PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
1335417-0	1992	Characterization of bradykinin B2 receptors on human IMR-90 lung fibroblasts: stimulation of 45Ca2+ efflux by D-Phe substituted bradykinin analogues.	D-phenylalanine	110-115	kininogen 1	Homo sapiens	20-30
1335417-1	1992	[3H]Bradykinin binds to intact human IMR-90 fetal lung fibroblasts in a time and dose-dependent manner.	Tritium	1-3	kininogen 1	Homo sapiens	4-14
1335417-2	1992	Binding equilibrium was attained by 120 minutes at 4 degrees C. [3H]Bradykinin binding was saturable; Scatchard analysis of saturation binding data demonstrated a single binding site having a KD = 1.8 +/- 0.2 nM and a receptor concentration of 17.4 +/- 4.0 fmol/10(5) cells.	Tritium	65-67	kininogen 1	Homo sapiens	68-78
1335417-8	1992	D-Phe7-substituted bradykinin analogues stimulated 45Ca2+ efflux dose dependently and this stimulation of 45Ca2+ efflux was inhibited by Hoe-140.	d-phe7	0-6	kininogen 1	Homo sapiens	19-29
1335417-9	1992	These results suggest that D-Phe7 substituted bradykinin analogues are agonists at the bradykinin B2 receptor in IMR-90 cells.	d-phe7	27-33	kininogen 1	Homo sapiens	46-56
1335417-9	1992	These results suggest that D-Phe7 substituted bradykinin analogues are agonists at the bradykinin B2 receptor in IMR-90 cells.	d-phe7	27-33	kininogen 1	Homo sapiens	87-97
1424001-11	1992	The difference in bradykinin-induced relaxations may reflect a prostaglandin metabolism in the gastroepiploic artery different from that in the left internal mammary artery.	Prostaglandins	63-76	kininogen 1	Homo sapiens	18-28
1452374-7	1992	Diltiazem also tended to decrease plasma bradykinin, thromboxane B2, and 6-keto-prostaglandin F1 alpha levels.	Diltiazem	0-9	kininogen 1	Homo sapiens	41-51
1452374-9	1992	Further, bradykinin was significantly decreased by diltiazem only in patients with exercise-induced silent ischemia or no exercise-induced ischemia, while the thromboxane B2/6-keto-prostaglandin F1 alpha ratio was unaffected by the administration of diltiazem.	Diltiazem	51-60	kininogen 1	Homo sapiens	9-19
1282721-0	1992	Effect of bradykinin on the cytosolic free calcium activity and phosphoinositol turnover in human glomerular epithelial cells.	Calcium	43-50	kininogen 1	Homo sapiens	10-20
1282721-0	1992	Effect of bradykinin on the cytosolic free calcium activity and phosphoinositol turnover in human glomerular epithelial cells.	phosphoinositol	64-79	kininogen 1	Homo sapiens	10-20
1282721-1	1992	The effect of bradykinin (BK) on the intracellular free calcium activity [Ca2+]i and phosphoinositide (PI) turnover was investigated in human glomerular epithelial cells (GEC) in culture.	Calcium	56-63	kininogen 1	Homo sapiens	14-24
1282721-1	1992	The effect of bradykinin (BK) on the intracellular free calcium activity [Ca2+]i and phosphoinositide (PI) turnover was investigated in human glomerular epithelial cells (GEC) in culture.	Calcium	56-63	kininogen 1	Homo sapiens	26-28
1282721-1	1992	The effect of bradykinin (BK) on the intracellular free calcium activity [Ca2+]i and phosphoinositide (PI) turnover was investigated in human glomerular epithelial cells (GEC) in culture.	Phosphatidylinositols	85-101	kininogen 1	Homo sapiens	14-24
1282721-1	1992	The effect of bradykinin (BK) on the intracellular free calcium activity [Ca2+]i and phosphoinositide (PI) turnover was investigated in human glomerular epithelial cells (GEC) in culture.	Phosphatidylinositols	85-101	kininogen 1	Homo sapiens	26-28
1282721-4	1992	The effect of BK (10(-8) mol/l) on the [Ca2+]i was inhibited by the BK2 antagonist Hoe 140 (IC50 10(-8) mol/l).	4-hydroxy-2-octenal	83-86	kininogen 1	Homo sapiens	14-16
1282721-6	1992	A transient increase in (1,4,5)-inositol-triphosphate (InsP3) formation from 1,445 +/- 119 to 4,629 +/- 323 cpm occurred after 5 s. Stimulation of protein kinase C (PKC) by short-term preincubation (15 min) of human GEC with phorbol-12-myristate-13-acetate (PMA) induced a dose-dependent inhibition of the BK-stimulated (10(-7) mol/l) inositol-phosphate formation.	(1,4,5)-inositol-triphosphate	24-53	kininogen 1	Homo sapiens	306-308
1417843-3	1992	Fibroblasts respond to bradykinin by large activations of phospholipase C and increases in [Ca2+]i in a manner that was abolished by D-Arg, [Hyp3,Thi5,8,D-Phe7]-bradykinin, thus indicating the presence of B2 kinin receptors.	D-Arginine	133-138	kininogen 1	Homo sapiens	23-33
1417843-3	1992	Fibroblasts respond to bradykinin by large activations of phospholipase C and increases in [Ca2+]i in a manner that was abolished by D-Arg, [Hyp3,Thi5,8,D-Phe7]-bradykinin, thus indicating the presence of B2 kinin receptors.	thi5	146-150	kininogen 1	Homo sapiens	23-33
1417843-3	1992	Fibroblasts respond to bradykinin by large activations of phospholipase C and increases in [Ca2+]i in a manner that was abolished by D-Arg, [Hyp3,Thi5,8,D-Phe7]-bradykinin, thus indicating the presence of B2 kinin receptors.	d-phe7	153-159	kininogen 1	Homo sapiens	23-33
1417843-3	1992	Fibroblasts respond to bradykinin by large activations of phospholipase C and increases in [Ca2+]i in a manner that was abolished by D-Arg, [Hyp3,Thi5,8,D-Phe7]-bradykinin, thus indicating the presence of B2 kinin receptors.	d-phe7	153-159	kininogen 1	Homo sapiens	161-171
1394917-17	1992	CONCLUSIONS: 1) The inhibition of ANF degradation causes sustained drop in left and right atrial pressures that appears to be mediated by an inhibition of neurohumoral activity; 2) concomitant inhibition of bradykinin breakdown (which in turn stimulates renal prostacyclin synthesis) contributes to natriuresis; 3) the close correlation between renal response and baseline cardiac index indicates that an inadequate renal perfusion secondary to low cardiac output diminishes the efficacy of this treatment modality.	Epoprostenol	260-272	kininogen 1	Homo sapiens	207-217
1464049-0	1992	Effect of topical application with capsaicin on skin responses to bradykinin and histamine in man.	Capsaicin	35-44	kininogen 1	Homo sapiens	66-76
1464049-3	1992	Capsaicin pre-treatment caused significant inhibition of the immediate mean flare responses (95% CI) to both bradykinin (from 51.5 [39.7-63.3] mm2 to 16.2 [8.0-24.5] mm2) (P < 0.01) and histamine (from 108.4 [80.4-136.4] mm2 to 52.3 [37.1-67.1] mm2) (P < 0.01).	Capsaicin	0-9	kininogen 1	Homo sapiens	109-119
1464049-3	1992	Capsaicin pre-treatment caused significant inhibition of the immediate mean flare responses (95% CI) to both bradykinin (from 51.5 [39.7-63.3] mm2 to 16.2 [8.0-24.5] mm2) (P < 0.01) and histamine (from 108.4 [80.4-136.4] mm2 to 52.3 [37.1-67.1] mm2) (P < 0.01).	Histamine	189-198	kininogen 1	Homo sapiens	109-119
1464049-5	1992	In addition, the effect of topical capsaicin was to completely inhibit the bradykinin induced weal response compared to control, the mean weal area (95% CI) being reduced from 13.4 (11.4-15.4) mm2 to 8.2 (5.3-11.0) mm2 (P < 0.01).	Capsaicin	35-44	kininogen 1	Homo sapiens	75-85
1464049-6	1992	Our findings show that repeated topical application with capsaicin led to a significant reduction of the skin responses to intradermal injections with both agonists, and particularly with bradykinin.	Capsaicin	57-66	kininogen 1	Homo sapiens	188-198
1464049-7	1992	The weal responsiveness to bradykinin may entirely follow neuropeptide release from sensory nerves within the skin and the same applies to the flare response, although this is not completely inhibited by topical application with capsaicin.	Capsaicin	229-238	kininogen 1	Homo sapiens	27-37
1453314-2	1992	Chlorpheniramine significantly attenuated the increase in cutaneous blood flow and erythema induced by bradykinin but not the weal response.	Chlorpheniramine	0-16	kininogen 1	Homo sapiens	103-113
1453314-4	1992	These results suggest that the cutaneous vasodilator effect of bradykinin is in part due to histamine release acting on histamine H1-receptors.	Histamine	92-101	kininogen 1	Homo sapiens	63-73
1479739-2	1992	BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK).	-arg9	54-59	kininogen 1	Homo sapiens	0-2
1479739-2	1992	BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK).	-arg9	54-59	kininogen 1	Homo sapiens	60-62
1479739-2	1992	BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK).	-arg9	54-59	kininogen 1	Homo sapiens	60-62
1479739-2	1992	BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK).	-arg9	54-59	kininogen 1	Homo sapiens	60-62
1479739-2	1992	BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK).	Bradykinin Fragment 1-7	75-91	kininogen 1	Homo sapiens	0-2
1479739-2	1992	BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK).	Arginine	55-58	kininogen 1	Homo sapiens	0-2
1479739-2	1992	BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK).	Arginine	55-58	kininogen 1	Homo sapiens	60-62
1479739-2	1992	BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK).	Arginine	55-58	kininogen 1	Homo sapiens	60-62
1479739-2	1992	BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK).	Arginine	55-58	kininogen 1	Homo sapiens	60-62
1479739-2	1992	BK, incubated with diluted plasma, was degraded to des-Arg9-BK (des-9-BK), des-Phe8-Arg9-BK (des-8,9-BK) and Arg-Pro-Pro-Gly-Phe ([1-5]BK).	pro-pro-gly-phe	113-128	kininogen 1	Homo sapiens	0-2
1479739-4	1992	D,L-2-Mercaptomethyl-3-guanidinoethyl-thiopropanoic acid inhibited the formation of des-9-BK from BK, whereas captopril inhibited the formation of des-8,9-BK from BK as well as that of [1-5]BK from des-9-BK or des-8,9-BK.	2-mercaptomethyl-3-guanidinoethylthiopropionic acid	0-56	kininogen 1	Homo sapiens	90-92
1479739-4	1992	D,L-2-Mercaptomethyl-3-guanidinoethyl-thiopropanoic acid inhibited the formation of des-9-BK from BK, whereas captopril inhibited the formation of des-8,9-BK from BK as well as that of [1-5]BK from des-9-BK or des-8,9-BK.	2-mercaptomethyl-3-guanidinoethylthiopropionic acid	0-56	kininogen 1	Homo sapiens	98-100
1479739-4	1992	D,L-2-Mercaptomethyl-3-guanidinoethyl-thiopropanoic acid inhibited the formation of des-9-BK from BK, whereas captopril inhibited the formation of des-8,9-BK from BK as well as that of [1-5]BK from des-9-BK or des-8,9-BK.	2-mercaptomethyl-3-guanidinoethylthiopropionic acid	0-56	kininogen 1	Homo sapiens	98-100
1479739-4	1992	D,L-2-Mercaptomethyl-3-guanidinoethyl-thiopropanoic acid inhibited the formation of des-9-BK from BK, whereas captopril inhibited the formation of des-8,9-BK from BK as well as that of [1-5]BK from des-9-BK or des-8,9-BK.	2-mercaptomethyl-3-guanidinoethylthiopropionic acid	0-56	kininogen 1	Homo sapiens	98-100
1479739-4	1992	D,L-2-Mercaptomethyl-3-guanidinoethyl-thiopropanoic acid inhibited the formation of des-9-BK from BK, whereas captopril inhibited the formation of des-8,9-BK from BK as well as that of [1-5]BK from des-9-BK or des-8,9-BK.	2-mercaptomethyl-3-guanidinoethylthiopropionic acid	0-56	kininogen 1	Homo sapiens	98-100
1479739-4	1992	D,L-2-Mercaptomethyl-3-guanidinoethyl-thiopropanoic acid inhibited the formation of des-9-BK from BK, whereas captopril inhibited the formation of des-8,9-BK from BK as well as that of [1-5]BK from des-9-BK or des-8,9-BK.	2-mercaptomethyl-3-guanidinoethylthiopropionic acid	0-56	kininogen 1	Homo sapiens	98-100
1479739-4	1992	D,L-2-Mercaptomethyl-3-guanidinoethyl-thiopropanoic acid inhibited the formation of des-9-BK from BK, whereas captopril inhibited the formation of des-8,9-BK from BK as well as that of [1-5]BK from des-9-BK or des-8,9-BK.	2-mercaptomethyl-3-guanidinoethylthiopropionic acid	0-56	kininogen 1	Homo sapiens	98-100
1479739-5	1992	The half lives of BK, des-9-BK, des-8,9-BK and [1-5]BK under the present experimental conditions were 60 min, 90 min, 14 min and 4.2 hr, respectively.	Diethylstilbestrol	22-25	kininogen 1	Homo sapiens	28-30
1479739-5	1992	The half lives of BK, des-9-BK, des-8,9-BK and [1-5]BK under the present experimental conditions were 60 min, 90 min, 14 min and 4.2 hr, respectively.	Diethylstilbestrol	22-25	kininogen 1	Homo sapiens	28-30
1479739-5	1992	The half lives of BK, des-9-BK, des-8,9-BK and [1-5]BK under the present experimental conditions were 60 min, 90 min, 14 min and 4.2 hr, respectively.	Diethylstilbestrol	22-25	kininogen 1	Homo sapiens	28-30
1479746-1	1992	The effects of hyaluronan (HA) on the release of arachidonic acid (AA) from phospholipids induced by bradykinin in synovial fibroblasts of osteoarthritic patients were examined.	Hyaluronic Acid	15-25	kininogen 1	Homo sapiens	101-111
1479746-1	1992	The effects of hyaluronan (HA) on the release of arachidonic acid (AA) from phospholipids induced by bradykinin in synovial fibroblasts of osteoarthritic patients were examined.	Hyaluronic Acid	27-29	kininogen 1	Homo sapiens	101-111
1479746-1	1992	The effects of hyaluronan (HA) on the release of arachidonic acid (AA) from phospholipids induced by bradykinin in synovial fibroblasts of osteoarthritic patients were examined.	Arachidonic Acid	49-65	kininogen 1	Homo sapiens	101-111
1479746-1	1992	The effects of hyaluronan (HA) on the release of arachidonic acid (AA) from phospholipids induced by bradykinin in synovial fibroblasts of osteoarthritic patients were examined.	Phospholipids	76-89	kininogen 1	Homo sapiens	101-111
1333726-0	1992	Bradykinin induces a B2 receptor-mediated calcium signal linked to prostanoid formation in human gingival fibroblasts in vitro.	Calcium	42-49	kininogen 1	Homo sapiens	0-10
1333726-0	1992	Bradykinin induces a B2 receptor-mediated calcium signal linked to prostanoid formation in human gingival fibroblasts in vitro.	Prostaglandins	67-77	kininogen 1	Homo sapiens	0-10
1333726-1	1992	The aim of the study was to determine the effect of bradykinin (BK) on the level of cytoplasmic-free Ca2+, [Ca2+]i, in human gingival fibroblasts and its relation to BK-induced prostanoid formation.	Prostaglandins	177-187	kininogen 1	Homo sapiens	52-62
1333726-1	1992	The aim of the study was to determine the effect of bradykinin (BK) on the level of cytoplasmic-free Ca2+, [Ca2+]i, in human gingival fibroblasts and its relation to BK-induced prostanoid formation.	Prostaglandins	177-187	kininogen 1	Homo sapiens	64-66
1333726-3	1992	The stimulatory effect of BK was seen in concentrations at or above 10(-8) M, with the most pronounced effect at 10(-6) M. D-Arg0-Hyp3-Thi5,8-DPhe7-BK, a BK B2 receptor antagonist, but not des-Arg9-Leu8-BK, a BK B1 receptor antagonist, blocked BK-induced rise in [Ca2+]i.	d-arg0-hyp3-thi5	123-139	kininogen 1	Homo sapiens	26-28
1333726-3	1992	The stimulatory effect of BK was seen in concentrations at or above 10(-8) M, with the most pronounced effect at 10(-6) M. D-Arg0-Hyp3-Thi5,8-DPhe7-BK, a BK B2 receptor antagonist, but not des-Arg9-Leu8-BK, a BK B1 receptor antagonist, blocked BK-induced rise in [Ca2+]i.	d-arg0-hyp3-thi5	123-139	kininogen 1	Homo sapiens	148-150
1333726-3	1992	The stimulatory effect of BK was seen in concentrations at or above 10(-8) M, with the most pronounced effect at 10(-6) M. D-Arg0-Hyp3-Thi5,8-DPhe7-BK, a BK B2 receptor antagonist, but not des-Arg9-Leu8-BK, a BK B1 receptor antagonist, blocked BK-induced rise in [Ca2+]i.	d-arg0-hyp3-thi5	123-139	kininogen 1	Homo sapiens	148-150
1333726-3	1992	The stimulatory effect of BK was seen in concentrations at or above 10(-8) M, with the most pronounced effect at 10(-6) M. D-Arg0-Hyp3-Thi5,8-DPhe7-BK, a BK B2 receptor antagonist, but not des-Arg9-Leu8-BK, a BK B1 receptor antagonist, blocked BK-induced rise in [Ca2+]i.	d-arg0-hyp3-thi5	123-139	kininogen 1	Homo sapiens	148-150
1333726-4	1992	The BK B2 receptor antagonist also significantly reduced BK-induced PGE2 formation.	Dinoprostone	68-72	kininogen 1	Homo sapiens	4-6
1333726-5	1992	When extracellular Ca2+ in the incubation medium was depleted, either by addition of EGTA or by omission of Ca2+ addition, BK still caused a significant stimulation of PGE2 formation.	Egtazic Acid	85-89	kininogen 1	Homo sapiens	123-125
1333726-5	1992	When extracellular Ca2+ in the incubation medium was depleted, either by addition of EGTA or by omission of Ca2+ addition, BK still caused a significant stimulation of PGE2 formation.	Dinoprostone	168-172	kininogen 1	Homo sapiens	123-125
1333726-6	1992	The calcium ionophores A23187 and ionomycin, similar to BK, caused a burst of PGE2 formation.	Ionomycin	34-43	kininogen 1	Homo sapiens	56-58
1333726-6	1992	The calcium ionophores A23187 and ionomycin, similar to BK, caused a burst of PGE2 formation.	Dinoprostone	78-82	kininogen 1	Homo sapiens	56-58
1333726-8	1992	The results indicate that BK-induced PGE2 formation in gingival fibroblasts is coupled to an increase in [Ca2+]i mediated by the BK B2 receptor, and which is independent of extracellular Ca2+.	Dinoprostone	37-41	kininogen 1	Homo sapiens	26-28
1330642-1	1992	The influence of an elevated level of cyclic AMP on the formation of nitric oxide was investigated in a neuronal cell line (108CC15; NG108-15), in which we had previously shown that nitric oxide mediates the activation of soluble guanylyl cyclase upon stimulation with the hormones bradykinin, endothelin, and serotonin.	Nitric Oxide	182-194	kininogen 1	Homo sapiens	282-292
1330642-2	1992	Maximal amplitude and duration of cyclic GMP response to bradykinin were about 2-fold greater in cells with cyclic AMP levels increased by forskolin pretreatment than in control cells with basal levels of cyclic AMP.	Cyclic AMP	108-118	kininogen 1	Homo sapiens	57-67
1330642-2	1992	Maximal amplitude and duration of cyclic GMP response to bradykinin were about 2-fold greater in cells with cyclic AMP levels increased by forskolin pretreatment than in control cells with basal levels of cyclic AMP.	Colforsin	139-148	kininogen 1	Homo sapiens	57-67
1330642-2	1992	Maximal amplitude and duration of cyclic GMP response to bradykinin were about 2-fold greater in cells with cyclic AMP levels increased by forskolin pretreatment than in control cells with basal levels of cyclic AMP.	Cyclic AMP	205-215	kininogen 1	Homo sapiens	57-67
1330642-3	1992	Phosphodiesterase inhibitors (isobutylmethylxanthine or M&B 22,948 (zaprinast)) similarly increased the maximal amplitude of the cyclic GMP response to bradykinin, but, in contrast, slowed down the decay phase of the cyclic GMP response to a much greater extent.	1-Methyl-3-isobutylxanthine	30-52	kininogen 1	Homo sapiens	156-166
1330642-3	1992	Phosphodiesterase inhibitors (isobutylmethylxanthine or M&B 22,948 (zaprinast)) similarly increased the maximal amplitude of the cyclic GMP response to bradykinin, but, in contrast, slowed down the decay phase of the cyclic GMP response to a much greater extent.	Acebutolol	56-61	kininogen 1	Homo sapiens	156-166
1330642-3	1992	Phosphodiesterase inhibitors (isobutylmethylxanthine or M&B 22,948 (zaprinast)) similarly increased the maximal amplitude of the cyclic GMP response to bradykinin, but, in contrast, slowed down the decay phase of the cyclic GMP response to a much greater extent.	zaprinast	72-81	kininogen 1	Homo sapiens	156-166
1330642-4	1992	The cyclic GMP responses to bradykinin were suppressed with the same potency by L-arginine analogues in control and in forskolin-treated cells (IC50 of NG-monomethyl-L-arginine 2 microM, of nitro-L-arginine 0.7 microM).	Arginine	80-90	kininogen 1	Homo sapiens	28-38
1330642-4	1992	The cyclic GMP responses to bradykinin were suppressed with the same potency by L-arginine analogues in control and in forskolin-treated cells (IC50 of NG-monomethyl-L-arginine 2 microM, of nitro-L-arginine 0.7 microM).	Colforsin	119-128	kininogen 1	Homo sapiens	28-38
1330642-4	1992	The cyclic GMP responses to bradykinin were suppressed with the same potency by L-arginine analogues in control and in forskolin-treated cells (IC50 of NG-monomethyl-L-arginine 2 microM, of nitro-L-arginine 0.7 microM).	omega-N-Methylarginine	152-176	kininogen 1	Homo sapiens	28-38
1330642-4	1992	The cyclic GMP responses to bradykinin were suppressed with the same potency by L-arginine analogues in control and in forskolin-treated cells (IC50 of NG-monomethyl-L-arginine 2 microM, of nitro-L-arginine 0.7 microM).	Nitroarginine	190-206	kininogen 1	Homo sapiens	28-38
1330642-5	1992	The transient rises of cyclic GMP levels induced by bradykinin and endothelin, which both cause release of Ca2+ from internal stores, were similarly enhanced by forskolin pretreatment.	Colforsin	161-170	kininogen 1	Homo sapiens	52-62
1511733-5	1992	Bradykinin-evoked [3H]inositol phosphate production was not affected by growth in high Zn2+.	[3h]inositol phosphate	18-40	kininogen 1	Homo sapiens	0-10
1335995-0	1992	Bradykinin and angiotensin II analogs containing a conformationally constrained proline analog.	Proline	80-87	kininogen 1	Homo sapiens	0-10
1335995-1	1992	Three analogs of bradykinin and one of angiotensin II have been prepared in which the naturally occurring proline residues have been replaced by the bicyclic amino acid, 2,4-methanoproline (2,4-MePro).	Proline	106-113	kininogen 1	Homo sapiens	17-27
1335995-1	1992	Three analogs of bradykinin and one of angiotensin II have been prepared in which the naturally occurring proline residues have been replaced by the bicyclic amino acid, 2,4-methanoproline (2,4-MePro).	bicyclic amino acid	149-168	kininogen 1	Homo sapiens	17-27
1335995-1	1992	Three analogs of bradykinin and one of angiotensin II have been prepared in which the naturally occurring proline residues have been replaced by the bicyclic amino acid, 2,4-methanoproline (2,4-MePro).	2,4-methanoproline	170-188	kininogen 1	Homo sapiens	17-27
1335995-1	1992	Three analogs of bradykinin and one of angiotensin II have been prepared in which the naturally occurring proline residues have been replaced by the bicyclic amino acid, 2,4-methanoproline (2,4-MePro).	2,4-methanoproline	190-199	kininogen 1	Homo sapiens	17-27
1335995-2	1992	The relative binding affinities for these analogs were determined to be significantly reduced in the cases of the three bradykinin analogs; [2,4-MePro3]-BK retains 1.3%, [2,4-MePro7]-BK retains 0.3% and [2,4-MePro2]-BK retains 0.021% of the binding affinity of bradykinin.	[2,4-mepro3]-bk	140-155	kininogen 1	Homo sapiens	120-130
1335995-2	1992	The relative binding affinities for these analogs were determined to be significantly reduced in the cases of the three bradykinin analogs; [2,4-MePro3]-BK retains 1.3%, [2,4-MePro7]-BK retains 0.3% and [2,4-MePro2]-BK retains 0.021% of the binding affinity of bradykinin.	2,4-mepro7]-bk	171-185	kininogen 1	Homo sapiens	120-130
1335995-2	1992	The relative binding affinities for these analogs were determined to be significantly reduced in the cases of the three bradykinin analogs; [2,4-MePro3]-BK retains 1.3%, [2,4-MePro7]-BK retains 0.3% and [2,4-MePro2]-BK retains 0.021% of the binding affinity of bradykinin.	[2,4-mepro2]-bk	203-218	kininogen 1	Homo sapiens	120-130
1279283-1	1992	Using a chemiluminescence method in the present study, we measured nitric oxide and one-electron oxidation products of nitric oxide (NOX) released from porcine coronary artery segments in response to bradykinin, ADP, and the calcium ionophore A23187.	Nitric Oxide	67-79	kininogen 1	Homo sapiens	200-210
1429767-3	1992	Ti and Si surfaces bound a-HMWK but no detectable amounts of a-fib, whereas the other metals bound both types of antisera.	Titanium	0-2	kininogen 1	Homo sapiens	27-31
1429767-3	1992	Ti and Si surfaces bound a-HMWK but no detectable amounts of a-fib, whereas the other metals bound both types of antisera.	Silicon	7-9	kininogen 1	Homo sapiens	27-31
1381726-7	1992	Lysylbradykinin was also degraded by NEP-24.11 (0.80 +/- 0.19 nmol/min per well); however, in the presence of phosphoramidon, AmM-mediated conversion to bradykinin (3.74 +/- 0.46 nmol/min per well) could be demonstrated.	phosphoramidon	110-124	kininogen 1	Homo sapiens	5-15
1512432-2	1992	Dose-response curves for bradykinin were constructed using the dorsal hand vein compliance technique in veins preconstricted with phenylephrine in 27 volunteers (16 male, 11 female) aged 18 to 81 years.	Phenylephrine	130-143	kininogen 1	Homo sapiens	25-35
1279283-1	1992	Using a chemiluminescence method in the present study, we measured nitric oxide and one-electron oxidation products of nitric oxide (NOX) released from porcine coronary artery segments in response to bradykinin, ADP, and the calcium ionophore A23187.	Nitric Oxide	119-131	kininogen 1	Homo sapiens	200-210
1279283-1	1992	Using a chemiluminescence method in the present study, we measured nitric oxide and one-electron oxidation products of nitric oxide (NOX) released from porcine coronary artery segments in response to bradykinin, ADP, and the calcium ionophore A23187.	Nitric Oxide	133-136	kininogen 1	Homo sapiens	200-210
1279283-4	1992	Bradykinin, ADP, and A23187 elicited vasorelaxation greater than that observed basally; A23187, but not bradykinin or ADP, caused additional release of NOX greater than that measured basally.	Nitric Oxide	152-155	kininogen 1	Homo sapiens	0-10
1279283-6	1992	We compared the amount of nitric oxide released under basal conditions and after stimulation with bradykinin, ADP, and A23187 with the amount of authentic nitric oxide necessary to elicit a bioequivalent response.	Nitric Oxide	26-38	kininogen 1	Homo sapiens	98-108
1375223-2	1992	We have previously characterized the calcium response of cultured human fibroblasts (HSWP cells) to stimulation by the mitogen Lys-bradykinin (BK).	Calcium	37-44	kininogen 1	Homo sapiens	131-141
1353791-6	1992	Similarly, culturing brain capillary ECs in the presence of aortic ECs increased their cGMP content in a manner that was amplified by bradykinin and that was inhibited by L-NG-monomethylarginine.	Cyclic GMP	87-91	kininogen 1	Homo sapiens	134-144
1284620-0	1992	Bradykinin inhibition of cyclic AMP accumulation in D384 astrocytoma cells.	Cyclic AMP	25-35	kininogen 1	Homo sapiens	0-10
1284620-2	1992	The present studies were performed in order to examine the possible role of cyclic GMP-stimulated phosphodiesterase (cGMP-PDE) activity in the inhibitory action of the inflammatory peptide bradykinin on cyclic AMP (cAMP) accumulation in D384 cells.	Cyclic AMP	203-213	kininogen 1	Homo sapiens	189-199
1284620-2	1992	The present studies were performed in order to examine the possible role of cyclic GMP-stimulated phosphodiesterase (cGMP-PDE) activity in the inhibitory action of the inflammatory peptide bradykinin on cyclic AMP (cAMP) accumulation in D384 cells.	Cyclic AMP	215-219	kininogen 1	Homo sapiens	189-199
1284620-3	1992	Bradykinin decreased the forskolin-stimulated cAMP accumulation in the presence of the phosphodiesterase inhibitor rolipram, and caused a transient 50% rise in cellular cGMP in the presence of the nonselective PDE inhibitor 3-isobutyl-1-methylxanthine (IBMX).	Colforsin	25-34	kininogen 1	Homo sapiens	0-10
1284620-3	1992	Bradykinin decreased the forskolin-stimulated cAMP accumulation in the presence of the phosphodiesterase inhibitor rolipram, and caused a transient 50% rise in cellular cGMP in the presence of the nonselective PDE inhibitor 3-isobutyl-1-methylxanthine (IBMX).	Cyclic AMP	46-50	kininogen 1	Homo sapiens	0-10
1284620-3	1992	Bradykinin decreased the forskolin-stimulated cAMP accumulation in the presence of the phosphodiesterase inhibitor rolipram, and caused a transient 50% rise in cellular cGMP in the presence of the nonselective PDE inhibitor 3-isobutyl-1-methylxanthine (IBMX).	Rolipram	115-123	kininogen 1	Homo sapiens	0-10
1284620-3	1992	Bradykinin decreased the forskolin-stimulated cAMP accumulation in the presence of the phosphodiesterase inhibitor rolipram, and caused a transient 50% rise in cellular cGMP in the presence of the nonselective PDE inhibitor 3-isobutyl-1-methylxanthine (IBMX).	Cyclic GMP	169-173	kininogen 1	Homo sapiens	0-10
1284620-3	1992	Bradykinin decreased the forskolin-stimulated cAMP accumulation in the presence of the phosphodiesterase inhibitor rolipram, and caused a transient 50% rise in cellular cGMP in the presence of the nonselective PDE inhibitor 3-isobutyl-1-methylxanthine (IBMX).	1-Methyl-3-isobutylxanthine	224-251	kininogen 1	Homo sapiens	0-10
1284620-3	1992	Bradykinin decreased the forskolin-stimulated cAMP accumulation in the presence of the phosphodiesterase inhibitor rolipram, and caused a transient 50% rise in cellular cGMP in the presence of the nonselective PDE inhibitor 3-isobutyl-1-methylxanthine (IBMX).	1-Methyl-3-isobutylxanthine	253-257	kininogen 1	Homo sapiens	0-10
1284620-4	1992	Both basal and bradykinin-stimulated cGMP accumulation were about 8 times higher in the presence of IBMX than in the presence of rolipram.	Cyclic GMP	37-41	kininogen 1	Homo sapiens	15-25
1284620-4	1992	Both basal and bradykinin-stimulated cGMP accumulation were about 8 times higher in the presence of IBMX than in the presence of rolipram.	1-Methyl-3-isobutylxanthine	100-104	kininogen 1	Homo sapiens	15-25
1284620-4	1992	Both basal and bradykinin-stimulated cGMP accumulation were about 8 times higher in the presence of IBMX than in the presence of rolipram.	Rolipram	129-137	kininogen 1	Homo sapiens	15-25
1284620-7	1992	The inhibitory effect of nitroprusside was totally reversed by blocking the soluble guanylate cyclase activity by methylene blue treatment; however, the inhibitory action of bradykinin on cAMP accumulation was not changed by this treatment.	Cyclic AMP	188-192	kininogen 1	Homo sapiens	174-184
1328896-2	1992	Addition of bradykinin to D384 cells resulted in a concentration-dependent (10(-11)-10(-6) M) increase in the accumulation of [3H]inositol phosphates and a similar concentration-dependent transient increase in specific [3H]beta-phorbol-12,13-dibutyrate binding which is indicative of translocation of protein kinase C from the cytosol to the membrane.	[3h]inositol phosphates	126-149	kininogen 1	Homo sapiens	12-22
1328896-2	1992	Addition of bradykinin to D384 cells resulted in a concentration-dependent (10(-11)-10(-6) M) increase in the accumulation of [3H]inositol phosphates and a similar concentration-dependent transient increase in specific [3H]beta-phorbol-12,13-dibutyrate binding which is indicative of translocation of protein kinase C from the cytosol to the membrane.	Tritium	127-129	kininogen 1	Homo sapiens	12-22
1328896-2	1992	Addition of bradykinin to D384 cells resulted in a concentration-dependent (10(-11)-10(-6) M) increase in the accumulation of [3H]inositol phosphates and a similar concentration-dependent transient increase in specific [3H]beta-phorbol-12,13-dibutyrate binding which is indicative of translocation of protein kinase C from the cytosol to the membrane.	beta-phorbol-12,13-dibutyrate	223-252	kininogen 1	Homo sapiens	12-22
1328896-3	1992	Changes in intracellular Ca2+ of single cells, measured using the fluorescent indicator dye fura-2, indicated that bradykinin produced a rapid, but transient, increase in intracellular calcium.	Fura-2	92-98	kininogen 1	Homo sapiens	115-125
1328896-3	1992	Changes in intracellular Ca2+ of single cells, measured using the fluorescent indicator dye fura-2, indicated that bradykinin produced a rapid, but transient, increase in intracellular calcium.	Calcium	185-192	kininogen 1	Homo sapiens	115-125
1328896-7	1992	The Ca2+ response to bradykinin could be partially reduced in the presence of the B2-receptor antagonist [D-Arg0-Hyp,D-Phe7,beta-(2-Thienyl)-Ala5,8]-bradykinin, whereas the B1-receptor agonists (Des-Arg9]-bradykinin and [Des-Arg10]-kallidin were ineffective.	d-arg0	106-112	kininogen 1	Homo sapiens	21-31
1328896-7	1992	The Ca2+ response to bradykinin could be partially reduced in the presence of the B2-receptor antagonist [D-Arg0-Hyp,D-Phe7,beta-(2-Thienyl)-Ala5,8]-bradykinin, whereas the B1-receptor agonists (Des-Arg9]-bradykinin and [Des-Arg10]-kallidin were ineffective.	d-arg0	106-112	kininogen 1	Homo sapiens	149-159
1328896-7	1992	The Ca2+ response to bradykinin could be partially reduced in the presence of the B2-receptor antagonist [D-Arg0-Hyp,D-Phe7,beta-(2-Thienyl)-Ala5,8]-bradykinin, whereas the B1-receptor agonists (Des-Arg9]-bradykinin and [Des-Arg10]-kallidin were ineffective.	d-arg0	106-112	kininogen 1	Homo sapiens	149-159
1328896-7	1992	The Ca2+ response to bradykinin could be partially reduced in the presence of the B2-receptor antagonist [D-Arg0-Hyp,D-Phe7,beta-(2-Thienyl)-Ala5,8]-bradykinin, whereas the B1-receptor agonists (Des-Arg9]-bradykinin and [Des-Arg10]-kallidin were ineffective.	des-arg10	221-230	kininogen 1	Homo sapiens	21-31
1328896-8	1992	Bradykinin was also found to attenuate dopamine stimulated cyclic AMP accumulation in D384 cells, at similar concentrations previously observed to stimulate the phospholipase C signal transduction pathway, in the presence of the phosphodiesterase inhibitor, rolipram.	Dopamine	39-47	kininogen 1	Homo sapiens	0-10
1328896-8	1992	Bradykinin was also found to attenuate dopamine stimulated cyclic AMP accumulation in D384 cells, at similar concentrations previously observed to stimulate the phospholipase C signal transduction pathway, in the presence of the phosphodiesterase inhibitor, rolipram.	Cyclic AMP	59-69	kininogen 1	Homo sapiens	0-10
1328896-8	1992	Bradykinin was also found to attenuate dopamine stimulated cyclic AMP accumulation in D384 cells, at similar concentrations previously observed to stimulate the phospholipase C signal transduction pathway, in the presence of the phosphodiesterase inhibitor, rolipram.	Rolipram	258-266	kininogen 1	Homo sapiens	0-10
1407558-2	1992	Prostaglandin I2 was applied intra-arterially close to the joint in doses of 0.3-30 micrograms per 0.3 ml bolus injection, and its effects on the spontaneous activity as well as on discharges evoked by mechanical and chemical stimulation (bradykinin) were monitored.	Epoprostenol	0-16	kininogen 1	Homo sapiens	239-249
1407558-7	1992	In 64% of 11 group III and 63% of eight group IV units studied the responses to bradykinin were enhanced by prostaglandin I2.	Epoprostenol	108-124	kininogen 1	Homo sapiens	80-90
1407558-12	1992	We conclude that prostaglandin I2 increases the sensitivity to mechanical stimuli as well as to chemical stimulation by bradykinin in the majority of articular group III and group IV fibers.	Epoprostenol	17-33	kininogen 1	Homo sapiens	120-130
1480537-1	1992	A double-blind, randomized, cross-over, placebo-controlled study was carried out to determine the extent and duration of potentiation of the action of bradykinin introduced intradermally by a long-acting novel angiotensin converting enzyme (ACE) inhibitor, trandolapril.	trandolapril	257-269	kininogen 1	Homo sapiens	151-161
1322838-4	1992	The effect of bradykinin is completely abolished in the presence of dimethylamiloride (100 mumol/l), which does not modify pHi in the absence of bradykinin.	5-dimethylamiloride	68-85	kininogen 1	Homo sapiens	14-24
1322838-8	1992	The effect of bradykinin on cell volume can be reversed by the reduction of extracellular NaCl concentration by 15 mmol/l NaCl in +ras cells and by 7 mmol/l NaCl in -ras cells.	Sodium Chloride	90-94	kininogen 1	Homo sapiens	14-24
1322838-8	1992	The effect of bradykinin on cell volume can be reversed by the reduction of extracellular NaCl concentration by 15 mmol/l NaCl in +ras cells and by 7 mmol/l NaCl in -ras cells.	Sodium Chloride	122-126	kininogen 1	Homo sapiens	14-24
1322838-8	1992	The effect of bradykinin on cell volume can be reversed by the reduction of extracellular NaCl concentration by 15 mmol/l NaCl in +ras cells and by 7 mmol/l NaCl in -ras cells.	Sodium Chloride	122-126	kininogen 1	Homo sapiens	14-24
1639798-7	1992	BK-stimulated formation of PGE2, derived from endogenous phospholipid, was decreased 60% by 5 microM PMC and eliminated by 50 microM PMC, compared with controls.	Dinoprostone	27-31	kininogen 1	Homo sapiens	0-2
1639798-7	1992	BK-stimulated formation of PGE2, derived from endogenous phospholipid, was decreased 60% by 5 microM PMC and eliminated by 50 microM PMC, compared with controls.	Phospholipids	57-69	kininogen 1	Homo sapiens	0-2
1616218-8	1992	The mechanism may involve accumulation of prostaglandins, kinins (such as bradykinin), or substance P (neurotransmitter present in respiratory tract C-fibers); both bradykinin and substance P are degraded by ACE.	Prostaglandins	42-56	kininogen 1	Homo sapiens	165-175
1330055-0	1992	On the signal transducing mechanisms involved in the synergistic interaction between interleukin-1 and bradykinin on prostaglandin biosynthesis in human gingival fibroblasts.	Prostaglandins	117-130	kininogen 1	Homo sapiens	103-113
1330055-1	1992	Recombinant human interleukin-1 beta (IL-1 beta) and bradykinin (BK) synergistically stimulate prostaglandin E2 (PGE2) formation in human gingival fibroblasts cultured for 24 h. Neither BK or IL-1 beta per se, nor their combinations, caused any acute stimulation of cellular cyclic AMP accumulation.	Dinoprostone	95-111	kininogen 1	Homo sapiens	53-63
1330055-1	1992	Recombinant human interleukin-1 beta (IL-1 beta) and bradykinin (BK) synergistically stimulate prostaglandin E2 (PGE2) formation in human gingival fibroblasts cultured for 24 h. Neither BK or IL-1 beta per se, nor their combinations, caused any acute stimulation of cellular cyclic AMP accumulation.	Dinoprostone	95-111	kininogen 1	Homo sapiens	65-67
1330055-1	1992	Recombinant human interleukin-1 beta (IL-1 beta) and bradykinin (BK) synergistically stimulate prostaglandin E2 (PGE2) formation in human gingival fibroblasts cultured for 24 h. Neither BK or IL-1 beta per se, nor their combinations, caused any acute stimulation of cellular cyclic AMP accumulation.	Dinoprostone	113-117	kininogen 1	Homo sapiens	53-63
1330055-1	1992	Recombinant human interleukin-1 beta (IL-1 beta) and bradykinin (BK) synergistically stimulate prostaglandin E2 (PGE2) formation in human gingival fibroblasts cultured for 24 h. Neither BK or IL-1 beta per se, nor their combinations, caused any acute stimulation of cellular cyclic AMP accumulation.	Dinoprostone	113-117	kininogen 1	Homo sapiens	65-67
1330055-1	1992	Recombinant human interleukin-1 beta (IL-1 beta) and bradykinin (BK) synergistically stimulate prostaglandin E2 (PGE2) formation in human gingival fibroblasts cultured for 24 h. Neither BK or IL-1 beta per se, nor their combinations, caused any acute stimulation of cellular cyclic AMP accumulation.	Cyclic AMP	275-285	kininogen 1	Homo sapiens	53-63
1330055-1	1992	Recombinant human interleukin-1 beta (IL-1 beta) and bradykinin (BK) synergistically stimulate prostaglandin E2 (PGE2) formation in human gingival fibroblasts cultured for 24 h. Neither BK or IL-1 beta per se, nor their combinations, caused any acute stimulation of cellular cyclic AMP accumulation.	Cyclic AMP	275-285	kininogen 1	Homo sapiens	65-67
1330055-2	1992	BK, but not IL-1 beta, caused a rapid, transient rise of intracellular Ca2+ concentration ([Ca2+]i), as assessed by recordings of fura-2 fluorescence in monolayers of prelabelled gingival fibroblasts.	Fura-2	130-136	kininogen 1	Homo sapiens	0-2
1420972-3	1992	The aromatic residues of substance P, bradykinin, and Des-Arg9 bradykinin all exhibited the 1-nm bathochromic shift in the presence of sodium dodecyl sulfate while those of Met-enkephalin did not.	Sodium Dodecyl Sulfate	135-157	kininogen 1	Homo sapiens	38-48
1420972-3	1992	The aromatic residues of substance P, bradykinin, and Des-Arg9 bradykinin all exhibited the 1-nm bathochromic shift in the presence of sodium dodecyl sulfate while those of Met-enkephalin did not.	Sodium Dodecyl Sulfate	135-157	kininogen 1	Homo sapiens	63-73
1461714-1	1992	Previous studies revealed that in NIH fibroblasts expressing the ras oncogene but not in other NIH fibroblasts, bradykinin leads to sustained, calcium dependent oscillations of cell membrane potential by repetitive activation of calcium-sensitive K+ channels.	Calcium	143-150	kininogen 1	Homo sapiens	112-122
1461714-10	1992	In conclusion, in cells expressing the ras oncogene bradykinin leads to sustained activation of calcium channels at the cell membrane, which cause oscillations of the cell membrane potential by triggering intracellular calcium release.	Calcium	96-103	kininogen 1	Homo sapiens	52-62
1321141-4	1992	The enzyme is active on furylacryloyl-Leu-Gly-Pro-Ala (FALGPA; pH optimum near 6.25), bradykinin (Bk), and several Bk-related peptides.	furylacryloyl-leu-gly-pro-ala	24-53	kininogen 1	Homo sapiens	98-100
1321141-4	1992	The enzyme is active on furylacryloyl-Leu-Gly-Pro-Ala (FALGPA; pH optimum near 6.25), bradykinin (Bk), and several Bk-related peptides.	Falgpa	55-61	kininogen 1	Homo sapiens	86-96
1321141-4	1992	The enzyme is active on furylacryloyl-Leu-Gly-Pro-Ala (FALGPA; pH optimum near 6.25), bradykinin (Bk), and several Bk-related peptides.	Falgpa	55-61	kininogen 1	Homo sapiens	98-100
1321141-7	1992	The shortest hydrolyzed peptide was FALGPA, the hydrolysis of which is strongly and competitively inhibited by Bk (Ki = 5.0 microM).	Falgpa	36-42	kininogen 1	Homo sapiens	111-113
1321141-11	1992	Since a Bk antagonist and a Bk-potentiating pentapeptide also were good substrates, it is possible that the enzyme hydrolyzes Bks and related peptides only because of the coincidental, specific amino acid sequence of those substrates.	Berkelium	126-129	kininogen 1	Homo sapiens	8-10
1321141-11	1992	Since a Bk antagonist and a Bk-potentiating pentapeptide also were good substrates, it is possible that the enzyme hydrolyzes Bks and related peptides only because of the coincidental, specific amino acid sequence of those substrates.	Berkelium	126-129	kininogen 1	Homo sapiens	28-30
1629199-9	1992	Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in the presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan.	Captopril	91-100	kininogen 1	Homo sapiens	0-10
1629199-9	1992	Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in the presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan.	Captopril	91-100	kininogen 1	Homo sapiens	153-163
1629199-9	1992	Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in the presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan.	Thiorphan	185-194	kininogen 1	Homo sapiens	0-10
1629199-9	1992	Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in the presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan.	Thiorphan	185-194	kininogen 1	Homo sapiens	153-163
1322053-1	1992	Previous data suggest that atrial natriuretic factor (ANF) and bradykinin (BK) interact to increase Na+ and water excretion.	Water	108-113	kininogen 1	Homo sapiens	63-73
1322053-1	1992	Previous data suggest that atrial natriuretic factor (ANF) and bradykinin (BK) interact to increase Na+ and water excretion.	Water	108-113	kininogen 1	Homo sapiens	75-77
1322053-7	1992	Because guanosine 3",5"-cyclic monophosphate (cGMP) and protein kinase C are implicated in the second messenger cascades of ANF and BK, we investigated their potential roles in mediating this interaction.	Cyclic GMP	8-44	kininogen 1	Homo sapiens	132-134
1322053-7	1992	Because guanosine 3",5"-cyclic monophosphate (cGMP) and protein kinase C are implicated in the second messenger cascades of ANF and BK, we investigated their potential roles in mediating this interaction.	Cyclic GMP	46-50	kininogen 1	Homo sapiens	132-134
1322053-8	1992	Dibutyryl-cGMP (10(-4) M) inhibited Isc from 33 +/- 4 to 22 +/- 3 microA/cm2 (P less than 0.05) in the presence of BK but not in its absence.	dibutyryl-cGMP	0-14	kininogen 1	Homo sapiens	115-117
1322053-9	1992	Staurosporine and calphostin C, inhibitors of protein kinase C, completely blocked the decrease in Isc caused by simultaneous addition of ANF and BK.	Staurosporine	0-13	kininogen 1	Homo sapiens	146-148
1322053-9	1992	Staurosporine and calphostin C, inhibitors of protein kinase C, completely blocked the decrease in Isc caused by simultaneous addition of ANF and BK.	calphostin C	18-30	kininogen 1	Homo sapiens	146-148
1330138-2	1992	In all cell types, bradykinin (1 nM-100 microM) caused significant time- and dose-dependent changes in the levels of inositol phosphates.	Inositol Phosphates	117-136	kininogen 1	Homo sapiens	19-29
1330138-3	1992	Neomycin inhibited the inositol phosphate response to bradykinin, while indomethacin had no effect.	Neomycin	0-8	kininogen 1	Homo sapiens	54-64
1330138-3	1992	Neomycin inhibited the inositol phosphate response to bradykinin, while indomethacin had no effect.	Inositol Phosphates	23-41	kininogen 1	Homo sapiens	54-64
1330138-4	1992	Bradykinin also elicited a dose-dependent increase in free cytosolic calcium concentration.	Calcium	69-76	kininogen 1	Homo sapiens	0-10
1330138-6	1992	Doses of des-Arg9-bradykinin, a B1 receptor agonist, up to 100 nM did not stimulate the osteoblastic inositol phosphate response.	-arg9	12-17	kininogen 1	Homo sapiens	18-28
1330138-7	1992	In addition, the bradykinin-stimulated inositol phosphate response was unaffected by des-Arg9-[Leu8]-bradykinin, a B1 receptor antagonist, while it was inhibited by D-Arg-[Hyp3-[beta-(2-thienyl)-Ala]5,8-D-Phe7]-bradykinin, a B2 receptor antagonist.	Inositol Phosphates	39-57	kininogen 1	Homo sapiens	17-27
1330138-8	1992	These results suggest that in osteoblastic cells the mechanism of action of bradykinin involves stimulation of the phosphoinositide metabolism and increases in cytosolic calcium levels through activation of B2 receptors.	Phosphatidylinositols	115-131	kininogen 1	Homo sapiens	76-86
1330138-8	1992	These results suggest that in osteoblastic cells the mechanism of action of bradykinin involves stimulation of the phosphoinositide metabolism and increases in cytosolic calcium levels through activation of B2 receptors.	Calcium	170-177	kininogen 1	Homo sapiens	76-86
1387041-5	1992	Bradykinin challenge induced mean maximal increases of 57%, 59%, 77% and 72% in NAR on the placebo, terfenadine, ipratropium bromide and terfenadine plus ipratropium bromide pretreatment days respectively.	Terfenadine	100-111	kininogen 1	Homo sapiens	0-10
1387041-5	1992	Bradykinin challenge induced mean maximal increases of 57%, 59%, 77% and 72% in NAR on the placebo, terfenadine, ipratropium bromide and terfenadine plus ipratropium bromide pretreatment days respectively.	Ipratropium	113-132	kininogen 1	Homo sapiens	0-10
1387041-5	1992	Bradykinin challenge induced mean maximal increases of 57%, 59%, 77% and 72% in NAR on the placebo, terfenadine, ipratropium bromide and terfenadine plus ipratropium bromide pretreatment days respectively.	Terfenadine	137-148	kininogen 1	Homo sapiens	0-10
1387041-5	1992	Bradykinin challenge induced mean maximal increases of 57%, 59%, 77% and 72% in NAR on the placebo, terfenadine, ipratropium bromide and terfenadine plus ipratropium bromide pretreatment days respectively.	Ipratropium	154-173	kininogen 1	Homo sapiens	0-10
1387041-8	1992	Bradykinin nasal challenge caused a mean maximal increase in albumin levels in recovered nasal lavages of 11.5, 13.0, 12.2 and 12.3 times of baseline levels on the placebo, terfenadine, ipratropium bromide and terfenadine plus ipratroprium bromide pretreatment days respectively.	Terfenadine	173-184	kininogen 1	Homo sapiens	0-10
1387041-8	1992	Bradykinin nasal challenge caused a mean maximal increase in albumin levels in recovered nasal lavages of 11.5, 13.0, 12.2 and 12.3 times of baseline levels on the placebo, terfenadine, ipratropium bromide and terfenadine plus ipratroprium bromide pretreatment days respectively.	Ipratropium	186-205	kininogen 1	Homo sapiens	0-10
1387041-8	1992	Bradykinin nasal challenge caused a mean maximal increase in albumin levels in recovered nasal lavages of 11.5, 13.0, 12.2 and 12.3 times of baseline levels on the placebo, terfenadine, ipratropium bromide and terfenadine plus ipratroprium bromide pretreatment days respectively.	Terfenadine	210-221	kininogen 1	Homo sapiens	0-10
1387041-8	1992	Bradykinin nasal challenge caused a mean maximal increase in albumin levels in recovered nasal lavages of 11.5, 13.0, 12.2 and 12.3 times of baseline levels on the placebo, terfenadine, ipratropium bromide and terfenadine plus ipratroprium bromide pretreatment days respectively.	ipratroprium bromide	227-247	kininogen 1	Homo sapiens	0-10
1333454-2	1992	[3H]BK binds to a single class of receptors on A431 cells in a saturable and reversible manner.	Tritium	1-3	kininogen 1	Homo sapiens	4-6
1437709-6	1992	Mantyl-bradykinin had excitation and fluorescence maxima at 350 nm and 426 nm in water and water/acetonitrile (ACN)/trifluoroacetic acid (TFA) solvent mixtures, respectively.	Water	81-86	kininogen 1	Homo sapiens	7-17
1437709-6	1992	Mantyl-bradykinin had excitation and fluorescence maxima at 350 nm and 426 nm in water and water/acetonitrile (ACN)/trifluoroacetic acid (TFA) solvent mixtures, respectively.	Water	91-96	kininogen 1	Homo sapiens	7-17
1437709-6	1992	Mantyl-bradykinin had excitation and fluorescence maxima at 350 nm and 426 nm in water and water/acetonitrile (ACN)/trifluoroacetic acid (TFA) solvent mixtures, respectively.	acetonitrile	97-109	kininogen 1	Homo sapiens	7-17
1437709-6	1992	Mantyl-bradykinin had excitation and fluorescence maxima at 350 nm and 426 nm in water and water/acetonitrile (ACN)/trifluoroacetic acid (TFA) solvent mixtures, respectively.	acn	111-114	kininogen 1	Homo sapiens	7-17
1437709-6	1992	Mantyl-bradykinin had excitation and fluorescence maxima at 350 nm and 426 nm in water and water/acetonitrile (ACN)/trifluoroacetic acid (TFA) solvent mixtures, respectively.	Trifluoroacetic Acid	116-136	kininogen 1	Homo sapiens	7-17
1437709-6	1992	Mantyl-bradykinin had excitation and fluorescence maxima at 350 nm and 426 nm in water and water/acetonitrile (ACN)/trifluoroacetic acid (TFA) solvent mixtures, respectively.	Trifluoroacetic Acid	138-141	kininogen 1	Homo sapiens	7-17
1508953-1	1992	Elevation of intracellular calcium in response to trypsin, bradykinin, thrombin or histamine is associated with a proportional increase in PGI2 production in cultured human umbilical vein endothelial cells (HUVEC), bovine pulmonary artery endothelial cells (CPAE), and bovine aortic endothelial cells (BAEC).	Calcium	27-34	kininogen 1	Homo sapiens	59-69
1508953-1	1992	Elevation of intracellular calcium in response to trypsin, bradykinin, thrombin or histamine is associated with a proportional increase in PGI2 production in cultured human umbilical vein endothelial cells (HUVEC), bovine pulmonary artery endothelial cells (CPAE), and bovine aortic endothelial cells (BAEC).	Epoprostenol	139-143	kininogen 1	Homo sapiens	59-69
1637084-2	1992	The mechanisms for CGRP release by low concentrations of capsaicin, electrical antidromic nerve stimulation, and bradykinin have several similar characteristics regarding sensitivity to TTX, CTX, and alpha 2-adrenoceptor activation.	Tetrodotoxin	186-189	kininogen 1	Homo sapiens	113-123
1318033-4	1992	Application of bradykinin after BHQ demonstrated that the BHQ-sensitive compartment partially overlapped the bradykinin-sensitive store.	2,5-di-tert-butylhydroquinone	58-61	kininogen 1	Homo sapiens	15-25
1318033-9	1992	Bradykinin-stimulated Ca2+ influx was increased at alkaline extracellular pH (pHo), and was inhibited by extracellular La3+, by depolarization of the membrane, and by the novel Ca(2+)-influx blocker 1-(beta-[3-(4-methoxyphenyl)propoxy]-4- methoxyphenethyl)-1H-imidazole hydrochloride (SKF 96365).	lanthanum(3+)	119-123	kininogen 1	Homo sapiens	0-10
1318033-9	1992	Bradykinin-stimulated Ca2+ influx was increased at alkaline extracellular pH (pHo), and was inhibited by extracellular La3+, by depolarization of the membrane, and by the novel Ca(2+)-influx blocker 1-(beta-[3-(4-methoxyphenyl)propoxy]-4- methoxyphenethyl)-1H-imidazole hydrochloride (SKF 96365).	1-(beta-[3-(4-methoxyphenyl)propoxy]-4- methoxyphenethyl)-1h-imidazole hydrochloride	199-283	kininogen 1	Homo sapiens	0-10
1318033-9	1992	Bradykinin-stimulated Ca2+ influx was increased at alkaline extracellular pH (pHo), and was inhibited by extracellular La3+, by depolarization of the membrane, and by the novel Ca(2+)-influx blocker 1-(beta-[3-(4-methoxyphenyl)propoxy]-4- methoxyphenethyl)-1H-imidazole hydrochloride (SKF 96365).	1,2,3,4-tetrahydroisoquinoline-7-sulfonamide	285-288	kininogen 1	Homo sapiens	0-10
1322819-1	1992	IMR90 human fetal lung fibroblasts express bradykinin receptors activating the pathway for biosynthesis of PGE2.	Dinoprostone	107-111	kininogen 1	Homo sapiens	43-53
1322819-2	1992	A receptor of the B2 subtype stimulates half-maximal PGE2 production at 4.8 nM bradykinin, and maximal output takes place at 25 nM bradykinin.	Dinoprostone	53-57	kininogen 1	Homo sapiens	79-89
1322819-3	1992	Radioligand binding studies reveal a population of [3H]bradykinin binding sites whose affinity correlates with this B2 receptor"s biologic activity, with a KD of 2.5 nM.	Tritium	52-54	kininogen 1	Homo sapiens	55-65
1322819-4	1992	As IMR90 cells reach 60% of their defined life span in culture, they spontaneously induce expression of a second site of lower affinity, with half-maximal binding of [3H]bradykinin at 44 nM.	Tritium	167-169	kininogen 1	Homo sapiens	170-180
1322819-8	1992	Expression of the second site changes the manner in which these fibroblasts control their PGE2 production; it affords a graded response of PGE2 production at bradykinin levels beyond those which would normally saturate the 2.5 nM site.	Dinoprostone	90-94	kininogen 1	Homo sapiens	158-168
1322819-8	1992	Expression of the second site changes the manner in which these fibroblasts control their PGE2 production; it affords a graded response of PGE2 production at bradykinin levels beyond those which would normally saturate the 2.5 nM site.	Dinoprostone	139-143	kininogen 1	Homo sapiens	158-168
1628727-0	1992	Repeated inhalation of bradykinin attenuates adenosine 5"-monophosphate (AMP) induced bronchoconstriction in asthmatic airways.	adenosine 5"-monophosphate	45-71	kininogen 1	Homo sapiens	23-33
1628727-0	1992	Repeated inhalation of bradykinin attenuates adenosine 5"-monophosphate (AMP) induced bronchoconstriction in asthmatic airways.	Adenosine Monophosphate	73-76	kininogen 1	Homo sapiens	23-33
1628727-2	1992	If adenosine 5"-monophosphate (AMP), another potent bronchoprovocant in asthma, and bradykinin share a common pathway in inducing bronchoconstriction in asthmatic subjects, then repeated bradykinin bronchoprovocation tests should reduce the response to subsequent inhalation of AMP.	Adenosine Monophosphate	31-34	kininogen 1	Homo sapiens	187-197
1628727-2	1992	If adenosine 5"-monophosphate (AMP), another potent bronchoprovocant in asthma, and bradykinin share a common pathway in inducing bronchoconstriction in asthmatic subjects, then repeated bradykinin bronchoprovocation tests should reduce the response to subsequent inhalation of AMP.	Adenosine Monophosphate	278-281	kininogen 1	Homo sapiens	84-94
1500097-1	1992	Contact of human plasma with a negatively charged surface such as dextran sulfate activates prekallikrein to kallikrein, which releases the vasoactive peptide bradykinin from high-molecular-weight kininogen.	Dextran Sulfate	66-81	kininogen 1	Homo sapiens	159-169
1500097-1	1992	Contact of human plasma with a negatively charged surface such as dextran sulfate activates prekallikrein to kallikrein, which releases the vasoactive peptide bradykinin from high-molecular-weight kininogen.	Dextran Sulfate	66-81	kininogen 1	Homo sapiens	175-206
1607246-5	1992	The results show that in the human ophthalmic artery, nitric oxide is released under basal conditions and that its production can be markedly stimulated by bradykinin, acetylcholine, and particularly histamine, which cause profound vascular relaxation.	Nitric Oxide	54-66	kininogen 1	Homo sapiens	156-166
1279283-10	1992	In contrast, omega-nitro-L-arginine methyl ester only partially reversed bradykinin-stimulated vasorelaxation.	NG-Nitroarginine Methyl Ester	13-48	kininogen 1	Homo sapiens	73-83
1583245-0	1992	Ibuprofen augments bradykinin-induced glycoconjugate secretion by human nasal mucosa in vivo.	Ibuprofen	0-9	kininogen 1	Homo sapiens	19-29
1583245-2	1992	Since some of the effects of BK may be mediated by autocrine generation of arachidonic acid metabolites, the influence of ibuprofen, a cyclooxygenase inhibitor, on BK-induced nasal secretion was studied.	Ibuprofen	122-131	kininogen 1	Homo sapiens	164-166
1583245-11	1992	Glycoconjugate secretion after ibuprofen treatment was significantly higher than normal at 10 nmol (p less than 0.05), 100 nmol (p less than 0.02), and 1000 nmol of BK (519 micrograms/ml +/- 74 versus 213 +/- 15 micrograms/ml; p less than 0.05).	Ibuprofen	31-40	kininogen 1	Homo sapiens	165-167
1583245-13	1992	Ibuprofen increases baseline secretion of glycoconjugate and enhances BK-induced glycoconjugate secretion.	Ibuprofen	0-9	kininogen 1	Homo sapiens	70-72
1317373-3	1992	To investigate the relative contribution of capsaicin-sensitive sensory neural stimulation to the action(s) of bradykinin, two randomized double-blind placebo-controlled studies have been undertaken comparing the nasal effects of single-dose administrations of bradykinin (1.88 x 10(-3) M) and capsaicin (3.28 x 10(-5) M).	Capsaicin	44-53	kininogen 1	Homo sapiens	111-121
1591276-0	1992	Bradykinin stimulates the production of prostaglandin E2 and interleukin-6 in human osteoblast-like cells.	Dinoprostone	40-56	kininogen 1	Homo sapiens	0-10
1591276-3	1992	However, BK stimulated the production of prostaglandin E2, an effect that was markedly enhanced by pre-incubation with recombinant interleukin-1 alpha (rhIL-1 alpha), but was apparently unaffected by BK receptor antagonists types 1 and 2.	Dinoprostone	41-57	kininogen 1	Homo sapiens	9-11
1591276-4	1992	Bradykinin stimulated the intracellular accumulation of total inositol phosphates suggesting that its effects were mediated by stimulation of phosphoinositide metabolism.	Inositol Phosphates	62-81	kininogen 1	Homo sapiens	0-10
1591276-4	1992	Bradykinin stimulated the intracellular accumulation of total inositol phosphates suggesting that its effects were mediated by stimulation of phosphoinositide metabolism.	Phosphatidylinositols	142-158	kininogen 1	Homo sapiens	0-10
1324051-2	1992	Bradykinin can release neuronal calcitonin gene-related peptide (CGRP) and adrenal medullary catecholamines, both of which could contribute to its cardiovascular effects in vivo.	Catecholamines	93-107	kininogen 1	Homo sapiens	0-10
1324051-20	1992	The results indicate that the increase in hindquarters blood flow following administration of bradykinin in vivo is largely due to activation of beta 2-adrenoceptors by catecholamines released subsequent to direct stimulation of the adrenal medulla by the peptide.	Catecholamines	169-183	kininogen 1	Homo sapiens	94-104
1562287-4	1992	In dextran sulfate-activated plasma, Neurotropin inhibited the formation of BK, the cleavage of high molecular weight kininogen (HK) and the formation of kallikrein-C1 inhibitor and activated coagulation factor XII (FXIIa)-C1 inhibitor complexes.	Dextran Sulfate	3-18	kininogen 1	Homo sapiens	76-78
1562287-4	1992	In dextran sulfate-activated plasma, Neurotropin inhibited the formation of BK, the cleavage of high molecular weight kininogen (HK) and the formation of kallikrein-C1 inhibitor and activated coagulation factor XII (FXIIa)-C1 inhibitor complexes.	Dextran Sulfate	3-18	kininogen 1	Homo sapiens	96-132
1558194-1	1992	Experiments were designed to study the effects of converting-enzyme inhibitors (captopril and S 10211) on the endothelium-dependent relaxation to bradykinin in isolated porcine arteries.	Captopril	80-89	kininogen 1	Homo sapiens	146-156
1558194-1	1992	Experiments were designed to study the effects of converting-enzyme inhibitors (captopril and S 10211) on the endothelium-dependent relaxation to bradykinin in isolated porcine arteries.	zabiciprilat	94-101	kininogen 1	Homo sapiens	146-156
1550208-6	1992	In amiloride-treated HNE, the electrical pattern of the BK-induced response was identical, but the magnitude of the Ieq was reduced by 54% and the change in Ieq could be abolished by removal of bath Cl-.	Amiloride	3-12	kininogen 1	Homo sapiens	56-58
1558194-7	1992	In the presence of indomethacin, the response to bradykinin was not modified and no potentiation from the inhibitor could be observed.	Indomethacin	19-31	kininogen 1	Homo sapiens	49-59
1550208-8	1992	We conclude that BK stimulates both Na+ absorption in untreated HNE and Cl- secretion in amiloride-treated HNE by activating a basolateral (K+) conductance.	Amiloride	89-98	kininogen 1	Homo sapiens	17-19
1536948-9	1992	Studies with 125I-light chain of HK showed that it specifically bound directly to platelets in the presence of zinc, since it was blocked by HK, light chain of HK, or EDTA, but not by LK, C1s, C1 inhibitor, plasmin, factor XIII, or fibrinogen.	Edetic Acid	167-171	kininogen 1	Homo sapiens	33-35
1318290-4	1992	Specificity of [3H]BK binding was confirmed by the ability of several BK peptide agonists and antagonists to inhibit binding in a dose dependent manner.	Tritium	16-18	kininogen 1	Homo sapiens	19-21
1572444-7	1992	For the whole group and for atopic subjects, there were significant correlations between the PC15 values for bradykinin and histamine (r = 0.82 and r = 0.85, respectively).	Histamine	124-133	kininogen 1	Homo sapiens	109-119
1318290-4	1992	Specificity of [3H]BK binding was confirmed by the ability of several BK peptide agonists and antagonists to inhibit binding in a dose dependent manner.	Tritium	16-18	kininogen 1	Homo sapiens	70-72
1318290-6	1992	The addition of BK to HSF caused a time and concentration dependent increase in PGE2 production.	Dinoprostone	80-84	kininogen 1	Homo sapiens	16-18
1318290-7	1992	This BK induced PGE2 production was blocked by specific B2 type BK antagonists and not by B1 antagonists.	Dinoprostone	16-20	kininogen 1	Homo sapiens	5-7
1318290-7	1992	This BK induced PGE2 production was blocked by specific B2 type BK antagonists and not by B1 antagonists.	Dinoprostone	16-20	kininogen 1	Homo sapiens	64-66
1627761-2	1992	Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins.	Nitric Oxide	179-191	kininogen 1	Homo sapiens	152-162
1521904-3	1992	Although the bradykinin concentration was markedly increased by passing the plasma through the column, this increment was suppressed by nafamostat mesilate which inhibits the initial contact phase of the intrinsic coagulation pathway.	nafamostat	136-155	kininogen 1	Homo sapiens	13-23
1627761-2	1992	Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins.	Prostaglandins	204-218	kininogen 1	Homo sapiens	152-162
1737988-0	1992	Bradykinin stimulates arachidonic acid release through the sequential actions of an sn-1 diacylglycerol lipase and a monoacylglycerol lipase.	Arachidonic Acid	22-38	kininogen 1	Homo sapiens	0-10
1737988-1	1992	In cultured dorsal root ganglion (DRG) neurons prelabeled with [3H]arachidonic acid [( 3H]AA), bradykinin (BK) stimulation resulted in increased levels of radioactive diacylglycerol, monoacylglycerol, and free AA.	[3h]arachidonic acid	63-83	kininogen 1	Homo sapiens	95-105
1737988-1	1992	In cultured dorsal root ganglion (DRG) neurons prelabeled with [3H]arachidonic acid [( 3H]AA), bradykinin (BK) stimulation resulted in increased levels of radioactive diacylglycerol, monoacylglycerol, and free AA.	[3h]arachidonic acid	63-83	kininogen 1	Homo sapiens	107-109
1737988-1	1992	In cultured dorsal root ganglion (DRG) neurons prelabeled with [3H]arachidonic acid [( 3H]AA), bradykinin (BK) stimulation resulted in increased levels of radioactive diacylglycerol, monoacylglycerol, and free AA.	Tritium	64-66	kininogen 1	Homo sapiens	95-105
1737988-1	1992	In cultured dorsal root ganglion (DRG) neurons prelabeled with [3H]arachidonic acid [( 3H]AA), bradykinin (BK) stimulation resulted in increased levels of radioactive diacylglycerol, monoacylglycerol, and free AA.	Tritium	64-66	kininogen 1	Homo sapiens	107-109
1737988-1	1992	In cultured dorsal root ganglion (DRG) neurons prelabeled with [3H]arachidonic acid [( 3H]AA), bradykinin (BK) stimulation resulted in increased levels of radioactive diacylglycerol, monoacylglycerol, and free AA.	Diglycerides	167-181	kininogen 1	Homo sapiens	95-105
1737988-1	1992	In cultured dorsal root ganglion (DRG) neurons prelabeled with [3H]arachidonic acid [( 3H]AA), bradykinin (BK) stimulation resulted in increased levels of radioactive diacylglycerol, monoacylglycerol, and free AA.	Diglycerides	167-181	kininogen 1	Homo sapiens	107-109
1737988-1	1992	In cultured dorsal root ganglion (DRG) neurons prelabeled with [3H]arachidonic acid [( 3H]AA), bradykinin (BK) stimulation resulted in increased levels of radioactive diacylglycerol, monoacylglycerol, and free AA.	Monoglycerides	183-199	kininogen 1	Homo sapiens	95-105
1737988-1	1992	In cultured dorsal root ganglion (DRG) neurons prelabeled with [3H]arachidonic acid [( 3H]AA), bradykinin (BK) stimulation resulted in increased levels of radioactive diacylglycerol, monoacylglycerol, and free AA.	Monoglycerides	183-199	kininogen 1	Homo sapiens	107-109
1737988-4	1992	BK stimulation resulted in a preferential increase in content of 1-stearoyl-2-arachidonoyl diacylglycerol.	1-stearoyl-2-arachidonoyl diacylglycerol	65-105	kininogen 1	Homo sapiens	0-2
1737988-5	1992	When DRG cultures were labeled with [3H]stearic acid, treatment with BK increased the amount of label in diacylglycerol and free stearic acid, but not in monoacylglycerol.	Tritium	36-39	kininogen 1	Homo sapiens	69-71
1737988-5	1992	When DRG cultures were labeled with [3H]stearic acid, treatment with BK increased the amount of label in diacylglycerol and free stearic acid, but not in monoacylglycerol.	stearic acid	40-52	kininogen 1	Homo sapiens	69-71
1737988-5	1992	When DRG cultures were labeled with [3H]stearic acid, treatment with BK increased the amount of label in diacylglycerol and free stearic acid, but not in monoacylglycerol.	Diglycerides	105-119	kininogen 1	Homo sapiens	69-71
1737988-5	1992	When DRG cultures were labeled with [3H]stearic acid, treatment with BK increased the amount of label in diacylglycerol and free stearic acid, but not in monoacylglycerol.	stearic acid	129-141	kininogen 1	Homo sapiens	69-71
1737988-5	1992	When DRG cultures were labeled with [3H]stearic acid, treatment with BK increased the amount of label in diacylglycerol and free stearic acid, but not in monoacylglycerol.	Monoglycerides	154-170	kininogen 1	Homo sapiens	69-71
1540646-8	1992	Hydrolysis of the substrate was strongly inhibited by bradykinin and those of its lower homologs that contain two adjacent proline residues.	Proline	123-130	kininogen 1	Homo sapiens	54-64
1631319-4	1992	However, after specific stimulation of prostaglandins with bradykinin (at normocalcic and isotonic conditions) a rigidification of plasma membranes was observed in living cells.	Prostaglandins	39-53	kininogen 1	Homo sapiens	59-69
1631319-5	1992	Fluidisation of membranes and bradykinin activate phospholipase A2 and induce prostaglandin synthesis.	Prostaglandins	78-91	kininogen 1	Homo sapiens	30-40
1555632-2	1992	Electrophysiological experiments revealed that in +ras fibroblasts but not in -ras fibroblasts, bradykinin leads to sustained, calcium-dependent oscillations of cell membrane potential by repetitive activation of calcium-sensitive K+ channels, resulting from oscillating intracellular calcium activity.	Calcium	127-134	kininogen 1	Homo sapiens	96-106
1544400-1	1992	The ability of (S)-alpha-methylproline (alpha-MePro) to stabilise reverse-turn conformations in the peptide hormone bradykinin (BK = Arg1-Pro2-Pro3-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9) has been investigated.	2-methylproline	40-51	kininogen 1	Homo sapiens	116-126
1606187-4	1992	Bradykinin had a stimulating effect on human and bovine endothelial cells and led to a threefold increase of nitrite/nitrate in endothelial cell column perfusates compared to those of unstimulated cells.	Nitrites	109-116	kininogen 1	Homo sapiens	0-10
1544400-0	1992	Beta-turns induced in bradykinin by (S)-alpha-methylproline.	2-methylproline	36-59	kininogen 1	Homo sapiens	22-32
1544400-1	1992	The ability of (S)-alpha-methylproline (alpha-MePro) to stabilise reverse-turn conformations in the peptide hormone bradykinin (BK = Arg1-Pro2-Pro3-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9) has been investigated.	2-methylproline	15-38	kininogen 1	Homo sapiens	116-126
1371395-3	1992	The flare evoked by bradykinin was abolished by pretreatment with lignocaine (local anesthetic), compound 48/80 (mast-cell histamine liberator), mepyramine (H1-receptor antagonist) and indomethacin (cyclo-oxygenase inhibitor) but was unaffected by atropine and ketanserin (serotonin antagonist).	Lidocaine	66-76	kininogen 1	Homo sapiens	20-30
1371395-3	1992	The flare evoked by bradykinin was abolished by pretreatment with lignocaine (local anesthetic), compound 48/80 (mast-cell histamine liberator), mepyramine (H1-receptor antagonist) and indomethacin (cyclo-oxygenase inhibitor) but was unaffected by atropine and ketanserin (serotonin antagonist).	Pyrilamine	145-155	kininogen 1	Homo sapiens	20-30
1599453-0	1992	Ion selectivity of Ba2+ inward current oscillations in ras-transformed fibroblasts that elicit cytoplasmic Ca2+ oscillations by bradykinin.	N-methyl-valyl-amiclenomycin	19-23	kininogen 1	Homo sapiens	128-138
1599453-2	1992	Application of bradykinin onto DT cells in 50 mM Ba2+ solution initiated Ba2+ inward current oscillations.	Thymidine	31-33	kininogen 1	Homo sapiens	15-25
1599453-2	1992	Application of bradykinin onto DT cells in 50 mM Ba2+ solution initiated Ba2+ inward current oscillations.	N-methyl-valyl-amiclenomycin	49-53	kininogen 1	Homo sapiens	15-25
1599453-2	1992	Application of bradykinin onto DT cells in 50 mM Ba2+ solution initiated Ba2+ inward current oscillations.	N-methyl-valyl-amiclenomycin	73-77	kininogen 1	Homo sapiens	15-25
1309839-0	1992	Human decidua is a target tissue for bradykinin and kallikrein: phosphoinositide hydrolysis accompanies arachidonic acid release in uterine decidua cells in vitro.	Phosphatidylinositols	64-80	kininogen 1	Homo sapiens	37-47
1309839-0	1992	Human decidua is a target tissue for bradykinin and kallikrein: phosphoinositide hydrolysis accompanies arachidonic acid release in uterine decidua cells in vitro.	Arachidonic Acid	104-120	kininogen 1	Homo sapiens	37-47
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	Arachidonic Acid	54-70	kininogen 1	Homo sapiens	0-10
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	Arachidonic Acid	54-70	kininogen 1	Homo sapiens	272-282
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	Arachidonic Acid	54-70	kininogen 1	Homo sapiens	327-337
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	inositol 1,2,3-trisphosphate	117-139	kininogen 1	Homo sapiens	0-10
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	inositol 1,2,3-trisphosphate	117-139	kininogen 1	Homo sapiens	272-282
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	inositol 1,2,3-trisphosphate	117-139	kininogen 1	Homo sapiens	327-337
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	Phorbol Esters	204-217	kininogen 1	Homo sapiens	0-10
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	Phorbol Esters	204-217	kininogen 1	Homo sapiens	272-282
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	Phorbol Esters	204-217	kininogen 1	Homo sapiens	327-337
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	Arachidonic Acid	227-243	kininogen 1	Homo sapiens	0-10
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	Calcimycin	306-312	kininogen 1	Homo sapiens	0-10
1309839-4	1992	Bradykinin (100 nmol/L) stimulated a rapid release of arachidonic acid (within 2 min) associated with an increase in inositol trisphosphate which was detectable after 20 s. Protein kinase C activation by phorbol ester enhanced arachidonic acid release in response to both bradykinin and the Ca++ ionophore A23187 but inhibited bradykinin-stimulated phosphoinositide hydrolysis.	Phosphatidylinositols	349-365	kininogen 1	Homo sapiens	0-10
1309839-5	1992	Epidermal growth factor also enhanced arachidonate release in response to both bradykinin and A23187.	Arachidonic Acid	38-50	kininogen 1	Homo sapiens	79-89
1309839-8	1992	Bradykinin also stimulated prostaglandin F2 alpha production in both primary decidua cell cultures and fibroblasts in the presence of interleukin-1 beta.	Dinoprost	27-49	kininogen 1	Homo sapiens	0-10
1309839-9	1992	These findings are consistent with a mediatory role for bradykinin in the action of kallikrein on decidua cells and suggest that inositol phospholipid hydrolysis is instrumental for arachidonic acid release in response to bradykinin in these cells.	Inositol	129-137	kininogen 1	Homo sapiens	222-232
1309839-9	1992	These findings are consistent with a mediatory role for bradykinin in the action of kallikrein on decidua cells and suggest that inositol phospholipid hydrolysis is instrumental for arachidonic acid release in response to bradykinin in these cells.	Phospholipids	138-150	kininogen 1	Homo sapiens	222-232
1309839-9	1992	These findings are consistent with a mediatory role for bradykinin in the action of kallikrein on decidua cells and suggest that inositol phospholipid hydrolysis is instrumental for arachidonic acid release in response to bradykinin in these cells.	Arachidonic Acid	182-198	kininogen 1	Homo sapiens	222-232
1620579-1	1992	In NIH fibroblasts expressing the ras oncogene bradykinin leads to sustained, calcium-dependent oscillations of cell membrane potential by oscillating activity of calcium sensitive potassium channels.	Calcium	78-85	kininogen 1	Homo sapiens	47-57
1371395-3	1992	The flare evoked by bradykinin was abolished by pretreatment with lignocaine (local anesthetic), compound 48/80 (mast-cell histamine liberator), mepyramine (H1-receptor antagonist) and indomethacin (cyclo-oxygenase inhibitor) but was unaffected by atropine and ketanserin (serotonin antagonist).	Indomethacin	185-197	kininogen 1	Homo sapiens	20-30
1371395-3	1992	The flare evoked by bradykinin was abolished by pretreatment with lignocaine (local anesthetic), compound 48/80 (mast-cell histamine liberator), mepyramine (H1-receptor antagonist) and indomethacin (cyclo-oxygenase inhibitor) but was unaffected by atropine and ketanserin (serotonin antagonist).	Atropine	248-256	kininogen 1	Homo sapiens	20-30
1371395-3	1992	The flare evoked by bradykinin was abolished by pretreatment with lignocaine (local anesthetic), compound 48/80 (mast-cell histamine liberator), mepyramine (H1-receptor antagonist) and indomethacin (cyclo-oxygenase inhibitor) but was unaffected by atropine and ketanserin (serotonin antagonist).	Ketanserin	261-271	kininogen 1	Homo sapiens	20-30
1371395-3	1992	The flare evoked by bradykinin was abolished by pretreatment with lignocaine (local anesthetic), compound 48/80 (mast-cell histamine liberator), mepyramine (H1-receptor antagonist) and indomethacin (cyclo-oxygenase inhibitor) but was unaffected by atropine and ketanserin (serotonin antagonist).	Serotonin	273-282	kininogen 1	Homo sapiens	20-30
1561233-0	1992	Interaction of paracrine factors during labour: interleukin-1 beta causes amplification of decidua cell prostaglandin F2 alpha production in response to bradykinin and epidermal growth factor.	Dinoprost	104-126	kininogen 1	Homo sapiens	153-163
1561233-2	1992	The aim of the present study is to investigate a potential interaction between interleukin-1 beta (IL-1) and bradykinin (BK) in the regulation of decidual PGF2 alpha production and PG precursor release.	Dinoprost	155-159	kininogen 1	Homo sapiens	109-119
1561233-2	1992	The aim of the present study is to investigate a potential interaction between interleukin-1 beta (IL-1) and bradykinin (BK) in the regulation of decidual PGF2 alpha production and PG precursor release.	Dinoprost	155-159	kininogen 1	Homo sapiens	121-123
1561233-2	1992	The aim of the present study is to investigate a potential interaction between interleukin-1 beta (IL-1) and bradykinin (BK) in the regulation of decidual PGF2 alpha production and PG precursor release.	Prostaglandins	155-157	kininogen 1	Homo sapiens	109-119
1561233-2	1992	The aim of the present study is to investigate a potential interaction between interleukin-1 beta (IL-1) and bradykinin (BK) in the regulation of decidual PGF2 alpha production and PG precursor release.	Prostaglandins	155-157	kininogen 1	Homo sapiens	121-123
1561233-3	1992	Pretreatment of primary decidua cell cultures with IL-1 significantly enhanced PGF2 alpha production in response to BK.	Dinoprost	79-83	kininogen 1	Homo sapiens	116-118
1561233-5	1992	Bradykinin also stimulated arachidonic acid release in decidual fibroblasts, an effect which was potentiated in the presence of epidermal growth factor (EGF), but which was not accompanied by an increase in PGF2 alpha production.	Arachidonic Acid	27-43	kininogen 1	Homo sapiens	0-10
1370482-4	1992	The okadaic acid-induced pattern of protein phosphorylation is distinct from that observed in cells treated with phorbol 12-myristate 13-acetate or with ligands like epidermal growth factor, cyclic AMP agonists, bradykinin, or interferons.	Okadaic Acid	4-16	kininogen 1	Homo sapiens	212-222
1739750-7	1992	Histamine, A23187 and bradykinin stimulated PGI2 synthesis in untreated but not in 2DG and OG treated cells.	Epoprostenol	44-48	kininogen 1	Homo sapiens	22-32
1309439-3	1992	Bradykinin stimulated a dose-dependent increase in inositol lipid hydrolysis and cytosolic Ca2+ levels in serum-starved fibroblasts derived from both normal and breast tumor tissue.	inositol lipid	51-65	kininogen 1	Homo sapiens	0-10
1309439-4	1992	Bradykinin also caused a dose-dependent decrease in cell growth and [3H]thymidine incorporation into DNA in breast fibroblasts.	Tritium	69-71	kininogen 1	Homo sapiens	0-10
1309439-7	1992	The binding of 125I-labeled EGF to fibroblasts was also inhibited by BK.	Iodine-125	15-19	kininogen 1	Homo sapiens	69-71
1309439-8	1992	Prostaglandin E2 also inhibited fibroblast DNA synthesis, and the cyclooxygenase inhibitor indomethacin partially reversed the inhibitory action of BK on DNA synthesis.	Indomethacin	91-103	kininogen 1	Homo sapiens	148-150
1309439-9	1992	Studies with BK receptor antagonists and agonists indicate that inositol lipid signalling and arachidonic acid mobilization in response to BK are B2 receptor-mediated pathways, whereas the inhibition of DNA synthesis appears to be via B1 receptors.	inositol lipid	64-78	kininogen 1	Homo sapiens	13-15
1309439-10	1992	Although these data support a role for prostaglandins and EGF receptor down-modulation in the inhibitory action of BK on DNA synthesis in breast fibroblasts, a B1 receptor-mediated pathway is also implicated.	Prostaglandins	39-53	kininogen 1	Homo sapiens	115-117
1531011-4	1992	It also produced hydrolysis at the Xaa-Phe, Xaa-Leu, or Xaa-Ile bonds of other peptide hormones such as bradykinin, somatostatin 14, litorin, substance P, neuromedin C and angiotensin II.	xanthenone-4-acetic acid	35-38	kininogen 1	Homo sapiens	104-114
1531011-4	1992	It also produced hydrolysis at the Xaa-Phe, Xaa-Leu, or Xaa-Ile bonds of other peptide hormones such as bradykinin, somatostatin 14, litorin, substance P, neuromedin C and angiotensin II.	Phenylalanine	39-42	kininogen 1	Homo sapiens	104-114
1620579-3	1992	In cells expressing the oncogene, but not in NIH fibroblasts not expressing the oncogene, bradykinin elicits calcium oscillations, which are detected by fura-2 fluorescence and amplified by a decrease of extracellular sodium activity.	Calcium	109-116	kininogen 1	Homo sapiens	90-100
1620579-3	1992	In cells expressing the oncogene, but not in NIH fibroblasts not expressing the oncogene, bradykinin elicits calcium oscillations, which are detected by fura-2 fluorescence and amplified by a decrease of extracellular sodium activity.	Fura-2	153-159	kininogen 1	Homo sapiens	90-100
1620579-3	1992	In cells expressing the oncogene, but not in NIH fibroblasts not expressing the oncogene, bradykinin elicits calcium oscillations, which are detected by fura-2 fluorescence and amplified by a decrease of extracellular sodium activity.	Sodium	218-224	kininogen 1	Homo sapiens	90-100
1620579-5	1992	It is concluded that in cells expressing the ras oncogene, bradykinin activates lanthanum sensitive calcium entry from the extracellular space.	Lanthanum	80-89	kininogen 1	Homo sapiens	59-69
1620579-5	1992	It is concluded that in cells expressing the ras oncogene, bradykinin activates lanthanum sensitive calcium entry from the extracellular space.	Calcium	100-107	kininogen 1	Homo sapiens	59-69
1620579-6	1992	Ras oncogene expression leads to enhanced bradykinin-induced formation of both, 1, 4, 5 inositoltrisphosphate and 1, 3, 4, 5 inositoltetrakisphosphate, an effect probably accounting for the oscillations of intracellular calcium activity.	1, 4, 5 inositoltrisphosphate	80-109	kininogen 1	Homo sapiens	42-52
1620579-6	1992	Ras oncogene expression leads to enhanced bradykinin-induced formation of both, 1, 4, 5 inositoltrisphosphate and 1, 3, 4, 5 inositoltetrakisphosphate, an effect probably accounting for the oscillations of intracellular calcium activity.	1, 3, 4, 5 inositoltetrakisphosphate	114-150	kininogen 1	Homo sapiens	42-52
1620579-6	1992	Ras oncogene expression leads to enhanced bradykinin-induced formation of both, 1, 4, 5 inositoltrisphosphate and 1, 3, 4, 5 inositoltetrakisphosphate, an effect probably accounting for the oscillations of intracellular calcium activity.	Calcium	220-227	kininogen 1	Homo sapiens	42-52
1595396-4	1992	The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes.	Evans Blue	87-97	kininogen 1	Homo sapiens	17-27
1317654-10	1992	By contrast, nanomolar concentrations of bradykinin, which increases Ca(2+)-levels and protein kinase C activity in D384 cells, reduced NECA-induced cyclic AMP accumulation in control and pertussis toxin-treated cells.	Adenosine-5'-(N-ethylcarboxamide)	136-140	kininogen 1	Homo sapiens	41-51
1317654-10	1992	By contrast, nanomolar concentrations of bradykinin, which increases Ca(2+)-levels and protein kinase C activity in D384 cells, reduced NECA-induced cyclic AMP accumulation in control and pertussis toxin-treated cells.	Cyclic AMP	149-159	kininogen 1	Homo sapiens	41-51
1281369-1	1992	Bradykinin stimulates Ca2+ entry in cultured human fibroblasts via nitrendipine-sensitive Ca2+ channels in cultured human fibroblasts.	Nitrendipine	67-79	kininogen 1	Homo sapiens	0-10
1281378-2	1992	Enalaprilat, moexiprilat and ramiprilat similarly potentiated the increase in [Ca2+]i elicited by bradykinin and caused an increase in resting [Ca2+]i when given alone.	Enalaprilat	0-11	kininogen 1	Homo sapiens	98-108
1281378-2	1992	Enalaprilat, moexiprilat and ramiprilat similarly potentiated the increase in [Ca2+]i elicited by bradykinin and caused an increase in resting [Ca2+]i when given alone.	moexiprilat	13-24	kininogen 1	Homo sapiens	98-108
1281378-2	1992	Enalaprilat, moexiprilat and ramiprilat similarly potentiated the increase in [Ca2+]i elicited by bradykinin and caused an increase in resting [Ca2+]i when given alone.	ramiprilat	29-39	kininogen 1	Homo sapiens	98-108
1334331-1	1992	Bradykinin (BK) is a weak stimulus for prostaglandin E2 (PGE2) release in untreated human synovial cells, but a potent stimulus in interleukin-1 (IL-1) pretreated cells.	Dinoprostone	39-55	kininogen 1	Homo sapiens	0-10
1334331-1	1992	Bradykinin (BK) is a weak stimulus for prostaglandin E2 (PGE2) release in untreated human synovial cells, but a potent stimulus in interleukin-1 (IL-1) pretreated cells.	Dinoprostone	39-55	kininogen 1	Homo sapiens	12-14
1334331-1	1992	Bradykinin (BK) is a weak stimulus for prostaglandin E2 (PGE2) release in untreated human synovial cells, but a potent stimulus in interleukin-1 (IL-1) pretreated cells.	Dinoprostone	57-61	kininogen 1	Homo sapiens	0-10
1334331-1	1992	Bradykinin (BK) is a weak stimulus for prostaglandin E2 (PGE2) release in untreated human synovial cells, but a potent stimulus in interleukin-1 (IL-1) pretreated cells.	Dinoprostone	57-61	kininogen 1	Homo sapiens	12-14
1334628-2	1992	In oocytes expressing the receptor, bradykinin-induced chloride current is blocked by [Thi5,8 dPhe7]BK and is unaffected by des-Arg9-BK suggesting that the cDNA encodes a classical B2 type receptor.	Chlorides	55-63	kininogen 1	Homo sapiens	36-46
1311688-2	1992	In contrast to the G protein-independent Ca2+ entry evoked by ionomycin or digitonin, bradykinin-induced Ca2+ influx was antagonized by Ni2+ with an IC50 value of about 50 microM.	Nickel(2+)	136-140	kininogen 1	Homo sapiens	86-96
1311688-4	1992	This conclusion is supported by our findings that inhibition of GTPase by mepacrine amplified bradykinin-stimulated Ca2+ influx, but did not interfere with the effect of the Ca2+ ionophore A23187.	Quinacrine	74-83	kininogen 1	Homo sapiens	94-104
1311688-5	1992	Similar to its effect on Ca2+ influx, mepacrine also potentiated endothelium-derived relaxing factor (EDRF) formation by bradykinin and sodium fluoride, but did not affect A23187-induced EDRF biosynthesis.	Quinacrine	38-47	kininogen 1	Homo sapiens	121-131
1334628-2	1992	In oocytes expressing the receptor, bradykinin-induced chloride current is blocked by [Thi5,8 dPhe7]BK and is unaffected by des-Arg9-BK suggesting that the cDNA encodes a classical B2 type receptor.	thi5	87-91	kininogen 1	Homo sapiens	36-46
1334628-2	1992	In oocytes expressing the receptor, bradykinin-induced chloride current is blocked by [Thi5,8 dPhe7]BK and is unaffected by des-Arg9-BK suggesting that the cDNA encodes a classical B2 type receptor.	dphe7	94-99	kininogen 1	Homo sapiens	36-46
1361094-0	1992	Proline-specific aminopeptidases: potential role in bradykinin degradation.	Proline	0-7	kininogen 1	Homo sapiens	52-62
1361094-1	1992	The N-terminus of bradykinin is shown to be sequentially degraded by the human proline-specific aminopeptidases aminopeptidase P (EC 3.4.11.9) and dipeptidyl peptidase IV (EC 3.4.14.5).	Proline	79-86	kininogen 1	Homo sapiens	18-28
1466276-1	1992	High molecular weight kininogen (HK) or its procoagulant light-chain but not the heavy chain potentiated the heparin enhancement of antithrombin III inactivation of plasma kallikrein and factor XIa from 10-50-fold to approximately 1000-fold at I 0.15, pH 7.4, 25 degrees C. This potentiation resulted in antithrombin becoming a predominant inhibitor of kallikrein and factor XIa in heparinized normal but not HK-deficient plasmas.	Heparin	109-116	kininogen 1	Homo sapiens	0-36
1462830-1	1992	The rate of high molecular weight kininogen cleavage in human plasma treated with dextran sulfate depends largely on the length of preincubation at 37 degrees C and the sample size during preincubation.	Dextran Sulfate	82-97	kininogen 1	Homo sapiens	12-43
1606187-4	1992	Bradykinin had a stimulating effect on human and bovine endothelial cells and led to a threefold increase of nitrite/nitrate in endothelial cell column perfusates compared to those of unstimulated cells.	Nitrates	117-124	kininogen 1	Homo sapiens	0-10
1531101-3	1992	Mobilization of intracellular Ca2+ stores with either inhibitor depleted intracellular Ca2+ and greatly reduced subsequent mobilization of the inositol 1,4,5-trisphosphate (IP3)-sensitive intracellular Ca2+ pool by bradykinin.	Inositol 1,4,5-Trisphosphate	143-171	kininogen 1	Homo sapiens	215-225
1531101-3	1992	Mobilization of intracellular Ca2+ stores with either inhibitor depleted intracellular Ca2+ and greatly reduced subsequent mobilization of the inositol 1,4,5-trisphosphate (IP3)-sensitive intracellular Ca2+ pool by bradykinin.	Inositol 1,4,5-Trisphosphate	173-176	kininogen 1	Homo sapiens	215-225
1531101-4	1992	However, bradykinin-induced mobilization of the IP3-sensitive intracellular Ca2+ pool only partially reduced the subsequent response of cells to TG and BHQ.	Inositol 1,4,5-Trisphosphate	48-51	kininogen 1	Homo sapiens	9-19
1466276-1	1992	High molecular weight kininogen (HK) or its procoagulant light-chain but not the heavy chain potentiated the heparin enhancement of antithrombin III inactivation of plasma kallikrein and factor XIa from 10-50-fold to approximately 1000-fold at I 0.15, pH 7.4, 25 degrees C. This potentiation resulted in antithrombin becoming a predominant inhibitor of kallikrein and factor XIa in heparinized normal but not HK-deficient plasmas.	Heparin	109-116	kininogen 1	Homo sapiens	33-35
1466276-2	1992	The heparin chain-length and salt dependence of this potentiation suggested an anticoagulant action of HK analogous to its procoagulant action.	Heparin	4-11	kininogen 1	Homo sapiens	103-105
1466276-2	1992	The heparin chain-length and salt dependence of this potentiation suggested an anticoagulant action of HK analogous to its procoagulant action.	Salts	29-33	kininogen 1	Homo sapiens	103-105
1609649-0	1992	Bradykinin modulation of the hydroosmotic effect of the antidiuretic hormone in water-transporting epithelia.	Water	80-85	kininogen 1	Homo sapiens	0-10
1609649-2	1992	Amongst them, considerable evidence suggests that the diuretic effects of endogenous bradykinin are, in part, mediated by inhibition of vasopressin-stimulated water transport.	Water	159-164	kininogen 1	Homo sapiens	85-95
1531101-7	1992	Extracellular Ca2+ entered the cell through an activated cation entry pathway, since bradykinin, TG, and BHQ stimulated Mn2+ and 45Ca2+ entry.	Manganese(2+)	120-124	kininogen 1	Homo sapiens	85-95
1554240-4	1992	One of the six analogs (B4642) inhibited bradykinin-induced pain with at least one concentration in all subjects tested.	b4642	24-29	kininogen 1	Homo sapiens	41-51
1377514-5	1992	The interactions between both SP and BK and SDS, based on nmr results, may be characterized as intrinsic, and the interaction between ME and SDS may be characterized as extrinsic.	Sodium Dodecyl Sulfate	44-47	kininogen 1	Homo sapiens	37-39
1377514-6	1992	Two-dimensional nuclear Overhauser enhancement spectroscopy experiments proved the insertion of the phenylalanine residues on both SP and BK into the hydrophobic core of SDS micelles.	Phenylalanine	100-113	kininogen 1	Homo sapiens	138-140
1377514-6	1992	Two-dimensional nuclear Overhauser enhancement spectroscopy experiments proved the insertion of the phenylalanine residues on both SP and BK into the hydrophobic core of SDS micelles.	Sodium Dodecyl Sulfate	170-173	kininogen 1	Homo sapiens	138-140
1377514-7	1992	The interaction between SP and BK with LPC based on nmr results are characterized as extrinsic, with the interaction between ME and SDS characterized as weakly intrinsic.	Lysophosphatidylcholines	39-42	kininogen 1	Homo sapiens	31-33
1341917-2	1992	We have fractionated the bradykinin inactivating activity of human urine by stepwise elution chromatography on DEAE-cellulose and recovered 95% of the inactivating activity and 29% of the protein (absorbance at A280 nm).	DEAE-Cellulose	111-125	kininogen 1	Homo sapiens	25-35
1341917-5	1992	Sites of hydrolysis in bradykinin were determined by HPLC of the hydrolysates and fragments were compared with authentic peptides.	Peptides	121-129	kininogen 1	Homo sapiens	23-33
1339590-8	1992	Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan.	Captopril	87-96	kininogen 1	Homo sapiens	0-10
1339590-8	1992	Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan.	Captopril	87-96	kininogen 1	Homo sapiens	149-159
1339590-8	1992	Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan.	Thiorphan	181-190	kininogen 1	Homo sapiens	0-10
1339590-8	1992	Bradykinin, a natural substrate of NEP, was in part metabolized by NEP, in presence of captopril, since 50% of the formation of the major metabolite bradykinin 1-7 was inhibited by thiorphan.	Thiorphan	181-190	kininogen 1	Homo sapiens	149-159
1728438-10	1992	Captopril, but not Ro 42-5892, increased forearm blood flow (2.4 +/- 0.8 versus 1.9 +/- 0.8 ml/min/100 ml, p less than 0.01) and significantly enhanced the increase of forearm blood flow to brachial artery infusions of bradykinin (0.15, 1.5, 5, 15, and 50 ng/min/100 ml; 5 minutes each) from 744 +/- 632% to 1,383 +/- 514% (p less than 0.01).	Captopril	0-9	kininogen 1	Homo sapiens	219-229
1728438-11	1992	Furthermore, repeat bradykinin infusions resulted in further decreases of blood pressure (from mean pressure of 71.4 +/- 8.5 to 63.2 +/- 7.6 mm Hg, p less than 0.01) only after captopril.	Captopril	177-186	kininogen 1	Homo sapiens	20-30
1728438-12	1992	Changes of blood pressure after captopril were unrelated to baseline plasma renin activity but correlated with captopril-induced enhancement of vasodilation to bradykinin (r = 0.68, p less than 0.05).	Captopril	32-41	kininogen 1	Homo sapiens	160-170
1728438-12	1992	Changes of blood pressure after captopril were unrelated to baseline plasma renin activity but correlated with captopril-induced enhancement of vasodilation to bradykinin (r = 0.68, p less than 0.05).	Captopril	111-120	kininogen 1	Homo sapiens	160-170
1333254-3	1992	Furthermore, the ACE inhibitor-induced augmentation of vascular PGI2 synthesis observed in vitro was completely inhibited by the competitive bradykinin antagonist D-Arg[Hyp3,Thi5,8,D-Phe7]bradykinin suggesting that ACE inhibitors stimulate PGI2 generation by an enhancement of kinin activity.	Epoprostenol	64-68	kininogen 1	Homo sapiens	141-151
1333254-3	1992	Furthermore, the ACE inhibitor-induced augmentation of vascular PGI2 synthesis observed in vitro was completely inhibited by the competitive bradykinin antagonist D-Arg[Hyp3,Thi5,8,D-Phe7]bradykinin suggesting that ACE inhibitors stimulate PGI2 generation by an enhancement of kinin activity.	Epoprostenol	64-68	kininogen 1	Homo sapiens	188-198
1333254-3	1992	Furthermore, the ACE inhibitor-induced augmentation of vascular PGI2 synthesis observed in vitro was completely inhibited by the competitive bradykinin antagonist D-Arg[Hyp3,Thi5,8,D-Phe7]bradykinin suggesting that ACE inhibitors stimulate PGI2 generation by an enhancement of kinin activity.	D-Arginine	163-168	kininogen 1	Homo sapiens	141-151
1333254-3	1992	Furthermore, the ACE inhibitor-induced augmentation of vascular PGI2 synthesis observed in vitro was completely inhibited by the competitive bradykinin antagonist D-Arg[Hyp3,Thi5,8,D-Phe7]bradykinin suggesting that ACE inhibitors stimulate PGI2 generation by an enhancement of kinin activity.	D-Arginine	163-168	kininogen 1	Homo sapiens	188-198
1333254-3	1992	Furthermore, the ACE inhibitor-induced augmentation of vascular PGI2 synthesis observed in vitro was completely inhibited by the competitive bradykinin antagonist D-Arg[Hyp3,Thi5,8,D-Phe7]bradykinin suggesting that ACE inhibitors stimulate PGI2 generation by an enhancement of kinin activity.	thi5	174-178	kininogen 1	Homo sapiens	141-151
1333254-3	1992	Furthermore, the ACE inhibitor-induced augmentation of vascular PGI2 synthesis observed in vitro was completely inhibited by the competitive bradykinin antagonist D-Arg[Hyp3,Thi5,8,D-Phe7]bradykinin suggesting that ACE inhibitors stimulate PGI2 generation by an enhancement of kinin activity.	thi5	174-178	kininogen 1	Homo sapiens	188-198
1333254-3	1992	Furthermore, the ACE inhibitor-induced augmentation of vascular PGI2 synthesis observed in vitro was completely inhibited by the competitive bradykinin antagonist D-Arg[Hyp3,Thi5,8,D-Phe7]bradykinin suggesting that ACE inhibitors stimulate PGI2 generation by an enhancement of kinin activity.	d-phe7	181-187	kininogen 1	Homo sapiens	141-151
1333254-3	1992	Furthermore, the ACE inhibitor-induced augmentation of vascular PGI2 synthesis observed in vitro was completely inhibited by the competitive bradykinin antagonist D-Arg[Hyp3,Thi5,8,D-Phe7]bradykinin suggesting that ACE inhibitors stimulate PGI2 generation by an enhancement of kinin activity.	d-phe7	181-187	kininogen 1	Homo sapiens	188-198
1333254-3	1992	Furthermore, the ACE inhibitor-induced augmentation of vascular PGI2 synthesis observed in vitro was completely inhibited by the competitive bradykinin antagonist D-Arg[Hyp3,Thi5,8,D-Phe7]bradykinin suggesting that ACE inhibitors stimulate PGI2 generation by an enhancement of kinin activity.	Epoprostenol	240-244	kininogen 1	Homo sapiens	141-151
1333254-3	1992	Furthermore, the ACE inhibitor-induced augmentation of vascular PGI2 synthesis observed in vitro was completely inhibited by the competitive bradykinin antagonist D-Arg[Hyp3,Thi5,8,D-Phe7]bradykinin suggesting that ACE inhibitors stimulate PGI2 generation by an enhancement of kinin activity.	Epoprostenol	240-244	kininogen 1	Homo sapiens	188-198
1351052-5	1992	Airway epithelial damage in asthma exposes sensory nerves which may become sensitized by inflammatory products (including prostaglandins and cytokines) so that neuropeptides are released via a local reflex trigger such as bradykinin, resulting in exaggerated inflammation.	Prostaglandins	122-136	kininogen 1	Homo sapiens	222-232
1282625-8	1992	All circulatory actions of bradykinin are not mediated by prostaglandins, since inhibition of prostaglandin synthesis by indomethacin (100-150 mg) was without any effect.	Indomethacin	121-133	kininogen 1	Homo sapiens	27-37
1282625-9	1992	ACE inhibition by ramipril (5 mg) or captopril (50 mg) potentiated all effects of bradykinin about 20- to 50-fold, whereas it decreased angiotensin I effects only about four- to fivefold.	Ramipril	18-26	kininogen 1	Homo sapiens	82-92
1282625-9	1992	ACE inhibition by ramipril (5 mg) or captopril (50 mg) potentiated all effects of bradykinin about 20- to 50-fold, whereas it decreased angiotensin I effects only about four- to fivefold.	Captopril	37-46	kininogen 1	Homo sapiens	82-92
1282628-8	1992	Also, the effects of bradykinin may be influenced by enhanced formation of prostaglandins and/or endothelium-derived relaxing factor (EDRF), which may contribute to the confusion.	Prostaglandins	75-89	kininogen 1	Homo sapiens	21-31
1282632-6	1992	Mechanical removal of the endothelium or incubation with nitro-L-arginine or the bradykinin2-receptor antagonist Hoe 140 prevented the relaxations to bradykinin and lisinopril.	4-hydroxy-2-octenal	113-116	kininogen 1	Homo sapiens	81-91
1282632-6	1992	Mechanical removal of the endothelium or incubation with nitro-L-arginine or the bradykinin2-receptor antagonist Hoe 140 prevented the relaxations to bradykinin and lisinopril.	Lisinopril	165-175	kininogen 1	Homo sapiens	81-91
1282632-8	1992	Endothelium-dependent relaxations to lisinopril were also observed in human coronary arteries treated with bradykinin (> or = 10(-7) M).	Lisinopril	37-47	kininogen 1	Homo sapiens	107-117
1282633-0	1992	Role of prostaglandins in the cardiovascular effects of bradykinin and angiotensin-converting enzyme inhibitors.	Prostaglandins	8-22	kininogen 1	Homo sapiens	56-66
1282633-3	1992	Eicosanoid generation by bradykinin is started by binding of the peptide to specific B2 receptors at the plasma membrane.	Eicosanoids	0-10	kininogen 1	Homo sapiens	25-35
1282633-11	1992	This also includes inhibition of polymorphonuclear leukocyte (PMN) accumulation in injured myocardial tissue, which is antagonized by PGI2-related pathways, stimulated by ACE inhibition and/or bradykinin.	Epoprostenol	134-138	kininogen 1	Homo sapiens	193-203
1282634-4	1992	In vitro studies demonstrate that the relaxations to bradykinin are mostly endothelium dependent and are mediated by nitric oxide, endothelium-derived hyperpolarizing factor, and/or vasodilator prostaglandins; however, these endothelium-derived relaxing factors do not always contribute simultaneously to the relaxations in every artery.	Nitric Oxide	117-129	kininogen 1	Homo sapiens	53-63
1282634-4	1992	In vitro studies demonstrate that the relaxations to bradykinin are mostly endothelium dependent and are mediated by nitric oxide, endothelium-derived hyperpolarizing factor, and/or vasodilator prostaglandins; however, these endothelium-derived relaxing factors do not always contribute simultaneously to the relaxations in every artery.	Prostaglandins	194-208	kininogen 1	Homo sapiens	53-63
1282939-0	1992	Bradykinin-induced, N omega-nitro-L-arginine-insensitive endothelium-dependent relaxation of porcine coronary arteries is not mediated by bioassayable relaxing substances.	Nitroarginine	20-44	kininogen 1	Homo sapiens	0-10
1282939-1	1992	The effect of the arginine analogue, N omega-nitro-L-arginine (L-NNA) was studied on bradykinin-induced relaxation in porcine coronary arteries.	Arginine	18-26	kininogen 1	Homo sapiens	85-95
1282939-1	1992	The effect of the arginine analogue, N omega-nitro-L-arginine (L-NNA) was studied on bradykinin-induced relaxation in porcine coronary arteries.	Nitroarginine	37-61	kininogen 1	Homo sapiens	85-95
1282939-1	1992	The effect of the arginine analogue, N omega-nitro-L-arginine (L-NNA) was studied on bradykinin-induced relaxation in porcine coronary arteries.	Nitroarginine	63-68	kininogen 1	Homo sapiens	85-95
1282939-3	1992	In contrast to the findings in organ chamber experiments, bradykinin-induced release of endothelium-derived relaxing factor(s) (EDRFs) was abolished after 45 min of treatment of perfused porcine coronary artery segments with L-NNA (10(-4) M) in a superfusion bioassay system.	Nitroarginine	225-230	kininogen 1	Homo sapiens	58-68
1282939-4	1992	These results show that, in addition to the release of nitric oxide, endothelium-dependent relaxation of porcine coronary arteries to bradykinin involves an alternative mechanism(s), which accounts for the relaxation in the presence of L-NNA.	Nitroarginine	236-241	kininogen 1	Homo sapiens	134-144
1309239-0	1992	The epithelial phenotype of human neuroblastoma cells express bradykinin, endothelin, and angiotensin II receptors that stimulate phosphoinositide hydrolysis.	Phosphatidylinositols	130-146	kininogen 1	Homo sapiens	62-72
1309239-5	1992	The effects of the three peptides--bradykinin, endothelin, and angiotensin II--on phosphoinositide hydrolysis in SH-EP cells were additive, a result suggesting that the three kinds of receptors may activate distinct transducer proteins and/or phospholipase C subtypes.	Phosphatidylinositols	82-98	kininogen 1	Homo sapiens	35-45
1389687-10	1992	Bradykinin antagonists could abrogate the calcium response to bradykinin but not to other peptides.	Calcium	42-49	kininogen 1	Homo sapiens	0-10
1531101-4	1992	However, bradykinin-induced mobilization of the IP3-sensitive intracellular Ca2+ pool only partially reduced the subsequent response of cells to TG and BHQ.	Thapsigargin	145-147	kininogen 1	Homo sapiens	9-19
1531101-4	1992	However, bradykinin-induced mobilization of the IP3-sensitive intracellular Ca2+ pool only partially reduced the subsequent response of cells to TG and BHQ.	2,5-di-tert-butylhydroquinone	152-155	kininogen 1	Homo sapiens	9-19
1462847-1	1992	In NIH-3T3 fibroblasts expressing the ras oncogene (+ras) bradykinin (BK) elicits sustained oscillations (1/min) of cell membrane potential (PD) due to oscillations of intracellular calcium activity with subsequent activation of calcium sensitive K+ channels.	Calcium	182-189	kininogen 1	Homo sapiens	58-68
1389687-10	1992	Bradykinin antagonists could abrogate the calcium response to bradykinin but not to other peptides.	Calcium	42-49	kininogen 1	Homo sapiens	62-72
1501139-4	1992	Bradykinin induced concentration- and endothelium-dependent relaxations and hyperpolarization in tissues contracted with prostaglandin F2 alpha.	Dinoprost	121-143	kininogen 1	Homo sapiens	0-10
1501139-6	1992	The threshold concentration of bradykinin was the same for the nitro-L-arginine-resistant relaxations and the membrane hyperpolarization.	Nitroarginine	63-79	kininogen 1	Homo sapiens	31-41
1501139-8	1992	Nitro-L-arginine-resistant relaxations were evoked by several agents (A23187, thrombin and UK 14304) in addition to bradykinin.	Nitroarginine	0-16	kininogen 1	Homo sapiens	116-126
1501139-11	1992	Thrombin caused more transient relaxations and hyperpolarizations than bradykinin in the presence of nitro-L-arginine.	Nitroarginine	101-117	kininogen 1	Homo sapiens	71-81
1501139-13	1992	In tissues contracted with high K+ or tetrabutylammonium (a non-selective K(+)-channel blocker), bradykinin inhibited the contractions in a concentration-dependent manner, whereas membrane hyperpolarization was not observed.	tetrabutylammonium	38-56	kininogen 1	Homo sapiens	97-107
1531690-8	1992	These differences between captopril and enalapril suggest that increases in tissue bradykinin and vasodilatory prostaglandins may play an important role in the beneficial effects of captopril.	Captopril	26-35	kininogen 1	Homo sapiens	83-93
1531690-8	1992	These differences between captopril and enalapril suggest that increases in tissue bradykinin and vasodilatory prostaglandins may play an important role in the beneficial effects of captopril.	Enalapril	40-49	kininogen 1	Homo sapiens	83-93
1531690-8	1992	These differences between captopril and enalapril suggest that increases in tissue bradykinin and vasodilatory prostaglandins may play an important role in the beneficial effects of captopril.	Captopril	182-191	kininogen 1	Homo sapiens	83-93
1304876-1	1992	The histidine-glycine-rich region of the light chain of cleaved high molecular weight kininogen (HK) is thought to be responsible for binding to negatively charged surfaces and initiation of the intrinsic coagulation, fibrinolytic, and kinin-forming systems.	Histidine	4-13	kininogen 1	Homo sapiens	64-95
1462847-1	1992	In NIH-3T3 fibroblasts expressing the ras oncogene (+ras) bradykinin (BK) elicits sustained oscillations (1/min) of cell membrane potential (PD) due to oscillations of intracellular calcium activity with subsequent activation of calcium sensitive K+ channels.	Calcium	182-189	kininogen 1	Homo sapiens	70-72
1462848-0	1992	Regulation of bradykinin-induced chloride secretion in a human epithelial cell line.	Chlorides	33-41	kininogen 1	Homo sapiens	14-24
1462848-1	1992	The chloride secretory response to bradykinin in T84 cells is regulated.	Chlorides	4-12	kininogen 1	Homo sapiens	35-45
1462860-2	1992	Captopril enhanced BK release, but did not suppress the increase of AII release.	Captopril	0-9	kininogen 1	Homo sapiens	19-21
1462860-5	1992	These results suggest that cardioprotective effect of captopril might be dependent on local BK accumulation, but not on suppression of local AII generation.	Captopril	54-63	kininogen 1	Homo sapiens	92-94
1462875-0	1992	CP-0127, a novel potent bradykinin antagonist, increases survival in rat and rabbit models of endotoxin shock.	deltibant	0-7	kininogen 1	Homo sapiens	24-34
1462875-1	1992	The bradykinin antagonist dimer CP-0127 was found to be a potent and selective inhibitor of the depressor response to bradykinin in the anaesthetized rat and rabbit.	deltibant	32-39	kininogen 1	Homo sapiens	4-14
1462875-1	1992	The bradykinin antagonist dimer CP-0127 was found to be a potent and selective inhibitor of the depressor response to bradykinin in the anaesthetized rat and rabbit.	deltibant	32-39	kininogen 1	Homo sapiens	118-128
1462875-6	1992	The results of these experiments provide evidence for a significant role for the kallikrein-kinin system in these models of endotoxic shock, and indicate the therapeutic potential of a bradykinin antagonist such as CP-0127 for treating this disorder in man.	deltibant	215-222	kininogen 1	Homo sapiens	185-195
1304876-1	1992	The histidine-glycine-rich region of the light chain of cleaved high molecular weight kininogen (HK) is thought to be responsible for binding to negatively charged surfaces and initiation of the intrinsic coagulation, fibrinolytic, and kinin-forming systems.	Glycine	14-21	kininogen 1	Homo sapiens	64-95
1403848-1	1992	We have examined the ability of recombinant human epidermal growth factor (EGF) and bradykinin (BK) to stimulate formation of inositol polyphosphates and sn-1,2-diacylglycerol (DAG), and mobilize intracellular Ca2+ ([Ca2+]i) in adult human keratinocytes (KC).	inositol polyphosphates	126-149	kininogen 1	Homo sapiens	84-94
1403848-1	1992	We have examined the ability of recombinant human epidermal growth factor (EGF) and bradykinin (BK) to stimulate formation of inositol polyphosphates and sn-1,2-diacylglycerol (DAG), and mobilize intracellular Ca2+ ([Ca2+]i) in adult human keratinocytes (KC).	inositol polyphosphates	126-149	kininogen 1	Homo sapiens	96-98
1403848-1	1992	We have examined the ability of recombinant human epidermal growth factor (EGF) and bradykinin (BK) to stimulate formation of inositol polyphosphates and sn-1,2-diacylglycerol (DAG), and mobilize intracellular Ca2+ ([Ca2+]i) in adult human keratinocytes (KC).	sn-1,2-diacylglycerol	154-175	kininogen 1	Homo sapiens	84-94
1403848-1	1992	We have examined the ability of recombinant human epidermal growth factor (EGF) and bradykinin (BK) to stimulate formation of inositol polyphosphates and sn-1,2-diacylglycerol (DAG), and mobilize intracellular Ca2+ ([Ca2+]i) in adult human keratinocytes (KC).	sn-1,2-diacylglycerol	154-175	kininogen 1	Homo sapiens	96-98
1403848-1	1992	We have examined the ability of recombinant human epidermal growth factor (EGF) and bradykinin (BK) to stimulate formation of inositol polyphosphates and sn-1,2-diacylglycerol (DAG), and mobilize intracellular Ca2+ ([Ca2+]i) in adult human keratinocytes (KC).	dag	177-180	kininogen 1	Homo sapiens	96-98
1403848-8	1992	Treatment of cells with pertussis toxin (PTX) for 24 h significantly attenuated the BK-stimulated inositol polyphosphate formation and [Ca2+]i while the EGF response remained unaffected in both parameters.	4'-demethylepipodophyllotoxin	34-39	kininogen 1	Homo sapiens	84-86
1403848-8	1992	Treatment of cells with pertussis toxin (PTX) for 24 h significantly attenuated the BK-stimulated inositol polyphosphate formation and [Ca2+]i while the EGF response remained unaffected in both parameters.	Phytic Acid	98-120	kininogen 1	Homo sapiens	84-86
1403848-10	1992	These results demonstrate that the coupling and biochemical signals produced by stimulation of BK and EGF receptors in human KC are different and suggests that stimulation of second messenger formation from inositol lipid hydrolysis may not be an absolute requirement for the initiation of cell proliferation.	inositol lipid	207-221	kininogen 1	Homo sapiens	95-97
1794204-6	1991	The glomerular endothelial cells responded to the calcium-mobilizing agonists bradykinin, ATP, thrombin and platelet activating factor with a significant rise in cytosolic calcium concentrations.	Calcium	50-57	kininogen 1	Homo sapiens	78-88
1767868-9	1991	The reduced responses of CF cells to bradykinin and methacholine, in addition to isoproterenol, suggest that both Ca-dependent and adenosine 3",5"-cyclic monophosphate-dependent regulation of Cl secretion are defective in CF tracheobronchial glands.	Cyclic AMP	131-167	kininogen 1	Homo sapiens	37-47
1768563-17	1991	Furthermore, that endogenous bradykinin production after enalapril pretreatment either never reaches the supraphysiological concentrations used in previous experiments, or that bradykinin is rapidly and effectively broken down to inactive peptides by other carboxypeptidase enzymes.	Enalapril	57-66	kininogen 1	Homo sapiens	29-39
1752117-1	1991	Pain and hyperalgesia, the perceptual campanions of tissue injury and inflammation, are thought to be in part attributable to the sensitization of primary afferent nociceptors by endogenously released chemicals, such as bradykinin.	campanions	38-48	kininogen 1	Homo sapiens	220-230
1794204-6	1991	The glomerular endothelial cells responded to the calcium-mobilizing agonists bradykinin, ATP, thrombin and platelet activating factor with a significant rise in cytosolic calcium concentrations.	Calcium	172-179	kininogen 1	Homo sapiens	78-88
1661707-3	1991	The effects of both IL-1 alpha and IL-1 beta on PGE2 biosynthesis was synergistically potentiated by BK, in a dose-related manner.	Dinoprostone	48-52	kininogen 1	Homo sapiens	101-103
1661707-4	1991	The synergistic interaction between IL-1 beta and BK on PGE2 production was seen both with B1 (des-Arg9-BK) and B2 (BK, Lys-BK) BK receptor agonists.	Dinoprostone	56-60	kininogen 1	Homo sapiens	50-52
1661707-4	1991	The synergistic interaction between IL-1 beta and BK on PGE2 production was seen both with B1 (des-Arg9-BK) and B2 (BK, Lys-BK) BK receptor agonists.	Dinoprostone	56-60	kininogen 1	Homo sapiens	104-106
1661707-4	1991	The synergistic interaction between IL-1 beta and BK on PGE2 production was seen both with B1 (des-Arg9-BK) and B2 (BK, Lys-BK) BK receptor agonists.	Dinoprostone	56-60	kininogen 1	Homo sapiens	104-106
1661707-4	1991	The synergistic interaction between IL-1 beta and BK on PGE2 production was seen both with B1 (des-Arg9-BK) and B2 (BK, Lys-BK) BK receptor agonists.	Dinoprostone	56-60	kininogen 1	Homo sapiens	104-106
1661707-6	1991	These data suggest that BK and IL-1 act in concert to enhance prostanoid formation in inflammatory lesions and that the level of interaction is distal to phospholipase activity.	Prostaglandins	62-72	kininogen 1	Homo sapiens	24-26
1819708-7	1991	Diltiazem also inhibited bradykinin (10(-8) M) induced PAF synthesis.	Diltiazem	0-9	kininogen 1	Homo sapiens	25-35
1687595-1	1991	Acylation of the N-terminus of [D-Arg0, Hyp3, Thi5,8, D-Phe7] bradykinin with 1-adamantanecarboxylic acid results in an analogue with enhanced potency of at least 33-fold.	[d-arg0	31-38	kininogen 1	Homo sapiens	62-72
1687595-1	1991	Acylation of the N-terminus of [D-Arg0, Hyp3, Thi5,8, D-Phe7] bradykinin with 1-adamantanecarboxylic acid results in an analogue with enhanced potency of at least 33-fold.	adamantanecarboxylic acid	78-105	kininogen 1	Homo sapiens	62-72
1939151-0	1991	Des-Arg9 bradykinin modulates DNA synthesis, phospholipase C, and protein kinase C in cultured mesangial cells.	des-arg9	0-8	kininogen 1	Homo sapiens	9-19
1763597-1	1991	Heparin has been suggested as an activator of the plasma kallikrein-kinin system, with possible formation of bradykinin, a potent vasodilator.	Heparin	0-7	kininogen 1	Homo sapiens	109-119
1810149-0	1991	Action of bradykinin at the cyclooxygenase step in prostanoid synthesis through the arachidonic acid cascade.	Prostaglandins	51-61	kininogen 1	Homo sapiens	10-20
1810149-0	1991	Action of bradykinin at the cyclooxygenase step in prostanoid synthesis through the arachidonic acid cascade.	Arachidonic Acid	84-100	kininogen 1	Homo sapiens	10-20
1810149-1	1991	Bradykinin enhances prostanoid synthesis in aorta smooth muscle cells.	Prostaglandins	20-30	kininogen 1	Homo sapiens	0-10
1810149-2	1991	Free arachidonic acid also enhances prostanoid synthesis and bradykinin, unlike fatty acid releasing agents, has a synergistic effect with free arachidonic acid.	Arachidonic Acid	5-21	kininogen 1	Homo sapiens	61-71
1810149-2	1991	Free arachidonic acid also enhances prostanoid synthesis and bradykinin, unlike fatty acid releasing agents, has a synergistic effect with free arachidonic acid.	Arachidonic Acid	144-160	kininogen 1	Homo sapiens	61-71
1810149-3	1991	Bradykinin promotes metabolite release from cells prelabeled with [14C]-arachidonic acid and this effect is blocked completely by indomethacin.	[14c]-arachidonic acid	66-88	kininogen 1	Homo sapiens	0-10
1810149-3	1991	Bradykinin promotes metabolite release from cells prelabeled with [14C]-arachidonic acid and this effect is blocked completely by indomethacin.	Indomethacin	130-142	kininogen 1	Homo sapiens	0-10
1810149-7	1991	Bradykinin behaves in all respects like another agent, bacterial lipopolysaccharide, and the action of both agents is consistent with a mechanism involving cyclooxygenase rather than fatty release in the arachidonic acid cascade.	Arachidonic Acid	204-220	kininogen 1	Homo sapiens	0-10
1662200-0	1991	N omega-nitro-L-arginine methyl ester selectively inhibits pulmonary vasodilator responses to acetylcholine and bradykinin.	NG-Nitroarginine Methyl Ester	0-37	kininogen 1	Homo sapiens	112-122
1951669-5	1991	The bradykinin-induced delta SCC was inhibited by piretanide, suggesting that a secretory movement of chloride was responsible for the change, and the effect was attenuated by an antagonist to kinin receptors.	piretanide	50-60	kininogen 1	Homo sapiens	4-14
1951669-5	1991	The bradykinin-induced delta SCC was inhibited by piretanide, suggesting that a secretory movement of chloride was responsible for the change, and the effect was attenuated by an antagonist to kinin receptors.	Chlorides	102-110	kininogen 1	Homo sapiens	4-14
1951669-6	1991	We conclude that both the production of true tissue kallikrein and the chloride secretory response to bradykinin can be regulated in T84 cells by changes in the cell environment.	Chlorides	71-79	kininogen 1	Homo sapiens	102-112
1662200-4	1991	When U-46619 was infused after L-NAME to raise lobar arterial pressure to levels similar to those attained during the control period, vasodilator responses to acetylcholine and bradykinin were reduced significantly, whereas responses to PGE1, lemakalim, and 8-bromo-cGMP were not altered, and responses to nitroprusside were increased.	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	5-12	kininogen 1	Homo sapiens	177-187
1944236-6	1991	The effects of ATP and UTP were not additive, whereas bradykinin- or histamine-stimulated inositol phosphate production was additive with the effects of ATP or UTP.	Inositol Phosphates	90-108	kininogen 1	Homo sapiens	54-64
1744575-0	1991	Bombesin and bradykinin increase inositol phosphates and cytosolic free Ca2+, and stimulate DNA synthesis in human endometrial stromal cells.	Inositol Phosphates	33-52	kininogen 1	Homo sapiens	13-23
1744575-2	1991	In human endometrial stromal cells, bombesin and bradykinin provoked an increase in intracellular free Ca2+ and in labelled inositol phosphates when pre-incubated with [3H]myoinositol.	Inositol Phosphates	124-143	kininogen 1	Homo sapiens	49-59
1744575-2	1991	In human endometrial stromal cells, bombesin and bradykinin provoked an increase in intracellular free Ca2+ and in labelled inositol phosphates when pre-incubated with [3H]myoinositol.	Tritium	169-171	kininogen 1	Homo sapiens	49-59
1744575-2	1991	In human endometrial stromal cells, bombesin and bradykinin provoked an increase in intracellular free Ca2+ and in labelled inositol phosphates when pre-incubated with [3H]myoinositol.	Inositol	172-183	kininogen 1	Homo sapiens	49-59
1744575-4	1991	[3H]Thymidine was added to human cultured endometrial stromal cells with bombesin, bradykinin, epidermal growth factor (EGF), prostaglandin F2 alpha, vasopressin and platelet-derived growth factor.	Thymidine	4-13	kininogen 1	Homo sapiens	83-93
1744575-5	1991	Bombesin, bradykinin and EGF stimulated the incorporation of [3H]thymidine into DNA in quiescent cells.	3h]thymidine	62-74	kininogen 1	Homo sapiens	10-20
1659406-0	1991	Bradykinin and ATP stimulate L-arginine uptake and nitric oxide release in vascular endothelial cells.	Arginine	29-39	kininogen 1	Homo sapiens	0-10
1659406-0	1991	Bradykinin and ATP stimulate L-arginine uptake and nitric oxide release in vascular endothelial cells.	Nitric Oxide	51-63	kininogen 1	Homo sapiens	0-10
1659406-2	1991	In the presence of nitro-L-arginine (100 microM), an inhibitor of NO synthase, the stimulatory effect of bradykinin on L-arginine uptake was partially inhibited while NO release was completely abolished.	Nitroarginine	19-35	kininogen 1	Homo sapiens	105-115
1659406-2	1991	In the presence of nitro-L-arginine (100 microM), an inhibitor of NO synthase, the stimulatory effect of bradykinin on L-arginine uptake was partially inhibited while NO release was completely abolished.	Arginine	25-35	kininogen 1	Homo sapiens	105-115
1953761-4	1991	The NO-release was markedly reduced by the inhibitor of NO-formation NG-momomethyl-L-arginine (L-NMMA, 10(-5) M) to 3% of the control levels (p less than 0.02, n = 4), but unaffected by acetylcholine, bradykinin or endothelin -1, -2 or -3.	omega-N-Methylarginine	95-101	kininogen 1	Homo sapiens	201-211
1944236-6	1991	The effects of ATP and UTP were not additive, whereas bradykinin- or histamine-stimulated inositol phosphate production was additive with the effects of ATP or UTP.	Adenosine Triphosphate	153-156	kininogen 1	Homo sapiens	54-64
1944236-6	1991	The effects of ATP and UTP were not additive, whereas bradykinin- or histamine-stimulated inositol phosphate production was additive with the effects of ATP or UTP.	Uridine Triphosphate	160-163	kininogen 1	Homo sapiens	54-64
1656721-7	1991	Indapamide enhanced the bradykinin-stimulated production of cyclic GMP in the presence of indomethacin and did not affect that evoked by 3 morpholino-sydnonimine, an exogenous donor of nitric oxide.	Indapamide	0-10	kininogen 1	Homo sapiens	24-34
1891022-7	1991	Prostacyclin release was stimulated by intravenous bradykinin.	Epoprostenol	0-12	kininogen 1	Homo sapiens	51-61
1891022-12	1991	The five- to sixfold increase in the prostacyclin metabolite induced by bradykinin was depressed by pretreatment for four days with 75 mg of immediate-release aspirin, but not by 75 mg of controlled-release aspirin.	Epoprostenol	37-49	kininogen 1	Homo sapiens	72-82
1891022-12	1991	The five- to sixfold increase in the prostacyclin metabolite induced by bradykinin was depressed by pretreatment for four days with 75 mg of immediate-release aspirin, but not by 75 mg of controlled-release aspirin.	Aspirin	159-166	kininogen 1	Homo sapiens	72-82
1656721-7	1991	Indapamide enhanced the bradykinin-stimulated production of cyclic GMP in the presence of indomethacin and did not affect that evoked by 3 morpholino-sydnonimine, an exogenous donor of nitric oxide.	Cyclic GMP	60-70	kininogen 1	Homo sapiens	24-34
1656721-7	1991	Indapamide enhanced the bradykinin-stimulated production of cyclic GMP in the presence of indomethacin and did not affect that evoked by 3 morpholino-sydnonimine, an exogenous donor of nitric oxide.	Indomethacin	90-102	kininogen 1	Homo sapiens	24-34
1656792-2	1991	Histamine and bradykinin stimulated phosphoinositol (PI) turnover in a dose-dependent manner, and phorbol-myristate-acetate inhibited hormone-dependent activation of PI turnover, indicating a feedback control of this process.	phosphoinositol	36-51	kininogen 1	Homo sapiens	14-24
1656023-5	1991	Six analogs had distinct excitatory response profile and the rank order of potency of these agonists according to pD2 (shown in parentheses) was D-Arg-[Hyp3Thi5,8D-Phe7]-BK (6.49 +/- 0.19) greater than [Thi5,8D-Phe7]-BK (5.61 +/- 0.26) greater than Lys-Lys-[Hyp3-Thi5,8D-Phe7]-BK (5.45 +/- 0.14) greater than BK (5.16 +/- 0.20) greater than [des-Arg9]-BK (4.95 +/- 0.08) greater than [D-Phe7]-BK (4.73 +/- 0.10).	D-Arginine	145-150	kininogen 1	Homo sapiens	170-172
1656792-3	1991	Activation of PI turnover by histamine and bradykinin is guanine nucleotide-dependent.	Guanine Nucleotides	57-75	kininogen 1	Homo sapiens	43-53
1656792-5	1991	Pertussis toxin blocked the histamine-dependent stimulation but did not affect the bradykinin-dependent stimulation of phospholipase C. By contrast, botulinum toxin (C2 + C3 components) blocked the bradykinin-dependent stimulation of phospholipase C but did not affect the histamine-dependent stimulation of this enzyme.	Histamine	273-282	kininogen 1	Homo sapiens	198-208
1768503-0	1991	Effect of nafamostat mesilate on bradykinin generation during low-density lipoprotein apheresis using a dextran sulfate cellulose column.	nafamostat	10-29	kininogen 1	Homo sapiens	33-43
1768503-6	1991	A distinct generation of bradykinin was observed by passing through the DS column, which led to an increase of blood bradykinin levels from 12.5 +/- 5.3(Mean +/- SEM) pg/ml to 127.3 +/- 67.1 pg/ml after 1000 ml plasma treatment.	Dextran Sulfate	72-74	kininogen 1	Homo sapiens	25-35
1768503-6	1991	A distinct generation of bradykinin was observed by passing through the DS column, which led to an increase of blood bradykinin levels from 12.5 +/- 5.3(Mean +/- SEM) pg/ml to 127.3 +/- 67.1 pg/ml after 1000 ml plasma treatment.	Dextran Sulfate	72-74	kininogen 1	Homo sapiens	117-127
1655653-0	1991	Ramiprilat enhances endothelial autacoid formation by inhibiting breakdown of endothelium-derived bradykinin.	ramiprilat	0-10	kininogen 1	Homo sapiens	98-108
1655653-9	1991	These data indicate that cultured endothelial cells from different species are capable of producing and releasing bradykinin into the extracellular space in amounts that lead to a sustained stimulation of nitric oxide and prostacyclin formation, provided that bradykinin degradation is prevented by angiotensin converting enzyme inhibition.	Nitric Oxide	205-217	kininogen 1	Homo sapiens	114-124
1655653-9	1991	These data indicate that cultured endothelial cells from different species are capable of producing and releasing bradykinin into the extracellular space in amounts that lead to a sustained stimulation of nitric oxide and prostacyclin formation, provided that bradykinin degradation is prevented by angiotensin converting enzyme inhibition.	Epoprostenol	222-234	kininogen 1	Homo sapiens	114-124
1656023-5	1991	Six analogs had distinct excitatory response profile and the rank order of potency of these agonists according to pD2 (shown in parentheses) was D-Arg-[Hyp3Thi5,8D-Phe7]-BK (6.49 +/- 0.19) greater than [Thi5,8D-Phe7]-BK (5.61 +/- 0.26) greater than Lys-Lys-[Hyp3-Thi5,8D-Phe7]-BK (5.45 +/- 0.14) greater than BK (5.16 +/- 0.20) greater than [des-Arg9]-BK (4.95 +/- 0.08) greater than [D-Phe7]-BK (4.73 +/- 0.10).	D-Arginine	145-150	kininogen 1	Homo sapiens	217-219
1656023-5	1991	Six analogs had distinct excitatory response profile and the rank order of potency of these agonists according to pD2 (shown in parentheses) was D-Arg-[Hyp3Thi5,8D-Phe7]-BK (6.49 +/- 0.19) greater than [Thi5,8D-Phe7]-BK (5.61 +/- 0.26) greater than Lys-Lys-[Hyp3-Thi5,8D-Phe7]-BK (5.45 +/- 0.14) greater than BK (5.16 +/- 0.20) greater than [des-Arg9]-BK (4.95 +/- 0.08) greater than [D-Phe7]-BK (4.73 +/- 0.10).	D-Arginine	145-150	kininogen 1	Homo sapiens	217-219
1656023-5	1991	Six analogs had distinct excitatory response profile and the rank order of potency of these agonists according to pD2 (shown in parentheses) was D-Arg-[Hyp3Thi5,8D-Phe7]-BK (6.49 +/- 0.19) greater than [Thi5,8D-Phe7]-BK (5.61 +/- 0.26) greater than Lys-Lys-[Hyp3-Thi5,8D-Phe7]-BK (5.45 +/- 0.14) greater than BK (5.16 +/- 0.20) greater than [des-Arg9]-BK (4.95 +/- 0.08) greater than [D-Phe7]-BK (4.73 +/- 0.10).	D-Arginine	145-150	kininogen 1	Homo sapiens	217-219
1656023-5	1991	Six analogs had distinct excitatory response profile and the rank order of potency of these agonists according to pD2 (shown in parentheses) was D-Arg-[Hyp3Thi5,8D-Phe7]-BK (6.49 +/- 0.19) greater than [Thi5,8D-Phe7]-BK (5.61 +/- 0.26) greater than Lys-Lys-[Hyp3-Thi5,8D-Phe7]-BK (5.45 +/- 0.14) greater than BK (5.16 +/- 0.20) greater than [des-Arg9]-BK (4.95 +/- 0.08) greater than [D-Phe7]-BK (4.73 +/- 0.10).	D-Arginine	145-150	kininogen 1	Homo sapiens	217-219
1656023-5	1991	Six analogs had distinct excitatory response profile and the rank order of potency of these agonists according to pD2 (shown in parentheses) was D-Arg-[Hyp3Thi5,8D-Phe7]-BK (6.49 +/- 0.19) greater than [Thi5,8D-Phe7]-BK (5.61 +/- 0.26) greater than Lys-Lys-[Hyp3-Thi5,8D-Phe7]-BK (5.45 +/- 0.14) greater than BK (5.16 +/- 0.20) greater than [des-Arg9]-BK (4.95 +/- 0.08) greater than [D-Phe7]-BK (4.73 +/- 0.10).	D-Arginine	145-150	kininogen 1	Homo sapiens	217-219
1656023-9	1991	The pA2 value of Lys-Lys-[Hyp3-Thi5,8D-Phe7]-BK was 6.92 +/- 0.17.	Lysine	17-20	kininogen 1	Homo sapiens	45-47
1656023-9	1991	The pA2 value of Lys-Lys-[Hyp3-Thi5,8D-Phe7]-BK was 6.92 +/- 0.17.	Lysine	21-24	kininogen 1	Homo sapiens	45-47
1656023-9	1991	The pA2 value of Lys-Lys-[Hyp3-Thi5,8D-Phe7]-BK was 6.92 +/- 0.17.	thi5	31-35	kininogen 1	Homo sapiens	45-47
1887943-0	1991	Bradykinin-induced prostaglandin synthesis is enhanced in keratinocytes and fibroblasts by UV injury.	Prostaglandins	19-32	kininogen 1	Homo sapiens	0-10
1665827-0	1991	ATP, bradykinin, TRH and TSH activate the Ca(2+)-phosphatidylinositol cascade of human thyrocytes in primary culture.	ca(2+)-phosphatidylinositol	42-69	kininogen 1	Homo sapiens	5-15
1665827-3	1991	The stimulation of IP3 generation followed two distinct kinetics: it was sustained when the cells were triggered with ATP and transient when the response was elicited by TRH or bradykinin.	Inositol 1,4,5-Trisphosphate	19-22	kininogen 1	Homo sapiens	177-187
1665827-5	1991	These data suggest that ATP, bradykinin, TRH and high TSH concentrations activate the Ca(2+)-phosphatidylinositol cascade of human thyrocytes.	ca(2+)-phosphatidylinositol	86-113	kininogen 1	Homo sapiens	29-39
1885582-7	1991	Enalapril dicarboxylic acid and Glu-Trp-Pro-Arg-ProGln-Ile-Pro-Pro which inhibit angiotensin-converting enzyme: angiotensin I, bradykinin, and N-[3-(2-furyl)acryloyl]Phe-Gly-Gly which are substrates; and chloride ions which activate angiotensin-converting enzyme did not modulate leukotriene A4 hydrolase/aminopeptidase activity.	enalapril dicarboxylic acid	0-27	kininogen 1	Homo sapiens	127-137
1885582-7	1991	Enalapril dicarboxylic acid and Glu-Trp-Pro-Arg-ProGln-Ile-Pro-Pro which inhibit angiotensin-converting enzyme: angiotensin I, bradykinin, and N-[3-(2-furyl)acryloyl]Phe-Gly-Gly which are substrates; and chloride ions which activate angiotensin-converting enzyme did not modulate leukotriene A4 hydrolase/aminopeptidase activity.	prolyl-proline	59-66	kininogen 1	Homo sapiens	127-137
1887943-4	1991	The ability of UV injury to increase bradykinin-stimulated prostaglandin synthesis is not limited to keratinocytes, as irradiation produced a similar response in fibroblasts.	Prostaglandins	59-72	kininogen 1	Homo sapiens	37-47
1720843-1	1991	In this study, the effect of bradykinin on coronary flow in the isolated rat heart was significantly potentiated when cysteine or the sulfhydryl-containing converting enzyme inhibitors captopril and zofenoprilat were administered simultaneously.	Cysteine	118-126	kininogen 1	Homo sapiens	29-39
1889254-4	1991	After treatment with budesonide, the response to both inhaled histamine and bradykinin was decreased when compared with placebo.	Budesonide	21-31	kininogen 1	Homo sapiens	76-86
1889254-8	1991	Inhaled budesonide therefore inhibits to the same extent the exaggerated response to both directly acting histamine and bradykinin which acts through airway nerves.	Budesonide	8-18	kininogen 1	Homo sapiens	120-130
24242689-2	1991	N-acetyl and O-methyl derivatives of bradykinin were used as mass shift species for assignment of N-terminal and C-terminal fragment ions.	isospaglumic acid	0-8	kininogen 1	Homo sapiens	37-47
24242689-2	1991	N-acetyl and O-methyl derivatives of bradykinin were used as mass shift species for assignment of N-terminal and C-terminal fragment ions.	o-methyl	13-21	kininogen 1	Homo sapiens	37-47
1720843-1	1991	In this study, the effect of bradykinin on coronary flow in the isolated rat heart was significantly potentiated when cysteine or the sulfhydryl-containing converting enzyme inhibitors captopril and zofenoprilat were administered simultaneously.	Captopril	185-194	kininogen 1	Homo sapiens	29-39
1720843-1	1991	In this study, the effect of bradykinin on coronary flow in the isolated rat heart was significantly potentiated when cysteine or the sulfhydryl-containing converting enzyme inhibitors captopril and zofenoprilat were administered simultaneously.	zofenoprilate	199-211	kininogen 1	Homo sapiens	29-39
1720843-2	1991	In contrast, the effect of concomitant administration of enalaprilat only slightly increased the effect of bradykinin on coronary flow.	Enalaprilat	57-68	kininogen 1	Homo sapiens	107-117
1720843-3	1991	In nitrate-tolerant hearts of rats pretreated with isosorbide dinitrate (15 mg daily), the increase in coronary flow by nitroglycerin and bradykinin was significantly less when compared to control hearts.	Nitrates	3-10	kininogen 1	Homo sapiens	138-148
1720843-3	1991	In nitrate-tolerant hearts of rats pretreated with isosorbide dinitrate (15 mg daily), the increase in coronary flow by nitroglycerin and bradykinin was significantly less when compared to control hearts.	Isosorbide Dinitrate	51-71	kininogen 1	Homo sapiens	138-148
1661345-5	1991	Thrombin- or bradykinin-stimulated PGI2 production was enhanced significantly, and the angiotensin converting enzyme (ACE) activity of cell lysate of PPAEC was significantly suppressed after a 24-hour incubation with 10(-4) M of paraquat.	Epoprostenol	35-39	kininogen 1	Homo sapiens	13-23
1770982-0	1991	Inositol phosphates and intracellular calcium after bradykinin stimulation in fibroblasts from young, normal aged and Alzheimer donors.	Inositol Phosphates	0-19	kininogen 1	Homo sapiens	52-62
1770982-5	1991	The bradykinin-induced formation of IP3 and IP2 increased significantly in fibroblasts from normal aged and Alzheimer donors compared to young subjects, but did not differ from each other.	Inositol 1,4,5-Trisphosphate	36-39	kininogen 1	Homo sapiens	4-14
1661345-5	1991	Thrombin- or bradykinin-stimulated PGI2 production was enhanced significantly, and the angiotensin converting enzyme (ACE) activity of cell lysate of PPAEC was significantly suppressed after a 24-hour incubation with 10(-4) M of paraquat.	Paraquat	229-237	kininogen 1	Homo sapiens	13-23
1770982-5	1991	The bradykinin-induced formation of IP3 and IP2 increased significantly in fibroblasts from normal aged and Alzheimer donors compared to young subjects, but did not differ from each other.	1D-myo-inositol 4,5-bisphosphate	44-47	kininogen 1	Homo sapiens	4-14
1770982-9	1991	The precise molecular basis and pathophysiological significance of the enhanced bradykinin-induced phosphoinositide cascade in fibroblasts from aged donors remains to be determined.	Phosphatidylinositols	99-115	kininogen 1	Homo sapiens	80-90
1770982-6	1991	Bradykinin-induced IP3 formation was 63-117% above the young group at time points between 10-60 s in normal aged or Alzheimer donors.	Inositol 1,4,5-Trisphosphate	19-22	kininogen 1	Homo sapiens	0-10
1770982-7	1991	Bradykinin-induced IP2 formation was 49-59% above the young group at time points between 10-60 s in normal aged or Alzheimer subjects.	1D-myo-inositol 4,5-bisphosphate	19-22	kininogen 1	Homo sapiens	0-10
1782603-8	1991	Removal of Ca2+ from the bathing saline only slightly attenuated the increase in intracellular free Ca2+ that resulted from stimulation with bradykinin.	Sodium Chloride	33-39	kininogen 1	Homo sapiens	141-151
1651669-0	1991	Effects of bradykinin on intracellular calcium regulation in human ciliated airway epithelium.	Calcium	39-46	kininogen 1	Homo sapiens	11-21
1651669-1	1991	The Ca(2+)-mobilizing action of bradykinin (BK) was investigated in ciliated human nasal epithelial (HNE) cells utilizing fura-2 fluorescence and microspectrofluorimetry.	Fura-2	122-128	kininogen 1	Homo sapiens	32-42
1651669-1	1991	The Ca(2+)-mobilizing action of bradykinin (BK) was investigated in ciliated human nasal epithelial (HNE) cells utilizing fura-2 fluorescence and microspectrofluorimetry.	Fura-2	122-128	kininogen 1	Homo sapiens	44-46
1875911-8	1991	Furthermore, the Ca2+ signals elicited by both bradykinin and epidermal growth factor were blocked in cells microinjected with the inositol 1,4,5-trisphosphate receptor antagonist heparin, whereas the intracellular Ca(2+)-ATPase inhibitor thapsigargin still mobilized Ca2+.	Thapsigargin	239-251	kininogen 1	Homo sapiens	47-57
1875911-4	1991	In nominally Ca(2+)-free medium, the addition of bradykinin to A431 cells rapidly but transiently increased inositol 1,4,5-trisphosphate and, in parallel fashion, transiently increased cytosolic Ca2+.	Inositol 1,4,5-Trisphosphate	108-136	kininogen 1	Homo sapiens	49-59
1875911-9	1991	Finally, histamine, a less efficacious guanine nucleotide-dependent protein-linked receptor agonist, as well as photolyzed, microinjected, caged inositol 1,4,5-trisphosphate, also mobilized Ca2+ after bradykinin.	Inositol 1,4,5-Trisphosphate	145-173	kininogen 1	Homo sapiens	201-211
1875911-7	1991	Epidermal growth factor stimulated additional inositol 1,4,5-trisphosphate formation in bradykinin-treated cells.	Inositol 1,4,5-Trisphosphate	46-74	kininogen 1	Homo sapiens	88-98
1875911-8	1991	Furthermore, the Ca2+ signals elicited by both bradykinin and epidermal growth factor were blocked in cells microinjected with the inositol 1,4,5-trisphosphate receptor antagonist heparin, whereas the intracellular Ca(2+)-ATPase inhibitor thapsigargin still mobilized Ca2+.	Heparin	180-187	kininogen 1	Homo sapiens	47-57
1719280-3	1991	Endothelium-dependent relaxations to bradykinin and serotonin were reduced to a similar extent in arteries contracted with endothelin-1 and KCl as compared to those contracted with the thromboxane analog U 46619 (p less than 0.05; n = 5-6).	Potassium Chloride	140-143	kininogen 1	Homo sapiens	37-47
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Phosphatidylcholines	0-19	kininogen 1	Homo sapiens	90-100
1663586-0	1991	Endothelium-derived bradykinin is responsible for the increase in calcium produced by angiotensin-converting enzyme inhibitors in human endothelial cells.	Calcium	66-73	kininogen 1	Homo sapiens	20-30
1663586-2	1991	The ACE inhibitors ramiprilat and enalaprilat (0.3 microM) enhanced the increase in [Ca2+]i elicited by bradykinin (3 nM) and also caused an increase in resting [Ca2+]i when given alone.	ramiprilat	19-29	kininogen 1	Homo sapiens	104-114
1663586-2	1991	The ACE inhibitors ramiprilat and enalaprilat (0.3 microM) enhanced the increase in [Ca2+]i elicited by bradykinin (3 nM) and also caused an increase in resting [Ca2+]i when given alone.	Enalaprilat	34-45	kininogen 1	Homo sapiens	104-114
1663586-6	1991	This endothelium-derived bradykinin can exert an autocrine function by stimulating endothelial B2-receptors with a subsequent increase in [Ca2+]i and nitric oxide formation.	Nitric Oxide	150-162	kininogen 1	Homo sapiens	25-35
2037585-0	1991	Phospholipid metabolism in bradykinin-stimulated human fibroblasts.	Phospholipids	0-12	kininogen 1	Homo sapiens	27-37
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Diglycerides	25-39	kininogen 1	Homo sapiens	161-171
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Diglycerides	25-39	kininogen 1	Homo sapiens	173-175
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Phosphatidylinositols	45-65	kininogen 1	Homo sapiens	161-171
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Phosphatidylinositols	45-65	kininogen 1	Homo sapiens	173-175
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Phosphatidylcholines	70-89	kininogen 1	Homo sapiens	161-171
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Phosphatidylcholines	70-89	kininogen 1	Homo sapiens	173-175
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Diglycerides	206-220	kininogen 1	Homo sapiens	161-171
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Diglycerides	206-220	kininogen 1	Homo sapiens	173-175
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Phosphatidic Acids	230-247	kininogen 1	Homo sapiens	161-171
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Phosphatidic Acids	230-247	kininogen 1	Homo sapiens	173-175
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Phosphatidic Acids	249-251	kininogen 1	Homo sapiens	161-171
2037585-1	1991	I. Biphasic formation of diacylglycerol from phosphatidylinositol and phosphatidylcholine, controlled by protein kinase C. Stimulation of human fibroblasts with bradykinin (BK) results in the generation of diacylglycerol (DG) and phosphatidic acid (PA).	Phosphatidic Acids	249-251	kininogen 1	Homo sapiens	173-175
2037585-5	1991	BK also generated free [3H]arachidonate and, to a lesser extent, mono[3H]arachidonoylglycerol.	[3h]arachidonate	23-39	kininogen 1	Homo sapiens	0-2
2037585-5	1991	BK also generated free [3H]arachidonate and, to a lesser extent, mono[3H]arachidonoylglycerol.	mono[3h]arachidonoylglycerol	65-93	kininogen 1	Homo sapiens	0-2
2037585-7	1991	Short pretreatment of the cells with phorbol 12-myristate 13-acetate (PMA) abolished the BK-induced breakdown of phosphoinositides, but did not affect the second-phase DGc level.	Tetradecanoylphorbol Acetate	37-68	kininogen 1	Homo sapiens	89-91
2037585-7	1991	Short pretreatment of the cells with phorbol 12-myristate 13-acetate (PMA) abolished the BK-induced breakdown of phosphoinositides, but did not affect the second-phase DGc level.	Tetradecanoylphorbol Acetate	70-73	kininogen 1	Homo sapiens	89-91
2037585-7	1991	Short pretreatment of the cells with phorbol 12-myristate 13-acetate (PMA) abolished the BK-induced breakdown of phosphoinositides, but did not affect the second-phase DGc level.	Phosphatidylinositols	113-130	kininogen 1	Homo sapiens	89-91
2037585-9	1991	Down-regulation of protein kinase C (PKC) by long term treatment with phorbol ester, prior to BK stimulation, resulted in (i) enhanced DGi and decreased PAi formation, suggesting that DG kinase activity is positively controlled by PKC; (ii) the unexpected manifestation of rapidly formed DGc; (iii) no change in the DGc levels obtained after 30-min BK stimulation, but complete suppression of PMA-induced DGc formation.	Phorbol Esters	70-83	kininogen 1	Homo sapiens	349-351
2037585-10	1991	In contrast, two inhibitors of PKC, staurosporin and 1-O-hexadecyl-2-O-methylglycerol, inhibited both BK- and PMA-induced DGc formation at 30 min, leaving the rapid response towards BK unaffected.	Staurosporine	36-48	kininogen 1	Homo sapiens	102-104
2037585-10	1991	In contrast, two inhibitors of PKC, staurosporin and 1-O-hexadecyl-2-O-methylglycerol, inhibited both BK- and PMA-induced DGc formation at 30 min, leaving the rapid response towards BK unaffected.	Staurosporine	36-48	kininogen 1	Homo sapiens	182-184
2037585-10	1991	In contrast, two inhibitors of PKC, staurosporin and 1-O-hexadecyl-2-O-methylglycerol, inhibited both BK- and PMA-induced DGc formation at 30 min, leaving the rapid response towards BK unaffected.	1-O-hexadecyl-2-O-methylglycerol	53-85	kininogen 1	Homo sapiens	102-104
2037585-10	1991	In contrast, two inhibitors of PKC, staurosporin and 1-O-hexadecyl-2-O-methylglycerol, inhibited both BK- and PMA-induced DGc formation at 30 min, leaving the rapid response towards BK unaffected.	1-O-hexadecyl-2-O-methylglycerol	53-85	kininogen 1	Homo sapiens	182-184
2037585-10	1991	In contrast, two inhibitors of PKC, staurosporin and 1-O-hexadecyl-2-O-methylglycerol, inhibited both BK- and PMA-induced DGc formation at 30 min, leaving the rapid response towards BK unaffected.	Tetradecanoylphorbol Acetate	110-113	kininogen 1	Homo sapiens	182-184
1309881-2	1992	We have previously shown bradykinin to be a potent stimulus for the release of prostanoids from interleukin-1 (IL-1)-treated, but not untreated, human synovial cells.	Prostaglandins	79-90	kininogen 1	Homo sapiens	25-35
1309881-4	1992	We performed [3H]bradykinin binding studies in intact human synovial tissue and in cultured human synovial cells.	Tritium	14-16	kininogen 1	Homo sapiens	17-27
1309881-5	1992	Specific, saturable [3H]bradykinin binding sites in intact synovia were identified by autoradiographic localization and were present in much higher density in rheumatoid, than in osteoarthritis, synovia.	Tritium	21-23	kininogen 1	Homo sapiens	24-34
1309881-7	1992	In matched experiments, IL-1 treatment enhanced specific [3H]bradykinin binding 1.5- to 2.0-fold above that observed in untreated cells.	Tritium	58-60	kininogen 1	Homo sapiens	61-71
1309881-9	1992	The potencies of a series of kinin analogs and antagonists and unrelated peptides in displacing [3H]bradykinin from IL-1-treated cells correlated well with their abilities to induce prostanoid release.	Tritium	97-99	kininogen 1	Homo sapiens	100-110
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Phosphatidylcholines	0-19	kininogen 1	Homo sapiens	102-104
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Phosphatidylcholines	181-200	kininogen 1	Homo sapiens	90-100
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Phosphatidylcholines	181-200	kininogen 1	Homo sapiens	102-104
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Phosphatidylcholines	202-204	kininogen 1	Homo sapiens	90-100
1653071-0	1991	Regulation of bradykinin receptor level by cholera toxin, pertussis toxin and forskolin in cultured human fibroblasts.	Colforsin	78-87	kininogen 1	Homo sapiens	14-24
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Phosphatidylcholines	202-204	kininogen 1	Homo sapiens	102-104
1653071-2	1991	The effect of bacterial toxins on bradykinin-triggered release of arachidonic acid was studied in serum-deprived human foreskin (HSWP) fibroblasts prelabelled with [3H]-arachidonic acid.	Arachidonic Acid	66-82	kininogen 1	Homo sapiens	34-44
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Phosphatidic Acids	258-275	kininogen 1	Homo sapiens	90-100
1653071-2	1991	The effect of bacterial toxins on bradykinin-triggered release of arachidonic acid was studied in serum-deprived human foreskin (HSWP) fibroblasts prelabelled with [3H]-arachidonic acid.	Tritium	165-167	kininogen 1	Homo sapiens	34-44
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Phosphatidic Acids	258-275	kininogen 1	Homo sapiens	102-104
1653071-2	1991	The effect of bacterial toxins on bradykinin-triggered release of arachidonic acid was studied in serum-deprived human foreskin (HSWP) fibroblasts prelabelled with [3H]-arachidonic acid.	Arachidonic Acid	169-185	kininogen 1	Homo sapiens	34-44
1653071-3	1991	An 18-h exposure of HSWP cells to cholera toxin, pertussis toxin, or forskolin enhanced the bradykinin-stimulated release of arachidonic acid and metabolites.	Colforsin	69-78	kininogen 1	Homo sapiens	92-102
1653071-3	1991	An 18-h exposure of HSWP cells to cholera toxin, pertussis toxin, or forskolin enhanced the bradykinin-stimulated release of arachidonic acid and metabolites.	Arachidonic Acid	125-141	kininogen 1	Homo sapiens	92-102
1653071-5	1991	Prolonged treatment of HSWP cells with these agents also caused a 3 to 4 fold rise in cell surface [3H]-bradykinin binding.	Tritium	100-102	kininogen 1	Homo sapiens	104-114
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Phosphatidic Acids	277-279	kininogen 1	Homo sapiens	90-100
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Phosphatidic Acids	277-279	kininogen 1	Homo sapiens	102-104
1653071-7	1991	In addition, cholera toxin and foreskolin increased [3H]-bradykinin binding in wildtype PC12 cells, but not in mutant PC12 cells with reduced cyclic AMP-dependent protein kinase type II activity.	foreskolin	31-41	kininogen 1	Homo sapiens	57-67
1653071-7	1991	In addition, cholera toxin and foreskolin increased [3H]-bradykinin binding in wildtype PC12 cells, but not in mutant PC12 cells with reduced cyclic AMP-dependent protein kinase type II activity.	Tritium	53-55	kininogen 1	Homo sapiens	57-67
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Diglycerides	285-299	kininogen 1	Homo sapiens	90-100
1653071-9	1991	In conclusion, cholera toxin, pertussis toxin and forskolin enhanced arachidonic acid release in response to bradykinin, and increased the number of bradykinin receptors in HSWP fibroblasts.	Colforsin	50-59	kininogen 1	Homo sapiens	109-119
1653071-9	1991	In conclusion, cholera toxin, pertussis toxin and forskolin enhanced arachidonic acid release in response to bradykinin, and increased the number of bradykinin receptors in HSWP fibroblasts.	Colforsin	50-59	kininogen 1	Homo sapiens	149-159
2037586-2	1991	Phosphatidylcholine breakdown by phospholipases C and D; involvement of protein kinase C. Bradykinin (BK) and phorbol 12-myristate 13-acetate (PMA) both stimulate the hydrolysis of phosphatidylcholine (PC) in human fibroblasts, resulting in the formation of phosphatidic acid (PA) and diacylglycerol (DG) (Van Blitterswijk, W.J., Hilkmann, H., de Widt, J., and Van der Bend, R.L.	Diglycerides	285-299	kininogen 1	Homo sapiens	102-104
1653071-9	1991	In conclusion, cholera toxin, pertussis toxin and forskolin enhanced arachidonic acid release in response to bradykinin, and increased the number of bradykinin receptors in HSWP fibroblasts.	Arachidonic Acid	69-85	kininogen 1	Homo sapiens	109-119
2037586-6	1991	Stimulation with BK resulted in the rapid and synchronous formation of [3H]choline and [3H]myristoyl-PA from the correspondingly prelabeled PC, indicative of phospholipase D (PLD) activity.	Tritium	72-74	kininogen 1	Homo sapiens	17-19
2037586-6	1991	Stimulation with BK resulted in the rapid and synchronous formation of [3H]choline and [3H]myristoyl-PA from the correspondingly prelabeled PC, indicative of phospholipase D (PLD) activity.	Choline	75-82	kininogen 1	Homo sapiens	17-19
2037586-6	1991	Stimulation with BK resulted in the rapid and synchronous formation of [3H]choline and [3H]myristoyl-PA from the correspondingly prelabeled PC, indicative of phospholipase D (PLD) activity.	Tritium	88-90	kininogen 1	Homo sapiens	17-19
2037586-6	1991	Stimulation with BK resulted in the rapid and synchronous formation of [3H]choline and [3H]myristoyl-PA from the correspondingly prelabeled PC, indicative of phospholipase D (PLD) activity.	myristoyl-pa	91-103	kininogen 1	Homo sapiens	17-19
2037586-6	1991	Stimulation with BK resulted in the rapid and synchronous formation of [3H]choline and [3H]myristoyl-PA from the correspondingly prelabeled PC, indicative of phospholipase D (PLD) activity.	Phosphatidylcholines	140-142	kininogen 1	Homo sapiens	17-19
2037586-12	1991	The protein kinase C (PKC) inhibitors staurosporin and 1-O-hexadecyl-2-O-methylglycerol inhibited BK- and PMA-induced activation of PLD.	Staurosporine	38-50	kininogen 1	Homo sapiens	98-100
2037586-12	1991	The protein kinase C (PKC) inhibitors staurosporin and 1-O-hexadecyl-2-O-methylglycerol inhibited BK- and PMA-induced activation of PLD.	1-O-hexadecyl-2-O-methylglycerol	55-87	kininogen 1	Homo sapiens	98-100
1851210-1	1991	Long-term ethanol exposure is known to inhibit bradykinin-stimulated phosphoinositide hydrolysis in cultures of neuroblastoma x glioma 108-15 cells.	Ethanol	10-17	kininogen 1	Homo sapiens	47-57
1851210-1	1991	Long-term ethanol exposure is known to inhibit bradykinin-stimulated phosphoinositide hydrolysis in cultures of neuroblastoma x glioma 108-15 cells.	Phosphatidylinositols	69-85	kininogen 1	Homo sapiens	47-57
1851210-3	1991	Ethanol exposure reduced guanosine 5"-O-(3-thiotriphosphate) [GTP(S)]- and, to a lesser extent, NaF/AlCl3-stimulated phosphoinositide hydrolysis, whereas it had no effect on the enzymatic activity of a phosphatidylinositol 4,5-bisphosphate-specific phospholipase C. [3H]Bradykinin binding in the absence of GTP(S) was not influenced by ethanol exposure.	Ethanol	0-7	kininogen 1	Homo sapiens	270-280
1851210-4	1991	However, the reduction in [3H]bradykinin binding seen in control cells after addition of GTP analogue was inhibited in cells grown in ethanol-containing medium.	Guanosine Triphosphate	89-92	kininogen 1	Homo sapiens	30-40
1851210-4	1991	However, the reduction in [3H]bradykinin binding seen in control cells after addition of GTP analogue was inhibited in cells grown in ethanol-containing medium.	Ethanol	134-141	kininogen 1	Homo sapiens	30-40
1652036-5	1991	Bradykinin and Ca ionophore A23187 enhanced PGI2 production, and increased the cytosolic free Ca++ concentration ([Ca++]i).	Epoprostenol	44-48	kininogen 1	Homo sapiens	0-10
1890650-3	1991	On 4 separate days, each separated by a week, subjects randomly underwent nasal challenge with incremental doses of either the B1 agonist [Des-Arg9]-bradykinin, the B2 agonists kallidin or bradykinin, or vehicle placebo in a double-blind comparative study.	des-arg9	139-147	kininogen 1	Homo sapiens	149-159
1716843-2	1991	Pertussis toxin (100 ng/ml) inhibited histamine release induced by compound 48/80, substance P, mastoparan, peptide 401, bradykinin and spermine showing that a G-protein sensitive to pertussis toxin was involved in the non-immunological histamine release.	Histamine	38-47	kininogen 1	Homo sapiens	121-131
1721246-0	1991	Bradykinin-induced cough reflex markedly increases in patients with cough associated with captopril and enalapril.	Captopril	90-99	kininogen 1	Homo sapiens	0-10
1721246-0	1991	Bradykinin-induced cough reflex markedly increases in patients with cough associated with captopril and enalapril.	Enalapril	104-113	kininogen 1	Homo sapiens	0-10
1708255-9	1991	The inactivation of bradykinin by intact neutrophils was decreased by phorbol 12-myristate 13-acetate, probably due to down-regulation by endocytosis of the neutral endopeptidase on the plasma membrane.	Tetradecanoylphorbol Acetate	70-101	kininogen 1	Homo sapiens	20-30
1651871-1	1991	Bradykinin (BK, 0.05 micrograms/kg) or glyceryl trinitrite (5 micrograms/kg) injected into the left circumflex coronary artery of anaesthetized, open-chest greyhounds, caused pronounced increases in large coronary artery diameter (CD) and coronary blood flow (CBF), whereas des-Arg9-BK (0.05-0.3 micrograms/kg), a selective bradykinin B1 agonist, dose dependently elevated CBF but had little effect on CD.	glycerine trinitrite	39-58	kininogen 1	Homo sapiens	283-285
2032802-4	1991	In arteries contracted with serotonin, bradykinin evoked potent endothelium-dependent relaxations; L-NMMA markedly reduced the sensitivity but not the maximal response.	Serotonin	28-37	kininogen 1	Homo sapiens	39-49
2032802-11	1991	Endothelium-derived nitric oxide is released both under basal conditions and after stimulation with acetylcholine and bradykinin.	Nitric Oxide	20-32	kininogen 1	Homo sapiens	118-128
1648132-6	1991	When GTP (1 mM) was included in the pipette solution, two additional ion channel populations were transiently augmented in response to bradykinin stimulation.	Guanosine Triphosphate	5-8	kininogen 1	Homo sapiens	135-145
1648132-11	1991	Video imaging of single-cell Fura-2 fluorescence from both intact cells and patch-clamped cells showed temporal correlation of the K+ current modulation and the Ca2+ transients in response to bradykinin stimulation.	Fura-2	29-35	kininogen 1	Homo sapiens	192-202
1651871-1	1991	Bradykinin (BK, 0.05 micrograms/kg) or glyceryl trinitrite (5 micrograms/kg) injected into the left circumflex coronary artery of anaesthetized, open-chest greyhounds, caused pronounced increases in large coronary artery diameter (CD) and coronary blood flow (CBF), whereas des-Arg9-BK (0.05-0.3 micrograms/kg), a selective bradykinin B1 agonist, dose dependently elevated CBF but had little effect on CD.	glycerine trinitrite	39-58	kininogen 1	Homo sapiens	324-334
1651871-2	1991	BK-induced increases in CD and CBF were not affected by the intracoronary infusion of a selective B1 receptor antagonist, des-Arg9-[Leu8]BK (40 micrograms/min), but were significantly reduced by the infusion of a selective B2 receptor antagonist, D-Arg0-[Hyp3,Thi5,8,D-Phe7] BK (10-12 micrograms/min).	d-arg0	247-253	kininogen 1	Homo sapiens	0-2
1651871-2	1991	BK-induced increases in CD and CBF were not affected by the intracoronary infusion of a selective B1 receptor antagonist, des-Arg9-[Leu8]BK (40 micrograms/min), but were significantly reduced by the infusion of a selective B2 receptor antagonist, D-Arg0-[Hyp3,Thi5,8,D-Phe7] BK (10-12 micrograms/min).	[hyp3	254-259	kininogen 1	Homo sapiens	0-2
1651871-2	1991	BK-induced increases in CD and CBF were not affected by the intracoronary infusion of a selective B1 receptor antagonist, des-Arg9-[Leu8]BK (40 micrograms/min), but were significantly reduced by the infusion of a selective B2 receptor antagonist, D-Arg0-[Hyp3,Thi5,8,D-Phe7] BK (10-12 micrograms/min).	thi5	260-264	kininogen 1	Homo sapiens	0-2
1651871-3	1991	The antagonism was reversible and specific for BK since responses to glyceryl trinitrate were not affected.	Nitroglycerin	69-88	kininogen 1	Homo sapiens	47-49
1651871-6	1991	(n = 5) resulted in significant attenuation of BK-induced increases in CBF but not that of CD.	C-(1-HYDROGYL-BETA-D-GLUCOPYRANOSYL) FORMAMIDE	71-74	kininogen 1	Homo sapiens	47-49
1880187-2	1991	The precolumn incubation of bradykinin, Tyr8-bradykinin and insulin A chain with biuret reagent for 20 min at 60 degrees C leads to the formation of biuret complexes which can be subjected to chromatography in acidic or basic eluents.	Biuret	81-87	kininogen 1	Homo sapiens	28-38
1656406-1	1991	Bradykinin (BK) analogs such as Lys-Lys-BK, des-Arg9-BK and [Leu8]des-Arg9-BK were poor substrates for angiotensin I converting enzyme (ACE), and analogs containing D-Phe7 residues, or a pseudopeptide C-terminal bond, were completely resistant.	d-phe7	165-171	kininogen 1	Homo sapiens	0-10
1656406-1	1991	Bradykinin (BK) analogs such as Lys-Lys-BK, des-Arg9-BK and [Leu8]des-Arg9-BK were poor substrates for angiotensin I converting enzyme (ACE), and analogs containing D-Phe7 residues, or a pseudopeptide C-terminal bond, were completely resistant.	d-phe7	165-171	kininogen 1	Homo sapiens	12-14
1880187-2	1991	The precolumn incubation of bradykinin, Tyr8-bradykinin and insulin A chain with biuret reagent for 20 min at 60 degrees C leads to the formation of biuret complexes which can be subjected to chromatography in acidic or basic eluents.	Biuret	81-87	kininogen 1	Homo sapiens	45-55
1880187-2	1991	The precolumn incubation of bradykinin, Tyr8-bradykinin and insulin A chain with biuret reagent for 20 min at 60 degrees C leads to the formation of biuret complexes which can be subjected to chromatography in acidic or basic eluents.	Biuret	149-155	kininogen 1	Homo sapiens	28-38
1880187-2	1991	The precolumn incubation of bradykinin, Tyr8-bradykinin and insulin A chain with biuret reagent for 20 min at 60 degrees C leads to the formation of biuret complexes which can be subjected to chromatography in acidic or basic eluents.	Biuret	149-155	kininogen 1	Homo sapiens	45-55
2010809-0	1991	Inhibition by bradykinin of voltage-activated barium current in a rat dorsal root ganglion cell line: role of protein kinase C. The whole-cell patch-clamp technique was used to record Ba2+ currents through voltage-activated calcium channels in the clonal dorsal root ganglion cell line F11-B9.	Barium	46-52	kininogen 1	Homo sapiens	14-24
2010809-1	1991	The pain-producing peptide bradykinin (BK; 100 nM) reduced the sustained Ba2+ current in F11-B9 cells by 30%.	N-methyl-valyl-amiclenomycin	73-77	kininogen 1	Homo sapiens	27-37
2010809-1	1991	The pain-producing peptide bradykinin (BK; 100 nM) reduced the sustained Ba2+ current in F11-B9 cells by 30%.	N-methyl-valyl-amiclenomycin	73-77	kininogen 1	Homo sapiens	39-41
2010809-2	1991	In cultures prelabeled with 3H-arachidonic acid and tested under ionic conditions similar to those used for recording Ba2+ currents, BK also induced a concentration-dependent, transient, 2.7-fold accumulation of 3H-diacylglycerol.	3h-arachidonic acid	28-47	kininogen 1	Homo sapiens	133-135
2010809-2	1991	In cultures prelabeled with 3H-arachidonic acid and tested under ionic conditions similar to those used for recording Ba2+ currents, BK also induced a concentration-dependent, transient, 2.7-fold accumulation of 3H-diacylglycerol.	N-methyl-valyl-amiclenomycin	118-122	kininogen 1	Homo sapiens	133-135
2010809-2	1991	In cultures prelabeled with 3H-arachidonic acid and tested under ionic conditions similar to those used for recording Ba2+ currents, BK also induced a concentration-dependent, transient, 2.7-fold accumulation of 3H-diacylglycerol.	3h-diacylglycerol	212-229	kininogen 1	Homo sapiens	133-135
2010809-3	1991	Both the elevation of 3H-diacylglycerol and the inhibition of Ba2+ current began within 5 sec following BK exposure, and the effective concentration range of BK was similar for the 2 responses.	N-methyl-valyl-amiclenomycin	62-66	kininogen 1	Homo sapiens	104-106
2010809-4	1991	In whole-cell recordings, extracellularly applied 1-oleoyl-2-acetylglycerol (OAG; 0.5-5 microM) mimicked the degree of block and occluded the block of sustained current by BK.	1-oleoyl-2-acetylglycerol	50-75	kininogen 1	Homo sapiens	172-174
2010809-4	1991	In whole-cell recordings, extracellularly applied 1-oleoyl-2-acetylglycerol (OAG; 0.5-5 microM) mimicked the degree of block and occluded the block of sustained current by BK.	1-oleoyl-2-acetylglycerol	77-80	kininogen 1	Homo sapiens	172-174
2010809-6	1991	The pseudosubstrate peptide PKC19-36 (2 microM in pipette) and the lipid staurosporine (100 nM in pipette), both inhibitors of PKC, reduced the effects of maximal concentrations of OAG or BK by 55-60%.	Staurosporine	73-86	kininogen 1	Homo sapiens	188-190
2010809-6	1991	The pseudosubstrate peptide PKC19-36 (2 microM in pipette) and the lipid staurosporine (100 nM in pipette), both inhibitors of PKC, reduced the effects of maximal concentrations of OAG or BK by 55-60%.	1-oleoyl-2-acetylglycerol	181-184	kininogen 1	Homo sapiens	188-190
2010809-8	1991	These data are consistent with the hypothesis that BK inhibits whole-cell sustained Ba2+ current in F11-B9 cells via a mechanism that involves activation of PKC.	N-methyl-valyl-amiclenomycin	84-88	kininogen 1	Homo sapiens	51-53
2010815-2	1991	However, there is evidence that kappa- and delta-opioid receptors are located on sympathetic postganglionic neuron (SPGN) terminals, which mediate bradykinin (BK) hyperalgesia via SPGN-terminal-dependent production of PGE2.	Dinoprostone	218-222	kininogen 1	Homo sapiens	147-157
1889623-0	1991	Arachidonate release consequent to bradykinin-stimulated phospholipid metabolism in dorsal root ganglion cells.	Arachidonic Acid	0-12	kininogen 1	Homo sapiens	35-45
2010815-2	1991	However, there is evidence that kappa- and delta-opioid receptors are located on sympathetic postganglionic neuron (SPGN) terminals, which mediate bradykinin (BK) hyperalgesia via SPGN-terminal-dependent production of PGE2.	Dinoprostone	218-222	kininogen 1	Homo sapiens	159-161
1889623-0	1991	Arachidonate release consequent to bradykinin-stimulated phospholipid metabolism in dorsal root ganglion cells.	Phospholipids	57-69	kininogen 1	Homo sapiens	35-45
1907204-0	1991	Transduction of the bradykinin response in human fibroblasts: prolonged elevation of diacylglycerol level and its correlation with protein kinase C activation.	Diglycerides	85-99	kininogen 1	Homo sapiens	20-30
2002040-8	1991	As evident from fura 2 fluorescence, bradykinin leads to a transient increase of intracellular calcium both in the presence and absence of extracellular calcium.	Fura-2	16-22	kininogen 1	Homo sapiens	37-47
2002040-8	1991	As evident from fura 2 fluorescence, bradykinin leads to a transient increase of intracellular calcium both in the presence and absence of extracellular calcium.	Calcium	95-102	kininogen 1	Homo sapiens	37-47
2002040-8	1991	As evident from fura 2 fluorescence, bradykinin leads to a transient increase of intracellular calcium both in the presence and absence of extracellular calcium.	Calcium	153-160	kininogen 1	Homo sapiens	37-47
2002040-9	1991	Oscillations of intracellular calcium could be observed in +ras cells, if bradykinin was applied at reduced extracellular sodium concentration possibly to impair calcium extrusion via the sodium/calcium exchange.	Calcium	30-37	kininogen 1	Homo sapiens	74-84
2002040-9	1991	Oscillations of intracellular calcium could be observed in +ras cells, if bradykinin was applied at reduced extracellular sodium concentration possibly to impair calcium extrusion via the sodium/calcium exchange.	Sodium	122-128	kininogen 1	Homo sapiens	74-84
2002040-9	1991	Oscillations of intracellular calcium could be observed in +ras cells, if bradykinin was applied at reduced extracellular sodium concentration possibly to impair calcium extrusion via the sodium/calcium exchange.	Calcium	162-169	kininogen 1	Homo sapiens	74-84
2002040-9	1991	Oscillations of intracellular calcium could be observed in +ras cells, if bradykinin was applied at reduced extracellular sodium concentration possibly to impair calcium extrusion via the sodium/calcium exchange.	Sodium	188-194	kininogen 1	Homo sapiens	74-84
2002040-9	1991	Oscillations of intracellular calcium could be observed in +ras cells, if bradykinin was applied at reduced extracellular sodium concentration possibly to impair calcium extrusion via the sodium/calcium exchange.	Calcium	162-169	kininogen 1	Homo sapiens	74-84
2002040-10	1991	Bradykinin induces oscillations of cell membrane potential similarly in -ras cells loaded with GTP[S], a nonhydrolyzable analogue of GTP.	Guanosine Triphosphate	95-98	kininogen 1	Homo sapiens	0-10
2002040-10	1991	Bradykinin induces oscillations of cell membrane potential similarly in -ras cells loaded with GTP[S], a nonhydrolyzable analogue of GTP.	Guanosine Triphosphate	133-136	kininogen 1	Homo sapiens	0-10
2002040-11	1991	Thus, the altered response of ras oncogene expressing cells to bradykinin relates to the GTP binding property of the ras protein.	Guanosine Triphosphate	89-92	kininogen 1	Homo sapiens	63-73
1907204-1	1991	Stimulation of quiescent human fibroblasts with the peptide mitogen bradykinin (BK) led to a biphasic elevation in cellular 1,2-diacylglycerol (DAG), as estimated by either measurement of total DAG mass or [3H]arachidonate incorporation.	3h]arachidonate	207-222	kininogen 1	Homo sapiens	68-78
1907204-1	1991	Stimulation of quiescent human fibroblasts with the peptide mitogen bradykinin (BK) led to a biphasic elevation in cellular 1,2-diacylglycerol (DAG), as estimated by either measurement of total DAG mass or [3H]arachidonate incorporation.	3h]arachidonate	207-222	kininogen 1	Homo sapiens	80-82
1907204-2	1991	A rapid initial transient that peaked 15 s after BK addition was followed by a decline to near basal levels then a second rise to a plateau phase during which DAG levels remained elevated for less than or equal to 45 min.	1,2-diacylglycerol	159-162	kininogen 1	Homo sapiens	49-51
1907204-3	1991	The source of the initial DAG transient appeared to be primarily polyphosphoinositides as these phospholipids were rapidly hydrolyzed after BK addition.	1,2-diacylglycerol	26-29	kininogen 1	Homo sapiens	140-142
1907204-3	1991	The source of the initial DAG transient appeared to be primarily polyphosphoinositides as these phospholipids were rapidly hydrolyzed after BK addition.	Phosphatidylinositol Phosphates	65-86	kininogen 1	Homo sapiens	140-142
1907204-6	1991	Subsequent addition of BK under these conditions caused only a relatively slow accumulation of [3H]DAG to a plateau level, without an initial transient.	[3h]dag	95-102	kininogen 1	Homo sapiens	23-25
1907204-1	1991	Stimulation of quiescent human fibroblasts with the peptide mitogen bradykinin (BK) led to a biphasic elevation in cellular 1,2-diacylglycerol (DAG), as estimated by either measurement of total DAG mass or [3H]arachidonate incorporation.	1,2-diacylglycerol	124-142	kininogen 1	Homo sapiens	68-78
1907204-7	1991	Together with the observation that PC was found to decrease upon BK stimulation, these observations suggest that the late phase of DAG accumulation may involve breakdown of other phospholipids including PC.	Phosphatidylcholines	35-37	kininogen 1	Homo sapiens	65-67
1907204-7	1991	Together with the observation that PC was found to decrease upon BK stimulation, these observations suggest that the late phase of DAG accumulation may involve breakdown of other phospholipids including PC.	1,2-diacylglycerol	131-134	kininogen 1	Homo sapiens	65-67
1907204-10	1991	Stimulation of [32P]-prelabeled fibroblasts with serum, BK, vasopressin, or 12-O-tetradecanoyl phorbol acetate, but not epidermal growth factor or calcium ionophores, resulted in the rapid phosphorylation of MARCKS.	Phosphorus-32	16-19	kininogen 1	Homo sapiens	56-58
1907204-13	1991	These studies show that the biphasic DAG signal in BK-stimulated human fibroblasts correlates well with the state of activation of PK-C.	1,2-diacylglycerol	37-40	kininogen 1	Homo sapiens	51-53
1907204-1	1991	Stimulation of quiescent human fibroblasts with the peptide mitogen bradykinin (BK) led to a biphasic elevation in cellular 1,2-diacylglycerol (DAG), as estimated by either measurement of total DAG mass or [3H]arachidonate incorporation.	1,2-diacylglycerol	124-142	kininogen 1	Homo sapiens	80-82
1907204-1	1991	Stimulation of quiescent human fibroblasts with the peptide mitogen bradykinin (BK) led to a biphasic elevation in cellular 1,2-diacylglycerol (DAG), as estimated by either measurement of total DAG mass or [3H]arachidonate incorporation.	1,2-diacylglycerol	144-147	kininogen 1	Homo sapiens	68-78
1907204-1	1991	Stimulation of quiescent human fibroblasts with the peptide mitogen bradykinin (BK) led to a biphasic elevation in cellular 1,2-diacylglycerol (DAG), as estimated by either measurement of total DAG mass or [3H]arachidonate incorporation.	1,2-diacylglycerol	144-147	kininogen 1	Homo sapiens	80-82
1907204-1	1991	Stimulation of quiescent human fibroblasts with the peptide mitogen bradykinin (BK) led to a biphasic elevation in cellular 1,2-diacylglycerol (DAG), as estimated by either measurement of total DAG mass or [3H]arachidonate incorporation.	1,2-diacylglycerol	194-197	kininogen 1	Homo sapiens	68-78
1907204-1	1991	Stimulation of quiescent human fibroblasts with the peptide mitogen bradykinin (BK) led to a biphasic elevation in cellular 1,2-diacylglycerol (DAG), as estimated by either measurement of total DAG mass or [3H]arachidonate incorporation.	1,2-diacylglycerol	194-197	kininogen 1	Homo sapiens	80-82
1847932-4	1991	However, both EGF and bradykinin stimulated the accumulation of inositol phosphates in [3H]inositol-labeled cells indicating that stimulation of PI turnover is not sufficient for the induction of changes in actin/gelsolin complex levels.	Inositol Phosphates	64-83	kininogen 1	Homo sapiens	22-32
1847932-4	1991	However, both EGF and bradykinin stimulated the accumulation of inositol phosphates in [3H]inositol-labeled cells indicating that stimulation of PI turnover is not sufficient for the induction of changes in actin/gelsolin complex levels.	3h]inositol	88-99	kininogen 1	Homo sapiens	22-32
1993889-0	1991	Changes in inositol 1,4,5-trisphosphate and inositol 1,3,4,5- tetrakisphosphate mass accumulations in cultured adrenal chromaffin cells in response to bradykinin and histamine.	Inositol 1,4,5-Trisphosphate	11-39	kininogen 1	Homo sapiens	151-161
1993889-3	1991	Bradykinin increased the mass of Ins(1,3,4,5)P4 despite the failure in earlier studies with [3H]inositol-labelled cells to observe a bradykinin-mediated increase in content of [3H]InsP4.	Tritium	177-179	kininogen 1	Homo sapiens	0-10
1993889-3	1991	Bradykinin increased the mass of Ins(1,3,4,5)P4 despite the failure in earlier studies with [3H]inositol-labelled cells to observe a bradykinin-mediated increase in content of [3H]InsP4.	Tritium	177-179	kininogen 1	Homo sapiens	133-143
1993889-0	1991	Changes in inositol 1,4,5-trisphosphate and inositol 1,3,4,5- tetrakisphosphate mass accumulations in cultured adrenal chromaffin cells in response to bradykinin and histamine.	inositol-1,3,4,5-tetrakisphosphate	44-79	kininogen 1	Homo sapiens	151-161
1993889-1	1991	In previous studies it has been shown that both bradykinin and histamine increase the formation of 3H-labeled inositol phosphates in adrenal chromaffin cells prelabelled with [3H]inositol and that both these agonists stimulate release of catecholamines by a mechanism dependent on extracellular calcium.	Tritium	99-101	kininogen 1	Homo sapiens	48-58
1993889-4	1991	Bradykinin elicited a very rapid increase in level of Ins(1,4,5)P3, which was maximal at 5-10 s and then rapidly decreased to a small but sustained elevation at 2 min.	ins(1,4	54-61	kininogen 1	Homo sapiens	0-10
1993889-5	1991	The bradykinin-elicited Ins(1,3,4,5)P4 response increased to a maximum at 30-60 s and at 2 min was still elevated severalfold above basal levels.	inositol-1,3,4,5-tetrakisphosphate	24-38	kininogen 1	Homo sapiens	4-14
1993889-1	1991	In previous studies it has been shown that both bradykinin and histamine increase the formation of 3H-labeled inositol phosphates in adrenal chromaffin cells prelabelled with [3H]inositol and that both these agonists stimulate release of catecholamines by a mechanism dependent on extracellular calcium.	Inositol Phosphates	110-129	kininogen 1	Homo sapiens	48-58
1993889-6	1991	Histamine, which produced a larger overall total inositol phosphate response in [3H]inositol-loaded cells, produced significantly smaller Ins(1,4,5)P3 and Ins(1,3,4,5)P4 responses compared with bradykinin.	Histamine	0-9	kininogen 1	Homo sapiens	194-204
1993889-7	1991	The bradykinin stimulation of Ins(1,4,5)P3 accumulation was partially dependent on a high (1.8 mM) extracellular Ca2+ concentration, whereas the Ins(1,3,4,5)P4 response was almost completely lost when the extracellular Ca2+ concentration was reduced to 100 nM.	Inositol 1,4,5-Trisphosphate	30-42	kininogen 1	Homo sapiens	4-14
1993889-1	1991	In previous studies it has been shown that both bradykinin and histamine increase the formation of 3H-labeled inositol phosphates in adrenal chromaffin cells prelabelled with [3H]inositol and that both these agonists stimulate release of catecholamines by a mechanism dependent on extracellular calcium.	chromaffin	141-151	kininogen 1	Homo sapiens	48-58
1993889-8	1991	Changes in the inositol polyphosphate second messengers are compared with the time course of bradykinin-stimulated increases in free intracellular Ca2+ concentrations and noradrenaline release.	Norepinephrine	171-184	kininogen 1	Homo sapiens	93-103
1993889-1	1991	In previous studies it has been shown that both bradykinin and histamine increase the formation of 3H-labeled inositol phosphates in adrenal chromaffin cells prelabelled with [3H]inositol and that both these agonists stimulate release of catecholamines by a mechanism dependent on extracellular calcium.	3h]inositol	176-187	kininogen 1	Homo sapiens	48-58
1993889-1	1991	In previous studies it has been shown that both bradykinin and histamine increase the formation of 3H-labeled inositol phosphates in adrenal chromaffin cells prelabelled with [3H]inositol and that both these agonists stimulate release of catecholamines by a mechanism dependent on extracellular calcium.	Catecholamines	238-252	kininogen 1	Homo sapiens	48-58
1993889-1	1991	In previous studies it has been shown that both bradykinin and histamine increase the formation of 3H-labeled inositol phosphates in adrenal chromaffin cells prelabelled with [3H]inositol and that both these agonists stimulate release of catecholamines by a mechanism dependent on extracellular calcium.	Calcium	295-302	kininogen 1	Homo sapiens	48-58
1993889-3	1991	Bradykinin increased the mass of Ins(1,3,4,5)P4 despite the failure in earlier studies with [3H]inositol-labelled cells to observe a bradykinin-mediated increase in content of [3H]InsP4.	inositol-1,3,4,5-tetrakisphosphate	33-47	kininogen 1	Homo sapiens	0-10
2001422-0	1991	Interactions between inositol phosphates and cytosolic free calcium following bradykinin stimulation in cultured human skin fibroblasts.	Inositol Phosphates	21-40	kininogen 1	Homo sapiens	78-88
2008223-4	1991	Enalapril inhibits angiotensin converting enzyme, which not only metabolizes angiotensin I but also bradykinin and "substance P".	Enalapril	0-9	kininogen 1	Homo sapiens	100-110
2001422-0	1991	Interactions between inositol phosphates and cytosolic free calcium following bradykinin stimulation in cultured human skin fibroblasts.	Calcium	60-67	kininogen 1	Homo sapiens	78-88
2001422-3	1991	Thus, in the present studies, a comparison of the temporal response of inositol phosphates (IP3, IP2 and IP) and [Ca2+]i to a wide range of bradykinin concentrations was used to examine the relation of these two signal transduction events in cultured human skin fibroblasts (GM3652).	Inositol Phosphates	71-90	kininogen 1	Homo sapiens	140-150
2001422-3	1991	Thus, in the present studies, a comparison of the temporal response of inositol phosphates (IP3, IP2 and IP) and [Ca2+]i to a wide range of bradykinin concentrations was used to examine the relation of these two signal transduction events in cultured human skin fibroblasts (GM3652).	Inositol 1,4,5-Trisphosphate	92-95	kininogen 1	Homo sapiens	140-150
2001422-4	1991	In addition, the effects of alterations in internal or external calcium on the response of these second messengers to bradykinin were determined.	Calcium	64-71	kininogen 1	Homo sapiens	118-128
2001422-5	1991	Bradykinin stimulated accumulation of inositol phosphates and a rise of [Ca2+]i in a time- and dose-dependent manner.	Inositol Phosphates	38-57	kininogen 1	Homo sapiens	0-10
2001422-6	1991	Decreasing the bradykinin concentration from 1 microM to 0.1 microM increased the time until the IP3 peak, and when the bradykinin concentration was reduced to 0.01 microM IP3 was not detected.	Inositol 1,4,5-Trisphosphate	97-100	kininogen 1	Homo sapiens	15-25
2001422-10	1991	Although the bradykinin-stimulated initial spike of [Ca2+]i did not depend on extracellular calcium, the subsequent sustained levels of [Ca2+]i were abolished in calcium free medium.	Calcium	162-169	kininogen 1	Homo sapiens	13-23
2001422-11	1991	The bradykinin-stimulated inositol phosphate formation was not dependent on the extracellular calcium nor on the elevation of [Ca2+]i that was produced with Br-A23187.	Inositol Phosphates	26-44	kininogen 1	Homo sapiens	4-14
2001422-11	1991	The bradykinin-stimulated inositol phosphate formation was not dependent on the extracellular calcium nor on the elevation of [Ca2+]i that was produced with Br-A23187.	br-a23187	157-166	kininogen 1	Homo sapiens	4-14
2001422-12	1991	These results demonstrate that bradykinin-induced IP3 formation can be independent of [Ca2+]i and of external calcium, whereas changes in [Ca2+]i are partially dependent on external calcium.	Inositol 1,4,5-Trisphosphate	50-53	kininogen 1	Homo sapiens	31-41
2001422-12	1991	These results demonstrate that bradykinin-induced IP3 formation can be independent of [Ca2+]i and of external calcium, whereas changes in [Ca2+]i are partially dependent on external calcium.	Calcium	110-117	kininogen 1	Homo sapiens	31-41
2001422-12	1991	These results demonstrate that bradykinin-induced IP3 formation can be independent of [Ca2+]i and of external calcium, whereas changes in [Ca2+]i are partially dependent on external calcium.	Calcium	182-189	kininogen 1	Homo sapiens	31-41
2015416-3	1991	In some of these tests the effects of the new compounds were compared with those of the antagonist D-Arg0-Hyp2-Thi5,8-D-Phe7-BK (compound IV), described by Stewart & Vavrek (1987).	d-arg0-hyp2-thi5	99-115	kininogen 1	Homo sapiens	125-127
1719954-4	1991	The results indicate that Ca(2+)-calmodulin directly activates the endothelial nitric oxide synthase, thereby transducing agonist-induced increases in intracellular free Ca2+ concentration to nitric oxide formation from L-arginine, K(+)-induced depolarization of the endothelial cells markedly inhibited the sustained, but not initial phase of the intracellular Ca2+ response to bradykinin, indicating that K(+)-induced depolarization depresses the transmembrane Ca2+ influx.	Nitric Oxide	79-91	kininogen 1	Homo sapiens	379-389
1992693-5	1991	In fact, in umbilical vessels collected from normal parturients, bradykinin at a dose of 20 pmol produces a release of endothelial-derived relaxing factor equivalent to a relaxation induced by 59.9 +/- 11.0 and 30.8 +/- 11.4 pmol of glyceryl trinitrate for the artery and vein, respectively.	Nitroglycerin	233-252	kininogen 1	Homo sapiens	65-75
1992693-6	1991	The same dose of bradykinin in umbilical vessels, collected from pregnancy-induced hypertensive parturients, produces a release equivalent to 6.6 +/- 2.2 and 5.7 +/- 3.5 pmol of glyceryl trinitrate equivalent for the artery and vein, respectively.	Nitroglycerin	178-197	kininogen 1	Homo sapiens	17-27
1991651-6	1991	Addition of L-arginine to arginine-deficient but not arginine-containing endothelial cells rapidly restored the capacity of shear stress and bradykinin to generate EDRF.	Arginine	12-22	kininogen 1	Homo sapiens	141-151
1991651-6	1991	Addition of L-arginine to arginine-deficient but not arginine-containing endothelial cells rapidly restored the capacity of shear stress and bradykinin to generate EDRF.	Arginine	14-22	kininogen 1	Homo sapiens	141-151
1991651-6	1991	Addition of L-arginine to arginine-deficient but not arginine-containing endothelial cells rapidly restored the capacity of shear stress and bradykinin to generate EDRF.	Arginine	26-34	kininogen 1	Homo sapiens	141-151
1703413-2	1991	The bradykinin analog was an effective histamine secretagogue, inducing a comparable maximal level of release to that observed for anti-IgE.	Histamine	39-48	kininogen 1	Homo sapiens	4-14
1703413-5	1991	The kinetics of [DArg0-Hyp3-DPhe7]-bradykinin-stimulated histamine release were rapid, with 50% of maximal release being achieved within 30 sec, compared to 2-3 min for anti-IgE.	Histamine	57-66	kininogen 1	Homo sapiens	35-45
1703413-7	1991	Studies of the signal transduction pathways that may be involved in [DArg0-Hyp3-DPhe7]-bradykinin-induced histamine release revealed striking differences to results obtained with anti-IgE.	Histamine	106-115	kininogen 1	Homo sapiens	87-97
1703413-9	1991	Similarly, staurosporine, a relatively selective inhibitor of protein kinase C, and the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA) an activator of this enzyme, both have pronounced effects on IgE-mediated histamine release from SMC but were completely inactive with regard to [DArg0-Hyp3-DPhe7]-bradykinin-stimulated release.	Staurosporine	11-24	kininogen 1	Homo sapiens	310-320
1703413-9	1991	Similarly, staurosporine, a relatively selective inhibitor of protein kinase C, and the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA) an activator of this enzyme, both have pronounced effects on IgE-mediated histamine release from SMC but were completely inactive with regard to [DArg0-Hyp3-DPhe7]-bradykinin-stimulated release.	Phorbol Esters	88-101	kininogen 1	Homo sapiens	310-320
1703413-9	1991	Similarly, staurosporine, a relatively selective inhibitor of protein kinase C, and the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA) an activator of this enzyme, both have pronounced effects on IgE-mediated histamine release from SMC but were completely inactive with regard to [DArg0-Hyp3-DPhe7]-bradykinin-stimulated release.	Tetradecanoylphorbol Acetate	103-139	kininogen 1	Homo sapiens	310-320
1703413-9	1991	Similarly, staurosporine, a relatively selective inhibitor of protein kinase C, and the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA) an activator of this enzyme, both have pronounced effects on IgE-mediated histamine release from SMC but were completely inactive with regard to [DArg0-Hyp3-DPhe7]-bradykinin-stimulated release.	Tetradecanoylphorbol Acetate	141-144	kininogen 1	Homo sapiens	310-320
1703413-13	1991	We conclude that histamine release from SMC in response to [DArg0-Hyp3-DPhe7]-bradykinin occurs via a completely different mechanism from that in response to IgE-mediated stimuli.	Histamine	17-26	kininogen 1	Homo sapiens	78-88
2037586-0	1991	Phospholipid metabolism in bradykinin-stimulated human fibroblasts.	Phospholipids	0-12	kininogen 1	Homo sapiens	27-37
1992790-7	1991	L-NMMA as well as the inhibitor of guanylate cyclase methylene blue (10(-5) M) prevented the relaxations induced by clonidine, reduced those to serotonin, but hardly affected those to bradykinin.	omega-N-Methylarginine	0-6	kininogen 1	Homo sapiens	184-194
1992790-7	1991	L-NMMA as well as the inhibitor of guanylate cyclase methylene blue (10(-5) M) prevented the relaxations induced by clonidine, reduced those to serotonin, but hardly affected those to bradykinin.	Methylene Blue	53-67	kininogen 1	Homo sapiens	184-194
1992790-10	1991	An endothelium-derived relaxing factor different from nitric oxide must mediate the relaxations to bradykinin and contribute to those evoked by serotonin.	Nitric Oxide	54-66	kininogen 1	Homo sapiens	99-109
1845801-1	1991	The possible role of cAMP and/or arachidonic acid (and metabolites) in the stimulation of glucose transport elicited by bradykinin in Swiss 3T3 fibroblasts was investigated with particular attention to the part of this effect inhibitable by pertussis toxin.	Cyclic AMP	21-25	kininogen 1	Homo sapiens	120-130
1845801-1	1991	The possible role of cAMP and/or arachidonic acid (and metabolites) in the stimulation of glucose transport elicited by bradykinin in Swiss 3T3 fibroblasts was investigated with particular attention to the part of this effect inhibitable by pertussis toxin.	Glucose	90-97	kininogen 1	Homo sapiens	120-130
1845801-3	1991	In contrast, arachidonic acid, which is released by the cells exposed to bradykinin, was able to markedly stimulate glucose transport, however, only at relatively high concentrations (EC50 approximately 30 microM).	Arachidonic Acid	13-29	kininogen 1	Homo sapiens	73-83
1845801-3	1991	In contrast, arachidonic acid, which is released by the cells exposed to bradykinin, was able to markedly stimulate glucose transport, however, only at relatively high concentrations (EC50 approximately 30 microM).	Glucose	116-123	kininogen 1	Homo sapiens	73-83
1845801-5	1991	Neither of the last treatments affected the glucose transport activated by bradykinin to a great extent.	Glucose	44-51	kininogen 1	Homo sapiens	75-85
1845801-6	1991	Moreover, the bradykinin-induced arachidonic acid release was unaffected by pertussis toxin and markedly inhibited by two treatments ineffective on glucose transport, the blockade of [Ca2+]i increases elicited by the peptide and the administration of the phospholipase A2 blocker, quinacrine.	Arachidonic Acid	33-49	kininogen 1	Homo sapiens	14-24
1845801-6	1991	Moreover, the bradykinin-induced arachidonic acid release was unaffected by pertussis toxin and markedly inhibited by two treatments ineffective on glucose transport, the blockade of [Ca2+]i increases elicited by the peptide and the administration of the phospholipase A2 blocker, quinacrine.	Glucose	148-155	kininogen 1	Homo sapiens	14-24
1845801-6	1991	Moreover, the bradykinin-induced arachidonic acid release was unaffected by pertussis toxin and markedly inhibited by two treatments ineffective on glucose transport, the blockade of [Ca2+]i increases elicited by the peptide and the administration of the phospholipase A2 blocker, quinacrine.	Quinacrine	281-291	kininogen 1	Homo sapiens	14-24
1794833-3	1991	In vitro, L-NAME induced an endothelium-dependent contraction, inhibited the endothelium-dependent relaxations to acetylcholine or bradykinin, and potentiated the relaxation evoked by the nitric oxide donor SIN-1.	NG-Nitroarginine Methyl Ester	10-16	kininogen 1	Homo sapiens	131-141
1845801-7	1991	These results exclude that glucose transport stimulation by bradykinin is mediated intracellularly via arachidonic acid release.	Glucose	27-34	kininogen 1	Homo sapiens	60-70
1845801-7	1991	These results exclude that glucose transport stimulation by bradykinin is mediated intracellularly via arachidonic acid release.	Arachidonic Acid	103-119	kininogen 1	Homo sapiens	60-70
1987286-0	1991	Inositol phosphate formation in the human squamous cell carcinoma line SCC-12 F: studies with bradykinin, the calcium ionophore A23187, and sodium fluoride.	Inositol Phosphates	0-18	kininogen 1	Homo sapiens	94-104
1660035-4	1991	Topical application of the alpha-adrenergic agonist oxymetazoline significantly reduced bradykinin-induced subjective nasal congestion scores, but did not lead to a significant decrease in total symptoms or in vascular permeability.	Oxymetazoline	52-65	kininogen 1	Homo sapiens	88-98
1777235-5	1991	On the contrary, the tumour promoting phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) and the bradykinin derivative Des-Arg9bradykinin that we have previously shown as mitogens for mesangial cells, fail to trigger DNA synthesis or cell proliferation upon staurosporine treatment or in protein kinase C-depleted cells.	Staurosporine	264-277	kininogen 1	Homo sapiens	103-113
1786245-3	1991	With the use of antibodies it was demonstrated and confirmed that immunologically detectable plasma protein antigens appear and disappear in a time- and concentration-dependent sequence [IgG followed by fibrinogen followed by high-molecular weight kininogen (HMWK)] on silica surfaces.	Silicon Dioxide	269-275	kininogen 1	Homo sapiens	226-257
1786245-3	1991	With the use of antibodies it was demonstrated and confirmed that immunologically detectable plasma protein antigens appear and disappear in a time- and concentration-dependent sequence [IgG followed by fibrinogen followed by high-molecular weight kininogen (HMWK)] on silica surfaces.	Silicon Dioxide	269-275	kininogen 1	Homo sapiens	259-263
1987286-5	1991	Only bradykinin was active, stimulating the PLC-dependent generation of inositol (1,4,5) triphosphate (Ins(1,4,5)P3).	Inositol 1,4,5-Trisphosphate	72-101	kininogen 1	Homo sapiens	5-15
1987286-5	1991	Only bradykinin was active, stimulating the PLC-dependent generation of inositol (1,4,5) triphosphate (Ins(1,4,5)P3).	Inositol 1,4,5-Trisphosphate	103-115	kininogen 1	Homo sapiens	5-15
1726113-3	1991	Vascular permeability increases were triggered by suffusing the cheek pouch with histamine, bradykinin, or Compound 48/80 which stimulated the formation of focal FITC-D leakage sites in the postcapillary venules resulting in marked increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance.	fitc-d	162-168	kininogen 1	Homo sapiens	92-102
1842001-7	1991	Up to now, most nonpeptide compounds reported to exhibit BK antagonistic activity have been derived from plants, including many flavonoids, terpenes, and also synthetic substances with various molecular structures.	Flavonoids	128-138	kininogen 1	Homo sapiens	57-59
1842001-7	1991	Up to now, most nonpeptide compounds reported to exhibit BK antagonistic activity have been derived from plants, including many flavonoids, terpenes, and also synthetic substances with various molecular structures.	Terpenes	140-148	kininogen 1	Homo sapiens	57-59
1726113-3	1991	Vascular permeability increases were triggered by suffusing the cheek pouch with histamine, bradykinin, or Compound 48/80 which stimulated the formation of focal FITC-D leakage sites in the postcapillary venules resulting in marked increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance.	Fluorescein-5-isothiocyanate	162-166	kininogen 1	Homo sapiens	92-102
1726113-6	1991	Bradykinin stimulated formation of venular FITC-D leakage sites and increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance were not affected by treatment with calmidazolium, cytochalasin B, DDAVP, diphenhydramine, tubulazole C, or verapamil.	Fluorescein-5-isothiocyanate	43-47	kininogen 1	Homo sapiens	0-10
1726113-6	1991	Bradykinin stimulated formation of venular FITC-D leakage sites and increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance were not affected by treatment with calmidazolium, cytochalasin B, DDAVP, diphenhydramine, tubulazole C, or verapamil.	fitc-d	43-49	kininogen 1	Homo sapiens	0-10
1726113-6	1991	Bradykinin stimulated formation of venular FITC-D leakage sites and increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance were not affected by treatment with calmidazolium, cytochalasin B, DDAVP, diphenhydramine, tubulazole C, or verapamil.	fitc-d	82-88	kininogen 1	Homo sapiens	0-10
1726113-6	1991	Bradykinin stimulated formation of venular FITC-D leakage sites and increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance were not affected by treatment with calmidazolium, cytochalasin B, DDAVP, diphenhydramine, tubulazole C, or verapamil.	fitc-d	82-88	kininogen 1	Homo sapiens	0-10
1726113-6	1991	Bradykinin stimulated formation of venular FITC-D leakage sites and increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance were not affected by treatment with calmidazolium, cytochalasin B, DDAVP, diphenhydramine, tubulazole C, or verapamil.	fitc-d	82-88	kininogen 1	Homo sapiens	0-10
1726113-6	1991	Bradykinin stimulated formation of venular FITC-D leakage sites and increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance were not affected by treatment with calmidazolium, cytochalasin B, DDAVP, diphenhydramine, tubulazole C, or verapamil.	calmidazolium	178-191	kininogen 1	Homo sapiens	0-10
1726113-6	1991	Bradykinin stimulated formation of venular FITC-D leakage sites and increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance were not affected by treatment with calmidazolium, cytochalasin B, DDAVP, diphenhydramine, tubulazole C, or verapamil.	Cytochalasin B	193-207	kininogen 1	Homo sapiens	0-10
1726113-6	1991	Bradykinin stimulated formation of venular FITC-D leakage sites and increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance were not affected by treatment with calmidazolium, cytochalasin B, DDAVP, diphenhydramine, tubulazole C, or verapamil.	Diphenhydramine	216-231	kininogen 1	Homo sapiens	0-10
1726113-6	1991	Bradykinin stimulated formation of venular FITC-D leakage sites and increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance were not affected by treatment with calmidazolium, cytochalasin B, DDAVP, diphenhydramine, tubulazole C, or verapamil.	tubulazole c	233-245	kininogen 1	Homo sapiens	0-10
1726113-6	1991	Bradykinin stimulated formation of venular FITC-D leakage sites and increases in [FITC-D]S, [FITC-D]S/[FITC-D]p. 10(-6), and FITC-D clearance were not affected by treatment with calmidazolium, cytochalasin B, DDAVP, diphenhydramine, tubulazole C, or verapamil.	Verapamil	250-259	kininogen 1	Homo sapiens	0-10
1826973-1	1991	Dexamethasone 21-acetate (DMS 21-A) time- and dose-dependently suppressed bradykinin-stimulated prostacyclin synthesis in porcine aortic endothelial cells.	dexamethasone acetate	0-24	kininogen 1	Homo sapiens	74-84
1812285-3	1991	In contrast to its effect on [Ca2+]i, bradykinin only transiently elevated 1,4,5-IP3 and 1,3,4,5-IP4 levels.	Inositol 1,4,5-Trisphosphate	75-84	kininogen 1	Homo sapiens	38-48
1812285-3	1991	In contrast to its effect on [Ca2+]i, bradykinin only transiently elevated 1,4,5-IP3 and 1,3,4,5-IP4 levels.	1,3,4,5-ip4	89-100	kininogen 1	Homo sapiens	38-48
1812285-4	1991	Ten minutes after addition of bradykinin, both 1,4,5-IP3 and 1,3,4,5-IP4 levels returned to basal values, whereas Ca(2+)-influx was still unaltered.	Inositol 1,4,5-Trisphosphate	47-56	kininogen 1	Homo sapiens	30-40
1812285-4	1991	Ten minutes after addition of bradykinin, both 1,4,5-IP3 and 1,3,4,5-IP4 levels returned to basal values, whereas Ca(2+)-influx was still unaltered.	1,3,4,5-ip4	61-72	kininogen 1	Homo sapiens	30-40
1812285-5	1991	Furthermore, preincubation of endothelial cell with phorbol-12-myristate-13-acetate (PMA) abolished the stimulatory effect of bradykinin on the formation of 1,4,5-IP3 and 1,3,4,5-IP4, but did not affect the longlasting Ca(2+)-influx.	Tetradecanoylphorbol Acetate	52-83	kininogen 1	Homo sapiens	126-136
1812285-5	1991	Furthermore, preincubation of endothelial cell with phorbol-12-myristate-13-acetate (PMA) abolished the stimulatory effect of bradykinin on the formation of 1,4,5-IP3 and 1,3,4,5-IP4, but did not affect the longlasting Ca(2+)-influx.	Tetradecanoylphorbol Acetate	85-88	kininogen 1	Homo sapiens	126-136
1812285-5	1991	Furthermore, preincubation of endothelial cell with phorbol-12-myristate-13-acetate (PMA) abolished the stimulatory effect of bradykinin on the formation of 1,4,5-IP3 and 1,3,4,5-IP4, but did not affect the longlasting Ca(2+)-influx.	Inositol 1,4,5-Trisphosphate	157-166	kininogen 1	Homo sapiens	126-136
1812285-5	1991	Furthermore, preincubation of endothelial cell with phorbol-12-myristate-13-acetate (PMA) abolished the stimulatory effect of bradykinin on the formation of 1,4,5-IP3 and 1,3,4,5-IP4, but did not affect the longlasting Ca(2+)-influx.	1,3,4,5-ip4	171-182	kininogen 1	Homo sapiens	126-136
2266124-5	1990	Na-K-2Cl cotransport, measured as bumetanide-sensitive potassium influx, was stimulated 118 +/- 30% by bradykinin (p less than 0.01) at physiologic ion concentrations.	Bumetanide	34-44	kininogen 1	Homo sapiens	103-113
2266124-7	1990	Simultaneous measurement of the binding of tracer [3H]bumetanide and its inhibition of potassium influx in medium containing 10 mM potassium and 130 mM chloride revealed a turnover number for the cotransporter of 293 +/- 68 s-1 which increased to 687 +/- 105 s-1 with bradykinin (p less than 0.001).	[3h]bumetanide	50-64	kininogen 1	Homo sapiens	268-278
2266124-9	1990	Bradykinin also increased the affinity of the cotransporter for bumetanide as indicated by a decrease in the Ki for potassium influx from 464 +/- 46 nM to 219 +/- 19 nM (p less than 0.005).	Bumetanide	64-74	kininogen 1	Homo sapiens	0-10
2266124-9	1990	Bradykinin also increased the affinity of the cotransporter for bumetanide as indicated by a decrease in the Ki for potassium influx from 464 +/- 46 nM to 219 +/- 19 nM (p less than 0.005).	Potassium	116-125	kininogen 1	Homo sapiens	0-10
2266124-12	1990	This, together with the increased affinity for bumetanide, strongly suggests that a change in cotransporter structure is occurring in response to bradykinin.	Bumetanide	47-57	kininogen 1	Homo sapiens	146-156
1849639-9	1991	Enalaprilat may compensate for the reduction of mucosal blood flow by limiting formation of angiotensin II and/or preventing degradation of bradykinin.	Enalaprilat	0-11	kininogen 1	Homo sapiens	140-150
1812285-1	1991	Since inositol 1,4,5-trisphosphate (1,4,5-IP3) and inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP4) have been described to modulate Ca(2+)-channels, we investigated the possible participation of 1,4,5-IP3 and/or 1,3,4,5-IP4 in the bradykinin-induced Ca(2+)-influx into cultured porcine aortic endothelial cells.	Inositol 1,4,5-Trisphosphate	6-34	kininogen 1	Homo sapiens	231-241
1812285-1	1991	Since inositol 1,4,5-trisphosphate (1,4,5-IP3) and inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP4) have been described to modulate Ca(2+)-channels, we investigated the possible participation of 1,4,5-IP3 and/or 1,3,4,5-IP4 in the bradykinin-induced Ca(2+)-influx into cultured porcine aortic endothelial cells.	Inositol 1,4,5-Trisphosphate	36-45	kininogen 1	Homo sapiens	231-241
1812285-1	1991	Since inositol 1,4,5-trisphosphate (1,4,5-IP3) and inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP4) have been described to modulate Ca(2+)-channels, we investigated the possible participation of 1,4,5-IP3 and/or 1,3,4,5-IP4 in the bradykinin-induced Ca(2+)-influx into cultured porcine aortic endothelial cells.	Inositol	6-14	kininogen 1	Homo sapiens	231-241
1812285-1	1991	Since inositol 1,4,5-trisphosphate (1,4,5-IP3) and inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP4) have been described to modulate Ca(2+)-channels, we investigated the possible participation of 1,4,5-IP3 and/or 1,3,4,5-IP4 in the bradykinin-induced Ca(2+)-influx into cultured porcine aortic endothelial cells.	,3,4,5-tetrakisphosphate	61-85	kininogen 1	Homo sapiens	231-241
1812285-1	1991	Since inositol 1,4,5-trisphosphate (1,4,5-IP3) and inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP4) have been described to modulate Ca(2+)-channels, we investigated the possible participation of 1,4,5-IP3 and/or 1,3,4,5-IP4 in the bradykinin-induced Ca(2+)-influx into cultured porcine aortic endothelial cells.	1,3,4,5-ip4	87-98	kininogen 1	Homo sapiens	231-241
1812285-1	1991	Since inositol 1,4,5-trisphosphate (1,4,5-IP3) and inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP4) have been described to modulate Ca(2+)-channels, we investigated the possible participation of 1,4,5-IP3 and/or 1,3,4,5-IP4 in the bradykinin-induced Ca(2+)-influx into cultured porcine aortic endothelial cells.	Inositol 1,4,5-Trisphosphate	195-204	kininogen 1	Homo sapiens	231-241
1812285-1	1991	Since inositol 1,4,5-trisphosphate (1,4,5-IP3) and inositol 1,3,4,5-tetrakisphosphate (1,3,4,5-IP4) have been described to modulate Ca(2+)-channels, we investigated the possible participation of 1,4,5-IP3 and/or 1,3,4,5-IP4 in the bradykinin-induced Ca(2+)-influx into cultured porcine aortic endothelial cells.	1,3,4,5-ip4	212-223	kininogen 1	Homo sapiens	231-241
2148087-0	1990	Enhancement of bradykinin-induced prostacyclin synthesis in porcine aortic endothelial cells by pertussis toxin.	Epoprostenol	34-46	kininogen 1	Homo sapiens	15-25
2148087-2	1990	Bradykinin-stimulated prostacyclin synthesis in porcine aortic endothelial cells was enhanced by pretreatment of the cells with pertussis toxin or islet-activating protein (IAP) for 5 hr or longer.	Epoprostenol	22-34	kininogen 1	Homo sapiens	0-10
2148087-3	1990	Although ADP-ribosylation of a protein with a molecular weight of 41-42 kD in the cell membranes was completed by 3 hr after the addition of IAP into the incubation medium, there was good correlation between enhancement of bradykinin-induced prostacyclin synthesis and ADP-ribosylation of the IAP substrate over a wide range of IAP concentrations.	Epoprostenol	242-254	kininogen 1	Homo sapiens	223-233
2148087-4	1990	Furthermore, even if IAP was removed from the incubation medium at 3 hr, bradykinin-induced prostaglandin synthesis at 24 hr was still potentiated.	Prostaglandins	92-105	kininogen 1	Homo sapiens	73-83
2148087-5	1990	Cycloheximide and actinomycin D enhanced bradykinin-induced prostacyclin synthesis and apparently blocked the effect of IAP.	Cycloheximide	0-13	kininogen 1	Homo sapiens	41-51
2148087-5	1990	Cycloheximide and actinomycin D enhanced bradykinin-induced prostacyclin synthesis and apparently blocked the effect of IAP.	Dactinomycin	18-31	kininogen 1	Homo sapiens	41-51
2148087-5	1990	Cycloheximide and actinomycin D enhanced bradykinin-induced prostacyclin synthesis and apparently blocked the effect of IAP.	Epoprostenol	60-72	kininogen 1	Homo sapiens	41-51
2148087-8	1990	These results suggest that the enhancement of bradykinin-induced prostacyclin synthesis by IAP is associated with a decrease in the level of lipocortin I.	Epoprostenol	65-77	kininogen 1	Homo sapiens	46-56
1964766-3	1990	HPLC analyses indicated that meprin cleaved bradykinin and nitrobradykinin between Phe5 (or Phe5(NO2)) and Ser6.	Nitrogen Dioxide	97-100	kininogen 1	Homo sapiens	44-54
1826973-1	1991	Dexamethasone 21-acetate (DMS 21-A) time- and dose-dependently suppressed bradykinin-stimulated prostacyclin synthesis in porcine aortic endothelial cells.	dms	26-29	kininogen 1	Homo sapiens	74-84
1826973-1	1991	Dexamethasone 21-acetate (DMS 21-A) time- and dose-dependently suppressed bradykinin-stimulated prostacyclin synthesis in porcine aortic endothelial cells.	Epoprostenol	96-108	kininogen 1	Homo sapiens	74-84
1826973-2	1991	The suppression was more prominent in the presence of pertussis toxin, which by itself could enhance bradykinin-induced prostacyclin synthesis.	Epoprostenol	120-132	kininogen 1	Homo sapiens	101-111
1826973-6	1991	The suppression of bradykinin-induced prostacyclin synthesis by DMS 21-A was completely blocked by cycloheximide.	Epoprostenol	38-50	kininogen 1	Homo sapiens	19-29
1826973-6	1991	The suppression of bradykinin-induced prostacyclin synthesis by DMS 21-A was completely blocked by cycloheximide.	dexamethasone acetate	64-72	kininogen 1	Homo sapiens	19-29
1826973-6	1991	The suppression of bradykinin-induced prostacyclin synthesis by DMS 21-A was completely blocked by cycloheximide.	Cycloheximide	99-112	kininogen 1	Homo sapiens	19-29
2081544-0	1990	Cytosolic calcium and membrane conductance in response to platelet-derived growth factor and bradykinin stimulation in single human fibroblasts.	Calcium	10-17	kininogen 1	Homo sapiens	93-103
2081544-1	1990	Bradykinin (BK) and platelet-derived growth factor (PDGF) act as mitogens and stimulate phosphatidylinositol (PI) turnover in human fibroblasts.	Phosphatidylinositols	88-108	kininogen 1	Homo sapiens	0-10
2174449-0	1990	Bradykinin induces phosphoinositide turnover, 1,2-diglyceride formation, and growth in cultured adult human keratinocytes.	Phosphatidylinositols	19-35	kininogen 1	Homo sapiens	0-10
2086448-2	1990	The present studies show that the human lymphocyte response to two positive chemokinetic signals (bradykinin and lymphocyte chemoattractant factor) can be interrupted by inhibitors of S-adenosyl-L-methionine-mediated transmethylation reactions.	Methionine	195-207	kininogen 1	Homo sapiens	98-108
2174449-0	1990	Bradykinin induces phosphoinositide turnover, 1,2-diglyceride formation, and growth in cultured adult human keratinocytes.	1,2-diglyceride	46-61	kininogen 1	Homo sapiens	0-10
2174449-2	1990	Keratinocytes specifically bound [3H]bradykinin with high affinity (kd = 3.4 nM) and displayed 1.5 X 10(5) binding sites/cell.	Tritium	34-36	kininogen 1	Homo sapiens	37-47
2174449-3	1990	Bradykinin caused a rapid dose-dependent increase in inositol trisphosphate (IP3) inositol bisphosphate, and inositol monophosphate.	inositol 1,2,3-trisphosphate	53-75	kininogen 1	Homo sapiens	0-10
2174449-3	1990	Bradykinin caused a rapid dose-dependent increase in inositol trisphosphate (IP3) inositol bisphosphate, and inositol monophosphate.	Inositol 1,4,5-Trisphosphate	77-80	kininogen 1	Homo sapiens	0-10
2174449-3	1990	Bradykinin caused a rapid dose-dependent increase in inositol trisphosphate (IP3) inositol bisphosphate, and inositol monophosphate.	inositol bisphosphate	82-103	kininogen 1	Homo sapiens	0-10
2261473-0	1990	Bradykinin and its Gly6 analogue are substrates of cyclophilin: a fluorine-19 magnetization transfer study.	Hexaglycine	19-23	kininogen 1	Homo sapiens	0-10
2174449-3	1990	Bradykinin caused a rapid dose-dependent increase in inositol trisphosphate (IP3) inositol bisphosphate, and inositol monophosphate.	Inositol Phosphates	109-131	kininogen 1	Homo sapiens	0-10
2261473-0	1990	Bradykinin and its Gly6 analogue are substrates of cyclophilin: a fluorine-19 magnetization transfer study.	Fluorine	66-74	kininogen 1	Homo sapiens	0-10
2174449-5	1990	Half maximal stimulation of IP3 formation was observed at 27 nM bradykinin.	Inositol 1,4,5-Trisphosphate	28-31	kininogen 1	Homo sapiens	64-74
2174449-6	1990	IP3 accumulation was equally elevated by bradykinin and lys-bradykinin but was not stimulated by des-Arg9-bradykinin, indicating that phospholipase C in cultured keratinocytes is coupled to B2 bradykinin receptors.	Inositol 1,4,5-Trisphosphate	0-3	kininogen 1	Homo sapiens	41-51
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	Tritium	151-153	kininogen 1	Homo sapiens	120-122
2174449-6	1990	IP3 accumulation was equally elevated by bradykinin and lys-bradykinin but was not stimulated by des-Arg9-bradykinin, indicating that phospholipase C in cultured keratinocytes is coupled to B2 bradykinin receptors.	Inositol 1,4,5-Trisphosphate	0-3	kininogen 1	Homo sapiens	60-70
2174449-6	1990	IP3 accumulation was equally elevated by bradykinin and lys-bradykinin but was not stimulated by des-Arg9-bradykinin, indicating that phospholipase C in cultured keratinocytes is coupled to B2 bradykinin receptors.	Inositol 1,4,5-Trisphosphate	0-3	kininogen 1	Homo sapiens	60-70
2174449-6	1990	IP3 accumulation was equally elevated by bradykinin and lys-bradykinin but was not stimulated by des-Arg9-bradykinin, indicating that phospholipase C in cultured keratinocytes is coupled to B2 bradykinin receptors.	Inositol 1,4,5-Trisphosphate	0-3	kininogen 1	Homo sapiens	60-70
2174449-7	1990	Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content.	Phorbol Esters	39-52	kininogen 1	Homo sapiens	100-110
2174449-7	1990	Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content.	Phorbol Esters	39-52	kininogen 1	Homo sapiens	208-218
2174449-7	1990	Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content.	Tetradecanoylphorbol Acetate	54-57	kininogen 1	Homo sapiens	100-110
2174449-7	1990	Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content.	Tetradecanoylphorbol Acetate	54-57	kininogen 1	Homo sapiens	208-218
2174449-7	1990	Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content.	Inositol 1,4,5-Trisphosphate	119-122	kininogen 1	Homo sapiens	100-110
2174449-7	1990	Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content.	1,2-diacylglycerol	258-276	kininogen 1	Homo sapiens	100-110
2174449-7	1990	Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content.	1,2-diacylglycerol	258-276	kininogen 1	Homo sapiens	208-218
2174449-7	1990	Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content.	1,2-diacylglycerol	278-281	kininogen 1	Homo sapiens	100-110
2174449-7	1990	Treatment of keratinocytes with active phorbol ester (TPA) caused a significant inhibition (50%) of bradykinin-induced IP3 accumulation, suggesting negative regulation of phospholipase C by protein kinase C. Bradykinin also caused a significant elevation in 1,2-diacylglycerol (DAG) content.	1,2-diacylglycerol	278-281	kininogen 1	Homo sapiens	208-218
2122744-0	1990	Different activation of L-arginine pathway by bradykinin, serotonin, and clonidine in coronary arteries.	Arginine	24-34	kininogen 1	Homo sapiens	46-56
2122744-6	1990	In contrast, L-NMMA, methylene blue, and hemoglobin caused a weak inhibition of the endothelium-dependent relaxation evoked by bradykinin; indomethacin and tranylcypromine had no effect.	N(G)-monomethylarginine acetate	13-19	kininogen 1	Homo sapiens	127-137
2122744-6	1990	In contrast, L-NMMA, methylene blue, and hemoglobin caused a weak inhibition of the endothelium-dependent relaxation evoked by bradykinin; indomethacin and tranylcypromine had no effect.	Methylene Blue	21-35	kininogen 1	Homo sapiens	127-137
2122744-9	1990	Thus endothelium-dependent relaxations to serotonin and to the alpha 2-adrenergic agonist clonidine are mediated through the release of nitric oxide formed from L-arginine in endothelial cells, whereas bradykinin evokes endothelium-dependent relaxations via a different pathway.	Clonidine	90-99	kininogen 1	Homo sapiens	202-212
1963797-10	1990	Pretreatment for 10 min with TPA (but not the relatively inactive 4-methoxy TPA) or the non-phorbol protein kinase C stimulator mezerein potently inhibited bradykinin- and histamine-stimulated accumulation of total [3H]-inositol phosphate; inhibition of [3H]-inositol phosphate formation was also seen with 24 h TPA treatment.	Tetradecanoylphorbol Acetate	29-32	kininogen 1	Homo sapiens	156-166
2244869-3	1990	Bradykinin caused a much larger increase in Ins(1,4,5)P3 than did angiotensin.	Inositol 1,4,5-Trisphosphate	44-56	kininogen 1	Homo sapiens	0-10
2244869-5	1990	Bradykinin, but not angiotensin, caused a rapid (within 2 s) fall in the levels of PtdIns(4,5)P2 and PtdIns(4)P.	Phosphatidylinositol 4,5-Diphosphate	83-96	kininogen 1	Homo sapiens	0-10
2244869-5	1990	Bradykinin, but not angiotensin, caused a rapid (within 2 s) fall in the levels of PtdIns(4,5)P2 and PtdIns(4)P.	phosphatidylinositol 4-phosphate	101-111	kininogen 1	Homo sapiens	0-10
1963797-10	1990	Pretreatment for 10 min with TPA (but not the relatively inactive 4-methoxy TPA) or the non-phorbol protein kinase C stimulator mezerein potently inhibited bradykinin- and histamine-stimulated accumulation of total [3H]-inositol phosphate; inhibition of [3H]-inositol phosphate formation was also seen with 24 h TPA treatment.	3h]-inositol phosphate	216-238	kininogen 1	Homo sapiens	156-166
1963797-10	1990	Pretreatment for 10 min with TPA (but not the relatively inactive 4-methoxy TPA) or the non-phorbol protein kinase C stimulator mezerein potently inhibited bradykinin- and histamine-stimulated accumulation of total [3H]-inositol phosphate; inhibition of [3H]-inositol phosphate formation was also seen with 24 h TPA treatment.	Tritium	216-219	kininogen 1	Homo sapiens	156-166
1963797-10	1990	Pretreatment for 10 min with TPA (but not the relatively inactive 4-methoxy TPA) or the non-phorbol protein kinase C stimulator mezerein potently inhibited bradykinin- and histamine-stimulated accumulation of total [3H]-inositol phosphate; inhibition of [3H]-inositol phosphate formation was also seen with 24 h TPA treatment.	Inositol Phosphates	220-238	kininogen 1	Homo sapiens	156-166
2211876-5	1990	Nanomolar concentrations of BK and PMA also stimulated Lucifer yellow uptake by the brain microvessel endothelial cell by 40 and 95%, respectively.	lucifer yellow	55-69	kininogen 1	Homo sapiens	28-30
2211876-8	1990	Results indicated that Ang II, saralasin, BK, and PMA produce similar stimulatory effects on brain microvessel endothelial cell fluid-phase endocytosis with only Ang II and saralasin, producing increases in brain microvessel endothelial cell fluid-phase endocytosis that appeared to be mediated by prostaglandins.	Prostaglandins	298-312	kininogen 1	Homo sapiens	42-44
2177500-0	1990	Bradykinin-2 receptor-mediated release of 3H-arachidonic acid and formation of prostaglandin E2 in human gingival fibroblasts.	3h-arachidonic acid	42-61	kininogen 1	Homo sapiens	0-10
2177500-1	1990	Bradykinin stimulated production of prostaglandin E2 (PGE2) and the release of 3H-arachidonic acid by gingival fibroblasts in a time- and dose-dependent manner.	Dinoprostone	54-58	kininogen 1	Homo sapiens	0-10
2177500-0	1990	Bradykinin-2 receptor-mediated release of 3H-arachidonic acid and formation of prostaglandin E2 in human gingival fibroblasts.	Dinoprostone	79-95	kininogen 1	Homo sapiens	0-10
2177500-1	1990	Bradykinin stimulated production of prostaglandin E2 (PGE2) and the release of 3H-arachidonic acid by gingival fibroblasts in a time- and dose-dependent manner.	3h-arachidonic acid	79-98	kininogen 1	Homo sapiens	0-10
2177500-1	1990	Bradykinin stimulated production of prostaglandin E2 (PGE2) and the release of 3H-arachidonic acid by gingival fibroblasts in a time- and dose-dependent manner.	Dinoprostone	36-52	kininogen 1	Homo sapiens	0-10
2177500-3	1990	Several structurally unrelated inhibitors of arachidonic acid metabolism via the cyclooxygenase pathway totally abolished the PGE2 response to bradykinin.	Arachidonic Acid	45-61	kininogen 1	Homo sapiens	143-153
2171345-2	1990	Serum or bradykinin dramatically stimulated HMA-sensitive Na+ influx in WI-38 cells, whereas in SV40-transformed WI-38 cells, serum, but not bradykinin, produced a large increase in HMA-sensitive Na+ influx.	5-(N,N-hexamethylene)amiloride	44-47	kininogen 1	Homo sapiens	9-19
2177500-3	1990	Several structurally unrelated inhibitors of arachidonic acid metabolism via the cyclooxygenase pathway totally abolished the PGE2 response to bradykinin.	Dinoprostone	126-130	kininogen 1	Homo sapiens	143-153
2177500-4	1990	The stimulation of PGE2 formation was seen at and above 10 nmol/l of bradykinin.	Dinoprostone	19-23	kininogen 1	Homo sapiens	69-79
2177500-5	1990	Des-Arg9-bradykinin was 100-fold less potent compared to bradykinin.	des-arg9	0-8	kininogen 1	Homo sapiens	9-19
2177500-7	1990	Met-Lys-bradykinin and Lys-bradykinin also enhanced PGE2 formation in gingival fibroblasts.	Dinoprostone	52-56	kininogen 1	Homo sapiens	8-18
2177500-7	1990	Met-Lys-bradykinin and Lys-bradykinin also enhanced PGE2 formation in gingival fibroblasts.	Dinoprostone	52-56	kininogen 1	Homo sapiens	27-37
2177500-8	1990	The stimulatory action of bradykinin on 3H-arachidonic acid release was observed after 30 s and progressively increased for at least 15 min.	3h-arachidonic acid	40-59	kininogen 1	Homo sapiens	26-36
2177500-9	1990	The stimulatory effect on 3H-arachidonic acid release by bradykinin was seen at and above 10 nmol/l, whereas des-Arg9-bradykinin was without effect up to a concentration of 1 mumol/l.	3h-arachidonic acid	26-45	kininogen 1	Homo sapiens	57-67
2177500-11	1990	These data show that bradykinin, via a B2-receptor-mediated pathway, can stimulate arachidonic acid release and subsequent prostanoid formation in gingival fibroblasts.	Arachidonic Acid	83-99	kininogen 1	Homo sapiens	21-31
2177500-11	1990	These data show that bradykinin, via a B2-receptor-mediated pathway, can stimulate arachidonic acid release and subsequent prostanoid formation in gingival fibroblasts.	Prostaglandins	123-133	kininogen 1	Homo sapiens	21-31
2177500-12	1990	Consequently, gingival fibroblasts may contribute, by a bradykinin-regulated reaction, to the enhanced amounts of prostanoids found in gingival tissues and crevicular fluids in patients with periodontal diseases.	Prostaglandins	114-125	kininogen 1	Homo sapiens	56-66
2261473-1	1990	Fluorine-19 magnetization transfer experiments have been used to determine the rates of cis/trans isomerization about the X-Pro7 peptide bond in [p-fluoro-Phe8]bradykinin (cis/trans ratio approximately 0.1) and its Gly6 analogue (cis/trans ratio approximately 0.4).	Fluorine	0-8	kininogen 1	Homo sapiens	160-170
2261473-1	1990	Fluorine-19 magnetization transfer experiments have been used to determine the rates of cis/trans isomerization about the X-Pro7 peptide bond in [p-fluoro-Phe8]bradykinin (cis/trans ratio approximately 0.1) and its Gly6 analogue (cis/trans ratio approximately 0.4).	-phe8	154-159	kininogen 1	Homo sapiens	160-170
2261473-1	1990	Fluorine-19 magnetization transfer experiments have been used to determine the rates of cis/trans isomerization about the X-Pro7 peptide bond in [p-fluoro-Phe8]bradykinin (cis/trans ratio approximately 0.1) and its Gly6 analogue (cis/trans ratio approximately 0.4).	Hexaglycine	215-219	kininogen 1	Homo sapiens	160-170
2261473-3	1990	Magnetization transfer measurements over the temperature range 40-75 degrees C in the absence of enzyme give activation energies of 22.8 and 23.0 kcal/mol for [p-fluoro-Phe8]bradykinin and its Gly6 analogue, respectively.	Hexaglycine	193-197	kininogen 1	Homo sapiens	174-184
2261473-5	1990	At a peptide concentration of 2.2 mM, the catalytic activity expressed as kc per micromolar cyclophilin was determined to be 1.2 s-1/microM for [p-fluoro-Phe8]bradykinin and 0.13 s-1/microM for the Gly6 analogue.	Hexaglycine	198-202	kininogen 1	Homo sapiens	159-169
2280902-0	1990	Divalent cations effectively replace Ca2+ and support bradykinin induced noradrenaline release.	Norepinephrine	73-86	kininogen 1	Homo sapiens	54-64
2280902-1	1990	Bradykinin (BK), a nonapeptide acting at the B2-type BK-receptor, and depolarization with high KCl (50 mM), induce catecholamine secretion in pheochromocytoma cells (PC-12).	Catecholamines	115-128	kininogen 1	Homo sapiens	0-10
2280902-1	1990	Bradykinin (BK), a nonapeptide acting at the B2-type BK-receptor, and depolarization with high KCl (50 mM), induce catecholamine secretion in pheochromocytoma cells (PC-12).	Catecholamines	115-128	kininogen 1	Homo sapiens	12-14
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	Barium	17-23	kininogen 1	Homo sapiens	120-122
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	N-methyl-valyl-amiclenomycin	25-29	kininogen 1	Homo sapiens	120-122
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	Strontium	32-41	kininogen 1	Homo sapiens	120-122
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	strontium cation	43-47	kininogen 1	Homo sapiens	120-122
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	Metals	9-14	kininogen 1	Homo sapiens	120-122
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	Manganese	74-83	kininogen 1	Homo sapiens	120-122
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	Manganese(2+)	85-89	kininogen 1	Homo sapiens	120-122
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	Lanthanum	94-103	kininogen 1	Homo sapiens	120-122
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	lanthanum(3+)	105-109	kininogen 1	Homo sapiens	120-122
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	Tritium	132-134	kininogen 1	Homo sapiens	120-122
2280902-3	1990	Alkaline metals, barium (Ba2+), strontium (Sr2+) and other metal cations, manganese (Mn2+) or lanthanum (La3+), support BK-induced [3H]noradrenaline ([3H]NA) release.	Norepinephrine	135-148	kininogen 1	Homo sapiens	120-122
2171345-2	1990	Serum or bradykinin dramatically stimulated HMA-sensitive Na+ influx in WI-38 cells, whereas in SV40-transformed WI-38 cells, serum, but not bradykinin, produced a large increase in HMA-sensitive Na+ influx.	5-(N,N-hexamethylene)amiloride	182-185	kininogen 1	Homo sapiens	9-19
2282472-4	1990	Angiotensins consistently elicited contractile responses, whereas both bradykinin and acetylcholine produced relaxation of the arterial rings when active tone was induced by prostaglandin F2 alpha.	Dinoprost	174-196	kininogen 1	Homo sapiens	71-81
2076202-6	1990	Sixty eight benign effusions were negative for Ile-Ser-bradykinin.	Ile-Ser	47-54	kininogen 1	Homo sapiens	55-65
2170274-5	1990	The endothelium-derived relaxing factor generated by bradykinin in this vascular bed is an oxygen radical generated in association with enhanced arachidonate metabolism via cyclooxygenase.	Reactive Oxygen Species	91-105	kininogen 1	Homo sapiens	53-63
2170274-5	1990	The endothelium-derived relaxing factor generated by bradykinin in this vascular bed is an oxygen radical generated in association with enhanced arachidonate metabolism via cyclooxygenase.	Arachidonic Acid	145-157	kininogen 1	Homo sapiens	53-63
2170274-6	1990	In the microcirculation of skeletal muscle, on the other hand, the vasodilation from bradykinin is mediated partly by prostacyclin and partly by an endothelium-derived relaxing factor similar to that generated by acetylcholine.	Epoprostenol	118-130	kininogen 1	Homo sapiens	85-95
2278039-6	1990	Incubation of Pt-XI with purified factor XII, HMWK, and kaolin produced activated platelet factor XI clotting activity and, concomitantly, the generation over time of a new chain on reduced SDS-PAGE of Mr = 44,500.	Sodium Dodecyl Sulfate	190-193	kininogen 1	Homo sapiens	46-50
2282472-8	1990	Relaxant responses to bradykinin were unchanged during blockade of thromboxane A2 synthesis by dazoxiben (30 microM) and proved to be largely resistant to blockade by indomethacin (1 microM) and the prostaglandin I2 (prostacyclin) synthesis inhibitor, tranylcypromine (40 microM).	dazoxiben	95-104	kininogen 1	Homo sapiens	22-32
2282472-8	1990	Relaxant responses to bradykinin were unchanged during blockade of thromboxane A2 synthesis by dazoxiben (30 microM) and proved to be largely resistant to blockade by indomethacin (1 microM) and the prostaglandin I2 (prostacyclin) synthesis inhibitor, tranylcypromine (40 microM).	Epoprostenol	217-229	kininogen 1	Homo sapiens	22-32
2282472-8	1990	Relaxant responses to bradykinin were unchanged during blockade of thromboxane A2 synthesis by dazoxiben (30 microM) and proved to be largely resistant to blockade by indomethacin (1 microM) and the prostaglandin I2 (prostacyclin) synthesis inhibitor, tranylcypromine (40 microM).	Tranylcypromine	252-267	kininogen 1	Homo sapiens	22-32
2284196-1	1990	We report that the acylation of the N-terminus of [D-Arg0,Hyp3,Thi5,8,D-Phe7]bradykinin, one of the most potent bradykinin antagonists described to date, with 1-adamantane-acetic acid, results in an analogue with more than ten times enhanced potency.	thi5	63-67	kininogen 1	Homo sapiens	77-87
2127257-3	1990	In vitro studies suggest that loss of bradykinin responsiveness may be due to the secondary generation of relaxant prostanoids.	Prostaglandins	115-126	kininogen 1	Homo sapiens	38-48
2127257-4	1990	We have used the potent cyclooxygenase inhibitor flurbiprofen to investigate the potential role of prostanoid generation in bradykinin tachyphylaxis in eight asthmatic patients.	Prostaglandins	99-109	kininogen 1	Homo sapiens	124-134
2127257-10	1990	This study demonstrates that repeated exposure to inhaled bradykinin results in loss of the bronchoconstrictor response which appears specific for this agonist and not secondary to the increased generation of protective prostanoids.	Prostaglandins	220-231	kininogen 1	Homo sapiens	58-68
2284196-1	1990	We report that the acylation of the N-terminus of [D-Arg0,Hyp3,Thi5,8,D-Phe7]bradykinin, one of the most potent bradykinin antagonists described to date, with 1-adamantane-acetic acid, results in an analogue with more than ten times enhanced potency.	thi5	63-67	kininogen 1	Homo sapiens	112-122
2284196-1	1990	We report that the acylation of the N-terminus of [D-Arg0,Hyp3,Thi5,8,D-Phe7]bradykinin, one of the most potent bradykinin antagonists described to date, with 1-adamantane-acetic acid, results in an analogue with more than ten times enhanced potency.	d-phe7	70-76	kininogen 1	Homo sapiens	77-87
2284196-1	1990	We report that the acylation of the N-terminus of [D-Arg0,Hyp3,Thi5,8,D-Phe7]bradykinin, one of the most potent bradykinin antagonists described to date, with 1-adamantane-acetic acid, results in an analogue with more than ten times enhanced potency.	d-phe7	70-76	kininogen 1	Homo sapiens	112-122
2284196-1	1990	We report that the acylation of the N-terminus of [D-Arg0,Hyp3,Thi5,8,D-Phe7]bradykinin, one of the most potent bradykinin antagonists described to date, with 1-adamantane-acetic acid, results in an analogue with more than ten times enhanced potency.	1-adamantaneacetic acid	159-183	kininogen 1	Homo sapiens	77-87
2284196-1	1990	We report that the acylation of the N-terminus of [D-Arg0,Hyp3,Thi5,8,D-Phe7]bradykinin, one of the most potent bradykinin antagonists described to date, with 1-adamantane-acetic acid, results in an analogue with more than ten times enhanced potency.	1-adamantaneacetic acid	159-183	kininogen 1	Homo sapiens	112-122
2175927-3	1990	The ACE is a glycoprotein with a molecular weight of 150,000 daltons and it cleaves C-terminal dipeptides of several oligo-peptides, including angiotensin I and bradykinin.	Dipeptides	95-105	kininogen 1	Homo sapiens	161-171
1963337-1	1990	Bradykinin triggered intracellular Ca mobilizations and ionic conductance changes were studied in the neuroblastoma x glioma hybrid cell line NG108-15 using Ca-sensitive fluorescent indicator fura-2 under patch pipette whole cell voltage clamp condition.	Fura-2	192-198	kininogen 1	Homo sapiens	0-10
1963337-6	1990	[Ca2+]i increase induced by high potassium depolarization was suppressed by bradykinin.	Potassium	33-42	kininogen 1	Homo sapiens	76-86
1963337-8	1990	Our results suggest that the modifications of ionic channels by bradykinin could be through the other mechanisms than the well established activation of the G-protein leading to the IP3 mechanisms and that the bradykinin receptor might couple with the pertussis toxin-insensitive G protein which regulates the calcium channels.	Inositol 1,4,5-Trisphosphate	182-185	kininogen 1	Homo sapiens	64-74
1974388-0	1990	Bradykinin attenuates glucagon-induced leucine oxidation in humans.	Glucagon	22-30	kininogen 1	Homo sapiens	0-10
1974388-3	1990	In the present study, the effect of glucagon and glucagon plus bradykinin on leucine and urea kinetics was examined in nine normal volunteers during somatostatin infusion and basal insulin replacement.	Leucine	77-84	kininogen 1	Homo sapiens	63-73
1974388-4	1990	Bradykinin was given because of its prostaglandin-stimulating qualities and the potential anabolic action of prostaglandins.	Prostaglandins	36-49	kininogen 1	Homo sapiens	0-10
1974388-4	1990	Bradykinin was given because of its prostaglandin-stimulating qualities and the potential anabolic action of prostaglandins.	Prostaglandins	109-123	kininogen 1	Homo sapiens	0-10
1974388-8	1990	Bradykinin, however, significantly attenuated the stimulation of leucine oxidation by glucagon.	Glucagon	86-94	kininogen 1	Homo sapiens	0-10
2400108-3	1990	Variants of synthetic bradykinin containing one or two hydroxyproline moieties were prepared by using manual Edman degradation and/or enzymatic methods.	Hydroxyproline	55-69	kininogen 1	Homo sapiens	22-32
2203794-5	1990	On hydrophobic polymers like polyethylene, the low amounts of adsorbed fibrinogen and HMW kininogen from plasma and concentrated plasma solutions may be due to a preferential adsorption of HDL.	Polymers	15-23	kininogen 1	Homo sapiens	86-99
2369723-8	1990	Cells exposed to 5 microM ET-18-OCH3 for 18 h showed no increase in resting [Ca2+]i but there was 95% inhibition of the [Ca2+]i response to platelet-derived growth factor, 63% inhibition of the response to bradykinin, and 55% inhibition of the response to vasopressin.	edelfosine	26-36	kininogen 1	Homo sapiens	206-216
2379387-2	1990	We have developed a new method, using microdialysis probes, for collecting tissue samples of immunoreactive bradykinin in both postoperative patients and rats injected with carrageenan.	Carrageenan	173-184	kininogen 1	Homo sapiens	108-118
2379387-5	1990	Preoperative administration of methylprednisolone (125 mg) reduced immunoreactive bradykinin levels by 62% (p less than 0.001) compared with placebo.	Methylprednisolone	31-49	kininogen 1	Homo sapiens	82-92
2379387-7	1990	In rats, dexamethasone suppressed tissue levels of immunoreactive bradykinin.	Dexamethasone	9-22	kininogen 1	Homo sapiens	66-76
2203794-5	1990	On hydrophobic polymers like polyethylene, the low amounts of adsorbed fibrinogen and HMW kininogen from plasma and concentrated plasma solutions may be due to a preferential adsorption of HDL.	Polyethylene	29-41	kininogen 1	Homo sapiens	86-99
2373690-10	1990	The LPA-induced Ca2+ signal is blocked completely by tetradecanoylphorbol acetate, but is not affected by prior stimulation of the cells with Ca2(+)-mobilizing agonists such as bradykinin or histamine.	lysophosphatidic acid	4-7	kininogen 1	Homo sapiens	177-187
2372310-2	1990	The use of NMR methods to study conformational and dynamic aspects of the proline residues in the nonapeptide bradykinin is reviewed.	Proline	74-81	kininogen 1	Homo sapiens	110-120
1698266-4	1990	In patch-clamped cells, pinacidil (1 mumol/l) and cromakalim (1 mumol/l) elicited outward currents carried by K+ and significantly prolonged the Ca2(+)-dependent K+ currents induced by bradykinin and ATP.	Pinacidil	24-33	kininogen 1	Homo sapiens	185-195
2114479-7	1990	Bradykinin also caused endothelium-dependent relaxation and this response was significantly attenuated by methylene blue but not indomethacin.	Methylene Blue	106-120	kininogen 1	Homo sapiens	0-10
1698266-4	1990	In patch-clamped cells, pinacidil (1 mumol/l) and cromakalim (1 mumol/l) elicited outward currents carried by K+ and significantly prolonged the Ca2(+)-dependent K+ currents induced by bradykinin and ATP.	Cromakalim	50-60	kininogen 1	Homo sapiens	185-195
1698266-9	1990	Likewise, in cells stimulated with bradykinin, pinacidil raised [Ca2+]i when applied during the decline of [Ca2+]i after the initial peak.	Pinacidil	47-56	kininogen 1	Homo sapiens	35-45
1698266-10	1990	Cicletanine elicited K+ currents in resting and attenuated K+ currents in bradykinin-stimulated cells.	cicletanine	0-11	kininogen 1	Homo sapiens	74-84
2351646-7	1990	Hydroxyproline, which was recently identified in the bradykinin sequence of kininogen from the ascitic fluid of a cancer patient, was not found in the kinin moiety of this mouse kininogen.	Hydroxyproline	0-14	kininogen 1	Homo sapiens	53-63
2165467-2	1990	The conformational properties of bradykinin in five molar excess sodium dodecyl sulfate (SDS) micelles have been examined by two-dimensional nuclear magnetic resonance (NMR) techniques at 500 MHz.	Sodium Dodecyl Sulfate	65-87	kininogen 1	Homo sapiens	33-43
2163209-0	1990	Isoproterenol, cAMP, and bradykinin stimulate diacylglycerol production in airway epithelium.	Diglycerides	46-60	kininogen 1	Homo sapiens	25-35
2163209-3	1990	Bradykinin increased cellular DAG at concentrations similar to those that increase inositol phosphates, suggesting that bradykinin stimulates phosphatidylinositol hydrolysis, as observed in other systems.	Diglycerides	30-33	kininogen 1	Homo sapiens	0-10
2163209-3	1990	Bradykinin increased cellular DAG at concentrations similar to those that increase inositol phosphates, suggesting that bradykinin stimulates phosphatidylinositol hydrolysis, as observed in other systems.	Diglycerides	30-33	kininogen 1	Homo sapiens	120-130
2163209-3	1990	Bradykinin increased cellular DAG at concentrations similar to those that increase inositol phosphates, suggesting that bradykinin stimulates phosphatidylinositol hydrolysis, as observed in other systems.	Phosphatidylinositols	142-162	kininogen 1	Homo sapiens	0-10
2163209-3	1990	Bradykinin increased cellular DAG at concentrations similar to those that increase inositol phosphates, suggesting that bradykinin stimulates phosphatidylinositol hydrolysis, as observed in other systems.	Phosphatidylinositols	142-162	kininogen 1	Homo sapiens	120-130
2163209-7	1990	Simultaneous addition of maximal concentrations of isoproterenol and bradykinin produced additive increases in DAG.	Diglycerides	111-114	kininogen 1	Homo sapiens	69-79
2163209-9	1990	Although phorbol ester and bradykinin stimulated phosphatidylcholine turnover, isoproterenol did not.	Phosphatidylcholines	49-68	kininogen 1	Homo sapiens	27-37
2163209-10	1990	These results suggest that isoproterenol and bradykinin generate DAG from the following different lipid sources: bradykinin stimulates phosphatidylinositol hydrolysis to produce DAG; isoproterenol stimulates an increase in DAG from unknown sources.	Diglycerides	65-68	kininogen 1	Homo sapiens	45-55
2163209-10	1990	These results suggest that isoproterenol and bradykinin generate DAG from the following different lipid sources: bradykinin stimulates phosphatidylinositol hydrolysis to produce DAG; isoproterenol stimulates an increase in DAG from unknown sources.	Diglycerides	65-68	kininogen 1	Homo sapiens	113-123
2163209-10	1990	These results suggest that isoproterenol and bradykinin generate DAG from the following different lipid sources: bradykinin stimulates phosphatidylinositol hydrolysis to produce DAG; isoproterenol stimulates an increase in DAG from unknown sources.	Phosphatidylinositols	135-155	kininogen 1	Homo sapiens	45-55
2163209-10	1990	These results suggest that isoproterenol and bradykinin generate DAG from the following different lipid sources: bradykinin stimulates phosphatidylinositol hydrolysis to produce DAG; isoproterenol stimulates an increase in DAG from unknown sources.	Phosphatidylinositols	135-155	kininogen 1	Homo sapiens	113-123
2163209-10	1990	These results suggest that isoproterenol and bradykinin generate DAG from the following different lipid sources: bradykinin stimulates phosphatidylinositol hydrolysis to produce DAG; isoproterenol stimulates an increase in DAG from unknown sources.	Diglycerides	178-181	kininogen 1	Homo sapiens	45-55
2163209-10	1990	These results suggest that isoproterenol and bradykinin generate DAG from the following different lipid sources: bradykinin stimulates phosphatidylinositol hydrolysis to produce DAG; isoproterenol stimulates an increase in DAG from unknown sources.	Diglycerides	178-181	kininogen 1	Homo sapiens	113-123
2163209-10	1990	These results suggest that isoproterenol and bradykinin generate DAG from the following different lipid sources: bradykinin stimulates phosphatidylinositol hydrolysis to produce DAG; isoproterenol stimulates an increase in DAG from unknown sources.	Isoproterenol	27-40	kininogen 1	Homo sapiens	113-123
2163209-10	1990	These results suggest that isoproterenol and bradykinin generate DAG from the following different lipid sources: bradykinin stimulates phosphatidylinositol hydrolysis to produce DAG; isoproterenol stimulates an increase in DAG from unknown sources.	Diglycerides	178-181	kininogen 1	Homo sapiens	45-55
2163209-10	1990	These results suggest that isoproterenol and bradykinin generate DAG from the following different lipid sources: bradykinin stimulates phosphatidylinositol hydrolysis to produce DAG; isoproterenol stimulates an increase in DAG from unknown sources.	Diglycerides	178-181	kininogen 1	Homo sapiens	113-123
2159719-3	1990	Coincubation of glomerular mesangial cells (GMC) with GEN augmented mesangial cell guanosine 3",5"-cyclic monophosphate (cGMP) content five- to sixfold, Bradykinin elicited a further concentration-dependent increase in GMC cGMP content in the presence but not absence of GEN.	Genistein	54-57	kininogen 1	Homo sapiens	153-163
2159719-3	1990	Coincubation of glomerular mesangial cells (GMC) with GEN augmented mesangial cell guanosine 3",5"-cyclic monophosphate (cGMP) content five- to sixfold, Bradykinin elicited a further concentration-dependent increase in GMC cGMP content in the presence but not absence of GEN.	Cyclic GMP	223-227	kininogen 1	Homo sapiens	153-163
2159719-4	1990	The GEN-dependent bradykinin-stimulated GMC cGMP accumulation was abolished by hemoglobin and methylene blue, blunted by gossypol, and augmented by superoxide dismutase.	Cyclic GMP	44-48	kininogen 1	Homo sapiens	18-28
2159719-4	1990	The GEN-dependent bradykinin-stimulated GMC cGMP accumulation was abolished by hemoglobin and methylene blue, blunted by gossypol, and augmented by superoxide dismutase.	Methylene Blue	94-108	kininogen 1	Homo sapiens	18-28
2159719-4	1990	The GEN-dependent bradykinin-stimulated GMC cGMP accumulation was abolished by hemoglobin and methylene blue, blunted by gossypol, and augmented by superoxide dismutase.	Gossypol	121-129	kininogen 1	Homo sapiens	18-28
2163328-4	1990	It was thus discovered that converting enzyme (CE) is identical with the bradykinin-degrading enzyme, kininase II, and CEIs can therefore potentiate the vasodepressor effects of bradykinin and thereby interact with the prostaglandin system.	Prostaglandins	219-232	kininogen 1	Homo sapiens	73-83
2163328-4	1990	It was thus discovered that converting enzyme (CE) is identical with the bradykinin-degrading enzyme, kininase II, and CEIs can therefore potentiate the vasodepressor effects of bradykinin and thereby interact with the prostaglandin system.	Prostaglandins	219-232	kininogen 1	Homo sapiens	178-188
2165467-0	1990	Three-dimensional structure of bradykinin in SDS micelles.	Sodium Dodecyl Sulfate	45-48	kininogen 1	Homo sapiens	31-41
2185292-2	1990	No change in the size of wheal-and-flare reactions to histamine occurred, but the size of wheal reactions to codeine and bradykinin increased in all study subjects after ingesting the ACE inhibitor, captopril.	Captopril	199-208	kininogen 1	Homo sapiens	121-131
2165467-2	1990	The conformational properties of bradykinin in five molar excess sodium dodecyl sulfate (SDS) micelles have been examined by two-dimensional nuclear magnetic resonance (NMR) techniques at 500 MHz.	Sodium Dodecyl Sulfate	89-92	kininogen 1	Homo sapiens	33-43
2165467-3	1990	Detailed structural information for bradykinin in SDS was obtained from quantitative 2-D nuclear Overhauser enhancement (n.O.e.)	Sodium Dodecyl Sulfate	50-53	kininogen 1	Homo sapiens	36-46
2165467-5	1990	The conformation of bradykinin in SDS micelles, as determined by these methods, is characterized by a beta-turn-like structure at residues 6-9.	Sodium Dodecyl Sulfate	34-37	kininogen 1	Homo sapiens	20-30
2194812-2	1990	Since ACE-inhibitors can prevent bradykinin breakdown and can stimulate prostaglandin production, it is thought that these cardioprotective effects are mediated by bradykinin and prostaglandins.	Prostaglandins	72-85	kininogen 1	Homo sapiens	164-174
1695464-0	1990	Histamine secretion from mast cells stimulated with bradykinin.	Histamine	0-9	kininogen 1	Homo sapiens	52-62
1695464-1	1990	Bradykinin and a range of peptide analogues induced a dose-dependent release of histamine from rat peritoneal mast cells.	Histamine	80-89	kininogen 1	Homo sapiens	0-10
1970226-0	1990	Contribution of histamine and prostanoids to bronchoconstriction provoked by inhaled bradykinin in atopic asthma.	Histamine	16-25	kininogen 1	Homo sapiens	85-95
1970226-0	1990	Contribution of histamine and prostanoids to bronchoconstriction provoked by inhaled bradykinin in atopic asthma.	Prostaglandins	30-41	kininogen 1	Homo sapiens	85-95
1970226-2	1990	Since bradykinin has been shown to stimulate mediator release from mast cells and augment the release of prostanoids, we have examined the effect of a selective histamine H1 receptor antagonist, terfenadine and a potent cyclooxygenase inhibitor, flurbiprofen on bronchoconstriction provoked by inhaled bradykinin in asthma.	Prostaglandins	105-116	kininogen 1	Homo sapiens	6-16
1970226-4	1990	In nine atopic asthmatic subjects, terfenadine 180 mg, when compared to placebo, increased the geometric mean provocation concentration of inhaled agonist required to reduce FEV1 by 20% of baseline (PC20) from 0.7 to greater than 22.9 mg/ml for histamine (P less than 0.01) and 0.3 to 0.5 mg/ml for bradykinin (P less than 0.01).	Terfenadine	35-46	kininogen 1	Homo sapiens	299-309
1970226-5	1990	In a further nine atopic asthmatics, flurbiprofen 150 mg when compared to placebo produced a small but significant protection of the airways against bradykinin, geometric mean PC20 increasing from 0.40 to 0.79 mg/ml (P less than 0.05).	Flurbiprofen	37-49	kininogen 1	Homo sapiens	149-159
1970226-7	1990	Pharmacological intervention with terfenadine and flurbiprofen led to a significant protection of the airways against the constrictor effect of bradykinin but the effect in each case was small.	Terfenadine	34-45	kininogen 1	Homo sapiens	144-154
1970226-7	1990	Pharmacological intervention with terfenadine and flurbiprofen led to a significant protection of the airways against the constrictor effect of bradykinin but the effect in each case was small.	Flurbiprofen	50-62	kininogen 1	Homo sapiens	144-154
1970226-8	1990	Thus, while histamine and prostanoids may contribute as mediators of bradykinin-induced bronchoconstriction, they are unlikely to account for the majority of the response.	Histamine	12-21	kininogen 1	Homo sapiens	69-79
1970226-8	1990	Thus, while histamine and prostanoids may contribute as mediators of bradykinin-induced bronchoconstriction, they are unlikely to account for the majority of the response.	Prostaglandins	26-37	kininogen 1	Homo sapiens	69-79
2194812-2	1990	Since ACE-inhibitors can prevent bradykinin breakdown and can stimulate prostaglandin production, it is thought that these cardioprotective effects are mediated by bradykinin and prostaglandins.	Prostaglandins	179-193	kininogen 1	Homo sapiens	33-43
2156873-0	1990	Bradykinin induces superoxide anion release from human endothelial cells.	Superoxides	19-35	kininogen 1	Homo sapiens	0-10
2156873-1	1990	The time-dependent release of superoxide anion (O2-) from bradykinin (Bk)-stimulated human umbilical vein endothelial cells (EC) was measured as the superoxide dismutase-inhibitable reduction of ferricytochrome C employing a novel application of microspectrophotometry.	Superoxides	30-46	kininogen 1	Homo sapiens	58-68
2156873-1	1990	The time-dependent release of superoxide anion (O2-) from bradykinin (Bk)-stimulated human umbilical vein endothelial cells (EC) was measured as the superoxide dismutase-inhibitable reduction of ferricytochrome C employing a novel application of microspectrophotometry.	Superoxides	30-46	kininogen 1	Homo sapiens	70-72
2156873-1	1990	The time-dependent release of superoxide anion (O2-) from bradykinin (Bk)-stimulated human umbilical vein endothelial cells (EC) was measured as the superoxide dismutase-inhibitable reduction of ferricytochrome C employing a novel application of microspectrophotometry.	Superoxides	48-50	kininogen 1	Homo sapiens	58-68
2156873-1	1990	The time-dependent release of superoxide anion (O2-) from bradykinin (Bk)-stimulated human umbilical vein endothelial cells (EC) was measured as the superoxide dismutase-inhibitable reduction of ferricytochrome C employing a novel application of microspectrophotometry.	Superoxides	48-50	kininogen 1	Homo sapiens	70-72
2156873-3	1990	EC exposure to Bk (10(-6) to 10(-5) M) resulted in a rapid release of O2-.	Superoxides	70-72	kininogen 1	Homo sapiens	15-17
2108678-3	1990	The pretreatment with 3 mM EGTA for 1 min caused a significant reduction in [Ca2+]i levels both of the basal (p less than 0.05) and BK-stimulated initial peak (p less than 0.001).	Egtazic Acid	27-31	kininogen 1	Homo sapiens	132-134
1695191-3	1990	Bradykinin, a pain producing substance, augmented the production of opioid peptides, for example, methionine and leucine enkephalins in in vitro and in vivo experiments.	Methionine	98-108	kininogen 1	Homo sapiens	0-10
2108678-4	1990	However, the BK-stimulated initial peak was retained in magnitude for at least 5 min under the treatment with EGTA.	Egtazic Acid	110-114	kininogen 1	Homo sapiens	13-15
2108678-6	1990	The BK-stimulated Ca2+ transient, once having been completely inhibited by ionomycin (10(-6) M) in the presence of EGTA, was rapidly (within 2 min) recovered to the untreated level by replacing it with fresh medium containing 1.5 mM Ca2+.	Ionomycin	75-84	kininogen 1	Homo sapiens	4-6
2108678-6	1990	The BK-stimulated Ca2+ transient, once having been completely inhibited by ionomycin (10(-6) M) in the presence of EGTA, was rapidly (within 2 min) recovered to the untreated level by replacing it with fresh medium containing 1.5 mM Ca2+.	Egtazic Acid	115-119	kininogen 1	Homo sapiens	4-6
2156727-0	1990	[Hyp3]-bradykinin and [Hyp3]-Lys-bradykinin interact with B2-bradykinin receptors and stimulate inositol phosphate production in cultured human fibroblasts.	Inositol Phosphates	96-114	kininogen 1	Homo sapiens	7-17
2156727-0	1990	[Hyp3]-bradykinin and [Hyp3]-Lys-bradykinin interact with B2-bradykinin receptors and stimulate inositol phosphate production in cultured human fibroblasts.	Inositol Phosphates	96-114	kininogen 1	Homo sapiens	33-43
2156727-0	1990	[Hyp3]-bradykinin and [Hyp3]-Lys-bradykinin interact with B2-bradykinin receptors and stimulate inositol phosphate production in cultured human fibroblasts.	Inositol Phosphates	96-114	kininogen 1	Homo sapiens	33-43
2156727-2	1990	Both ligands competed with [3H]bradykinin binding in a dose-dependent fashion with potencies similar to bradykinin (BK) and Lys-BK.	Tritium	28-30	kininogen 1	Homo sapiens	31-41
2178531-10	1990	Human nasal fragments secreted significantly increased amounts of RGC in response to 10 microM BK (15.0% +/- 1.8 compared with control values; mean +/- standard error of the mean; n = 7; p less than 0.01 by Student"s unpaired t test), 10 microM lys-BK (12.2% +/- 3.3; n = 5; p less than 0.05), and 100 microM methacholine (35.7% +/- 2.3; p less than 0.0001).	Methacholine Chloride	309-321	kininogen 1	Homo sapiens	95-97
2310660-0	1990	The effect of sulindac on dermal responses to bradykinin in normal subjects given an angiotensin converting enzyme inhibitor.	Sulindac	14-22	kininogen 1	Homo sapiens	46-56
2310660-1	1990	The ability of sulindac to modify the weal response to four doses of intradermal bradykinin in subjects given enalapril was tested in a double-blind cross-over study in normal volunteers.	Sulindac	15-23	kininogen 1	Homo sapiens	81-91
2310660-2	1990	The dose-dependent increase in skin thickness after bradykinin was significantly reduced by prior administration of sulindac.	Sulindac	116-124	kininogen 1	Homo sapiens	52-62
2156987-2	1990	The pD2 value of BK on the longitudinal muscle was 6.58 +/- 0.06 M. The maximal response of the longitudinal muscle to BK was 44% compared to carbachol.	Carbachol	142-151	kininogen 1	Homo sapiens	17-19
2156987-6	1990	The excitatory effect of BK and Thi5,8-d-Phe7-BK was not modified by tetrodotoxin (1 and 10 microM), atropine (1 microM) or indomethacin (1 and 10 microM), but was significantly (P less than .001) inhibited by nifedipine (1 and 10 microM).	thi5	32-36	kininogen 1	Homo sapiens	46-48
2156987-6	1990	The excitatory effect of BK and Thi5,8-d-Phe7-BK was not modified by tetrodotoxin (1 and 10 microM), atropine (1 microM) or indomethacin (1 and 10 microM), but was significantly (P less than .001) inhibited by nifedipine (1 and 10 microM).	Nifedipine	210-220	kininogen 1	Homo sapiens	25-27
2156987-7	1990	Three putative "tissue selective" BK antagonists, d-Phe2,7-BK (B4404), d-Phe7-Hyp8-BK and Phe2-d-Phe7-BK also had an agonistic effect on longitudinal muscle.	d-phe2	50-56	kininogen 1	Homo sapiens	34-36
2156998-4	1990	The PGs also enhanced the turnover of inositol phospholipids, but the PGE1-stimulated formation of inositol phosphates was small compared to that produced by bradykinin, which stimulates a similar degree of release.	Alprostadil	70-74	kininogen 1	Homo sapiens	158-168
2352486-7	1990	The formation or reduction of interendothelial gaps by histamine, bradykinin, and U-46619 and by 5-HT, respectively, was positively correlated to changes in monolayer permeability to EBA.	eba	183-186	kininogen 1	Homo sapiens	66-76
2274475-1	1990	The analgesic potency of the C-terminal dipeptide of tuftsin (Pro-Arg) was found to be much stronger than that of the C-terminal of bradykinin dipeptide Phe-Arg.	Dipeptides	143-152	kininogen 1	Homo sapiens	132-142
2274475-1	1990	The analgesic potency of the C-terminal dipeptide of tuftsin (Pro-Arg) was found to be much stronger than that of the C-terminal of bradykinin dipeptide Phe-Arg.	phenylalanylarginine	153-160	kininogen 1	Homo sapiens	132-142
2274475-2	1990	It was also found that the tripeptide fragment of bradykinin (Pro-Phe-Arg) and its D-Pro analog (D-Pro-Phe-Arg) are deprived of analgesic activity.	tripeptide K-26	27-37	kininogen 1	Homo sapiens	50-60
2274475-2	1990	It was also found that the tripeptide fragment of bradykinin (Pro-Phe-Arg) and its D-Pro analog (D-Pro-Phe-Arg) are deprived of analgesic activity.	Pro-Phe-Arg	62-73	kininogen 1	Homo sapiens	50-60
2274475-2	1990	It was also found that the tripeptide fragment of bradykinin (Pro-Phe-Arg) and its D-Pro analog (D-Pro-Phe-Arg) are deprived of analgesic activity.	D-proline	83-88	kininogen 1	Homo sapiens	50-60
2274475-2	1990	It was also found that the tripeptide fragment of bradykinin (Pro-Phe-Arg) and its D-Pro analog (D-Pro-Phe-Arg) are deprived of analgesic activity.	d-pro-phe-arg	97-110	kininogen 1	Homo sapiens	50-60
2106798-7	1990	The compound LY 83583 (which depletes vascular guanylate cyclase) reduced responses to nitroglycerin, nitric oxide, S-nitrosocysteine, bradykinin, and the calcium ionophore A23187 in microvessels of all sizes.	6-anilino-5,8-quinolinedione	13-21	kininogen 1	Homo sapiens	135-145
2160302-0	1990	Bradykinin stimulates prostaglandin E2 formation in isolated human osteoblast-like cells.	Dinoprostone	22-38	kininogen 1	Homo sapiens	0-10
2160302-1	1990	The effect of bradykinin on prostaglandin E2 formation in cells from human trabecular bone has been studied.	Dinoprostone	28-44	kininogen 1	Homo sapiens	14-24
2160302-3	1990	In these isolated human osteoblast-like cells, bradykinin (1 mumol/l) caused a rapid (5 min) stimulation of prostaglandin E2 formation.	Dinoprostone	108-124	kininogen 1	Homo sapiens	47-57
2160302-4	1990	This finding indicates that human osteoblasts are equipped with receptors for bradykinin linked to an increase in prostaglandin formation.	Prostaglandins	114-127	kininogen 1	Homo sapiens	78-88
2306703-4	1990	Suramin, 7 x 10(-5) M, caused a 49% decrease in the elevation of intracellular free Ca2+ concentration ([Ca2+]i) caused by platelet derived growth factor (PDGF) in intact Swiss 3T3 fibroblasts but did not block the increases in [Ca2+]i caused by bradykinin or vasopressin.	Suramin	0-7	kininogen 1	Homo sapiens	246-256
2298179-1	1990	Incubation of plasma from the red-eared turtle with glass beads in the presence of the kininase inhibitor 1,10-phenanthroline resulted in activation of the kallikrein-kinin system and generation of bradykinin-like immunoreactivity.	1,10-phenanthroline	106-125	kininogen 1	Homo sapiens	198-208
2312500-2	1990	Cultured PCMV endothelial cells were characterized by the capacity to produce prostacyclin in response to bradykinin.	Epoprostenol	78-90	kininogen 1	Homo sapiens	106-116
2156053-6	1990	The B2 kinin receptor antagonist, D-Arg0 [Hyp3, D-Phe7]bradykinin but not the B1 kinin receptor antagonists Leu8-des-Arg9 bradykinin and Leu9-des-Arg10 kallidin inhibited the production of cyclic GMP upon stimulation of the endothelial cells with either bradykinin or kallidin.	d-arg0	34-40	kininogen 1	Homo sapiens	55-65
2158065-6	1990	Histamine, bradykinin and isoproterenol transiently increased the intracellular calcium level and caused a parallel increase of the transcellular chloride current in both normal and CF cells.	Calcium	80-87	kininogen 1	Homo sapiens	11-21
2158065-6	1990	Histamine, bradykinin and isoproterenol transiently increased the intracellular calcium level and caused a parallel increase of the transcellular chloride current in both normal and CF cells.	Chlorides	146-154	kininogen 1	Homo sapiens	11-21
2408245-3	1990	The exact mechanism of action is not fully understood; the main role plays obviously the inhibition of the angiotensin converting enzyme itself; in addition may be effects on the kallikrein-bradykinin-prostaglandin-system are of importance.	Prostaglandins	201-214	kininogen 1	Homo sapiens	190-200
1967418-0	1990	Effect of low-dose bradykinin on glucose metabolism and nitrogen balance in surgical patients.	Glucose	33-40	kininogen 1	Homo sapiens	19-29
1967418-0	1990	Effect of low-dose bradykinin on glucose metabolism and nitrogen balance in surgical patients.	Nitrogen	56-64	kininogen 1	Homo sapiens	19-29
1967418-1	1990	Acute effects of a low-dose bradykinin infusion (30 ng/kg per min) on carbohydrate metabolism were studied in five patients after major burn injury.	Carbohydrates	70-82	kininogen 1	Homo sapiens	28-38
1967418-5	1990	Patients in the bradykinin group had a significantly improved rate of nitrogen retention (cumulative N balance, -0.014 [SE 0.064] vs -0.175 [0.048] g N/kg) in controls and significantly better nutritional indices.	Nitrogen	70-78	kininogen 1	Homo sapiens	16-26
1967418-6	1990	Manipulation of metabolism in surgical patients by bradykinin may have beneficial effects on nitrogen and protein dynamics, possibly mediated by improved aerobic and anaerobic glycolysis.	Nitrogen	93-101	kininogen 1	Homo sapiens	51-61
2128586-9	1990	SSEPs changed with high dose bradykinin and some glioma cyst infusates whilst CBF CO2 reactivity was locally impaired by all infusates except saline and arachidonic acid.	sseps	0-5	kininogen 1	Homo sapiens	29-39
1966711-3	1990	After ultracentrifugation, the enzyme was purified by gel filtration on Sepharose 6B CL and ion exchange chromatography followed by affinity chromatography of EDTA-inhibited enzyme on bradykinin-Sepharose.	Edetic Acid	159-163	kininogen 1	Homo sapiens	184-194
2389994-4	1990	In the concentration range between 10(-11) to 10(-6) M, des-arg9-bradykinin and T-kinin showed no significant change in motility of washed human spermatozoa.	des-arg9	56-64	kininogen 1	Homo sapiens	65-75
2389994-6	1990	The kinin receptor of human spermatozoa should be of subtype B2 because the specific B1-agonist, des-arg9-bradykinin, showed no influence on sperm motility.	des-arg9	97-105	kininogen 1	Homo sapiens	106-116
1697359-2	1990	Specific bradykinin (BK) receptor sites (B2 subtype) were measured by direct binding study and correlated with BK-induced biological effects such as the release of inositol phosphates, formation of prostacyclin (PGI2), and accumulation of cyclic 3"5" adenosine monophosphate (cAMP).	Inositol Phosphates	164-183	kininogen 1	Homo sapiens	9-19
1697359-2	1990	Specific bradykinin (BK) receptor sites (B2 subtype) were measured by direct binding study and correlated with BK-induced biological effects such as the release of inositol phosphates, formation of prostacyclin (PGI2), and accumulation of cyclic 3"5" adenosine monophosphate (cAMP).	Inositol Phosphates	164-183	kininogen 1	Homo sapiens	21-23
1697363-5	1990	The acute blood pressure-lowering action of ACE inhibitors is inhibited by indomethacin-type cyclooxygenase inhibitors, suggesting a contribution of bradykinin-induced release of vasodilator prostaglandins to their action.	Prostaglandins	191-205	kininogen 1	Homo sapiens	149-159
1697363-6	1990	Bradykinin stimulates the phospholipase-dependent release of arachidonic acid from membrane phospholipids, allowing for subsequent generation of its metabolites, the eicosanoids.	Arachidonic Acid	61-77	kininogen 1	Homo sapiens	0-10
1697359-2	1990	Specific bradykinin (BK) receptor sites (B2 subtype) were measured by direct binding study and correlated with BK-induced biological effects such as the release of inositol phosphates, formation of prostacyclin (PGI2), and accumulation of cyclic 3"5" adenosine monophosphate (cAMP).	Epoprostenol	198-210	kininogen 1	Homo sapiens	9-19
1697363-6	1990	Bradykinin stimulates the phospholipase-dependent release of arachidonic acid from membrane phospholipids, allowing for subsequent generation of its metabolites, the eicosanoids.	Phospholipids	92-105	kininogen 1	Homo sapiens	0-10
1697359-2	1990	Specific bradykinin (BK) receptor sites (B2 subtype) were measured by direct binding study and correlated with BK-induced biological effects such as the release of inositol phosphates, formation of prostacyclin (PGI2), and accumulation of cyclic 3"5" adenosine monophosphate (cAMP).	Epoprostenol	198-210	kininogen 1	Homo sapiens	21-23
1697363-6	1990	Bradykinin stimulates the phospholipase-dependent release of arachidonic acid from membrane phospholipids, allowing for subsequent generation of its metabolites, the eicosanoids.	Eicosanoids	166-177	kininogen 1	Homo sapiens	0-10
1697359-2	1990	Specific bradykinin (BK) receptor sites (B2 subtype) were measured by direct binding study and correlated with BK-induced biological effects such as the release of inositol phosphates, formation of prostacyclin (PGI2), and accumulation of cyclic 3"5" adenosine monophosphate (cAMP).	cyclic 3"5" adenosine monophosphate	239-274	kininogen 1	Homo sapiens	9-19
1697359-2	1990	Specific bradykinin (BK) receptor sites (B2 subtype) were measured by direct binding study and correlated with BK-induced biological effects such as the release of inositol phosphates, formation of prostacyclin (PGI2), and accumulation of cyclic 3"5" adenosine monophosphate (cAMP).	Cyclic AMP	276-280	kininogen 1	Homo sapiens	9-19
1697359-3	1990	Depending on the ambient concentration of BK in the culture medium, homologous receptor downregulation accompanied by a reduction in BK-stimulated PGI2 release occurred.	Epoprostenol	147-151	kininogen 1	Homo sapiens	42-44
1697359-3	1990	Depending on the ambient concentration of BK in the culture medium, homologous receptor downregulation accompanied by a reduction in BK-stimulated PGI2 release occurred.	Epoprostenol	147-151	kininogen 1	Homo sapiens	133-135
1697359-5	1990	The fate of receptor-bound [3H]BK was studied by the acetic acid "stripping technique" that completely removes surface-bound [3H]BK while leaving internalized material with the remaining cells.	Tritium	28-30	kininogen 1	Homo sapiens	31-33
1697359-5	1990	The fate of receptor-bound [3H]BK was studied by the acetic acid "stripping technique" that completely removes surface-bound [3H]BK while leaving internalized material with the remaining cells.	Acetic Acid	53-64	kininogen 1	Homo sapiens	31-33
1697359-5	1990	The fate of receptor-bound [3H]BK was studied by the acetic acid "stripping technique" that completely removes surface-bound [3H]BK while leaving internalized material with the remaining cells.	Acetic Acid	53-64	kininogen 1	Homo sapiens	129-131
1697359-5	1990	The fate of receptor-bound [3H]BK was studied by the acetic acid "stripping technique" that completely removes surface-bound [3H]BK while leaving internalized material with the remaining cells.	Tritium	126-128	kininogen 1	Homo sapiens	31-33
1697359-7	1990	High-performance liquid chromatography (HPLC) analysis of internalized 3H counts showed significant quantities of intact [3H]BK occurring in an intracellular compartment.	Tritium	71-73	kininogen 1	Homo sapiens	125-127
1697359-7	1990	High-performance liquid chromatography (HPLC) analysis of internalized 3H counts showed significant quantities of intact [3H]BK occurring in an intracellular compartment.	Tritium	122-124	kininogen 1	Homo sapiens	125-127
1697359-8	1990	Compounds or drugs that enhance intracellular cAMP levels or inhibit generation of eicosanoids were shown to modify the BK response by indirect means.	Cyclic AMP	46-50	kininogen 1	Homo sapiens	120-122
1697359-8	1990	Compounds or drugs that enhance intracellular cAMP levels or inhibit generation of eicosanoids were shown to modify the BK response by indirect means.	Eicosanoids	83-94	kininogen 1	Homo sapiens	120-122
2304952-0	1990	Characteristics of BANA-degrading enzyme in the tooth pulp activated by bradykinin.	Benzoylarginine-2-Naphthylamide	19-23	kininogen 1	Homo sapiens	72-82
33764894-7	2021	ACE2 cleaves lys-des-arginine9BK and arg-des-arginine9BK, the active metabolites of bradykinin, which stimulate the BKB1R receptor.	lys-des-arginine9bk	13-32	kininogen 1	Homo sapiens	84-94
2315457-1	1990	A study was made of the role of protein phosphorylation of mast cells and their cytoskeleton upon secretion induced by biogenic amines (histamine and serotonin) and bradykinin, a possible mediator of the effect of MEA, a sulfur-containing radioprotector.	Sulfur	221-227	kininogen 1	Homo sapiens	165-175
33764894-7	2021	ACE2 cleaves lys-des-arginine9BK and arg-des-arginine9BK, the active metabolites of bradykinin, which stimulate the BKB1R receptor.	arg-des-arginine9bk	37-56	kininogen 1	Homo sapiens	84-94
33794540-1	2021	Bradykinin increases skin blood flow via a cGMP mechanism but its role in sweating in vivo is unclear.	Cyclic GMP	43-47	kininogen 1	Homo sapiens	0-10
27884766-5	2017	RESULTS: Compared with control groups, there was reduced vasodilation with bradykinin (P = .005), a blunted effect of fluconazole on bradykinin-induced vasodilation (P = .03), and a trend toward reduced basal EET/dihydroxyepoxyeicosatrienoic acid ratio in patients with COPD (P = .08).	Fluconazole	118-129	kininogen 1	Homo sapiens	133-143
33032098-13	2020	In human omental arteries, sulforaphane induced vasodilation (p < 0.001), and prevented PEM-induced endothelial dysfunction by restoring arterial sensitivity to the endothelium-dependent vasodilator bradykinin (p = 0.008).	sulforaphane	27-39	kininogen 1	Homo sapiens	199-209
27884766-7	2017	In vitro, 10 muM GSK2256294 increased 11,12-EET-mediated vasodilation compared with vehicle (90% +- 4.2% vs 72.6% +- 6.2% maximal dilatation) and shifted the bradykinin half-maximal effective concentration (EC50) (-8.33 +- 0.172 logM vs -8.10 +- 0.118 logM; P = .001 for EC50).	N-((4-cyano-2-(trifluoromethyl)phenyl)methyl)-3-((4-methyl-6-(methylamino)-1,3,5-triazin-2-yl)amino)cyclohexanecarboxamide	17-27	kininogen 1	Homo sapiens	158-168
27884766-7	2017	In vitro, 10 muM GSK2256294 increased 11,12-EET-mediated vasodilation compared with vehicle (90% +- 4.2% vs 72.6% +- 6.2% maximal dilatation) and shifted the bradykinin half-maximal effective concentration (EC50) (-8.33 +- 0.172 logM vs -8.10 +- 0.118 logM; P = .001 for EC50).	11,12-epoxy-5,8,14-eicosatrienoic acid	38-47	kininogen 1	Homo sapiens	158-168
27884766-8	2017	In vivo, 18 mg GSK2256294 improved the maximum bradykinin response from 338% +- 46% before a dose to 566% +- 110% after a single dose (P = .02) and to 503% +- 123% after a chronic dose (P = .003).	N-((4-cyano-2-(trifluoromethyl)phenyl)methyl)-3-((4-methyl-6-(methylamino)-1,3,5-triazin-2-yl)amino)cyclohexanecarboxamide	15-25	kininogen 1	Homo sapiens	47-57
34153179-8	2021	RESULTS: In studying pharyngitis using organotypic human respiratory tissue stimulated with bradykinin, we saw an increase in PGE2 and interleukin-8 (IL-8) in response to bradykinin.	Dinoprostone	126-130	kininogen 1	Homo sapiens	92-102
7649580-1	1995	The aim of this study was to investigate angiotensin II (Ang II) receptor-, bradykinin receptor-, and beta-adrenergic receptor-mediated modulation of norepinephrine release from human renal sympathetic nerves and to characterize the respective receptor subtypes involved.	Norepinephrine	150-164	kininogen 1	Homo sapiens	76-86
34935423-8	2021	Exposure of endothelial cells to bradykinin caused calcium signaling and endothelial dysfunction (increased expression of von Willibrand Factor and decreased expression of Kruppel-like Factor 2) but did not adversely affect viability in primary human aortic endothelial cells.	Calcium	51-58	kininogen 1	Homo sapiens	33-43
34935423-10	2021	When tested in our in vitro model, we found evidence that aspirin can blunt cell signaling and endothelial dysfunction caused by bradykinin in these cells.	Aspirin	58-65	kininogen 1	Homo sapiens	129-139
32797891-9	2020	In this regard, bradykinin further benefitted from an organic fraction and a high amount of formic acid.	formic acid	92-103	kininogen 1	Homo sapiens	16-26
19255162-7	2009	Inhibition of NO synthase with asymmetric dimethylarginine and/or cyclooxygenase with indomethacin markedly reduced bradykinin and NS309 relaxation.	Indomethacin	86-98	kininogen 1	Homo sapiens	116-126
19255162-9	2009	Blocking of SK(Ca) and IK(Ca) channels with apamin plus charybdotoxin or blocking of SK(Ca) channels alone in the absence and the presence of indomethacin markedly reduced bradykinin and NS309 relaxation, whereas blocking of IK(Ca) channels had no significant effect.	Charybdotoxin	56-69	kininogen 1	Homo sapiens	172-182
19255162-9	2009	Blocking of SK(Ca) and IK(Ca) channels with apamin plus charybdotoxin or blocking of SK(Ca) channels alone in the absence and the presence of indomethacin markedly reduced bradykinin and NS309 relaxation, whereas blocking of IK(Ca) channels had no significant effect.	Indomethacin	142-154	kininogen 1	Homo sapiens	172-182
19255162-11	2009	CONCLUSIONS: In porcine retinal arterioles, NO and prostaglandins mediate endothelium-dependent relaxation to bradykinin and NS309.	Prostaglandins	51-65	kininogen 1	Homo sapiens	110-120
9051297-15	1997	ZnPP (10 microM) curtailed the relaxant response of the oxygen (30%)/indomethacin (2.8 microM)-contracted ductus to bradykinin (35 nM), while it left the sodium nitroprusside (35 nM) relaxation unchanged.	zinc protoporphyrin	0-4	kininogen 1	Homo sapiens	116-126
9051297-15	1997	ZnPP (10 microM) curtailed the relaxant response of the oxygen (30%)/indomethacin (2.8 microM)-contracted ductus to bradykinin (35 nM), while it left the sodium nitroprusside (35 nM) relaxation unchanged.	Oxygen	56-62	kininogen 1	Homo sapiens	116-126
9051297-15	1997	ZnPP (10 microM) curtailed the relaxant response of the oxygen (30%)/indomethacin (2.8 microM)-contracted ductus to bradykinin (35 nM), while it left the sodium nitroprusside (35 nM) relaxation unchanged.	Indomethacin	69-81	kininogen 1	Homo sapiens	116-126
34936240-4	2022	Bradykinin ligand agonist-decorated spermine-modified acetalated dextran NPs (SpAcDex NPs) could temporarily open the BTB by activating G-protein-coupled receptors that are expressed in tumor blood vessels and tumor cells, which increase transportation to and accumulation in tumor sites.	Spermine	36-44	kininogen 1	Homo sapiens	0-10
34936240-4	2022	Bradykinin ligand agonist-decorated spermine-modified acetalated dextran NPs (SpAcDex NPs) could temporarily open the BTB by activating G-protein-coupled receptors that are expressed in tumor blood vessels and tumor cells, which increase transportation to and accumulation in tumor sites.	acetalated dextran	54-72	kininogen 1	Homo sapiens	0-10
34153179-8	2021	RESULTS: In studying pharyngitis using organotypic human respiratory tissue stimulated with bradykinin, we saw an increase in PGE2 and interleukin-8 (IL-8) in response to bradykinin.	Dinoprostone	126-130	kininogen 1	Homo sapiens	171-181
34153179-9	2021	Acetyl salicylic acid (ASA), a nonspecific COX inhibitor, was able to mitigate a bradykinin-induced increase in PGE2 in our studies.	Aspirin	0-21	kininogen 1	Homo sapiens	81-91
34153179-9	2021	Acetyl salicylic acid (ASA), a nonspecific COX inhibitor, was able to mitigate a bradykinin-induced increase in PGE2 in our studies.	Aspirin	23-26	kininogen 1	Homo sapiens	81-91
34153179-9	2021	Acetyl salicylic acid (ASA), a nonspecific COX inhibitor, was able to mitigate a bradykinin-induced increase in PGE2 in our studies.	Dinoprostone	112-116	kininogen 1	Homo sapiens	81-91
34153179-10	2021	However, ASA was inflammatory above its therapeutic window, increasing the levels of PGE2 and IL-8 above those seen with bradykinin stimulation alone.	Aspirin	9-12	kininogen 1	Homo sapiens	121-131
34153179-10	2021	However, ASA was inflammatory above its therapeutic window, increasing the levels of PGE2 and IL-8 above those seen with bradykinin stimulation alone.	Dinoprostone	85-89	kininogen 1	Homo sapiens	121-131
34153179-13	2021	An ASA-based formula (Biovanta) mitigated bradykinin-induced inflammation more strongly than ASA alone in organotypic human respiratory tissues.	Aspirin	3-6	kininogen 1	Homo sapiens	42-52
34732115-5	2022	ACE2 metabolizes angiotensin II and several peptides, including apelin-13, neurotensin, kinetensin, dynorphin, (des-Arg9) bradykinin, and (Lys-des-Arg9)-bradykinin, which may elicit neuroprotective effects.	Peptides	44-52	kininogen 1	Homo sapiens	122-132
34732115-5	2022	ACE2 metabolizes angiotensin II and several peptides, including apelin-13, neurotensin, kinetensin, dynorphin, (des-Arg9) bradykinin, and (Lys-des-Arg9)-bradykinin, which may elicit neuroprotective effects.	Peptides	44-52	kininogen 1	Homo sapiens	153-163
34412518-6	2021	To explain this difference, we suggest a potentiation of the effect of bradykinin at the B2 receptor level by ramipril, which does not occur with quinapril.	Ramipril	110-118	kininogen 1	Homo sapiens	71-81
34539836-10	2021	Thus, these data indicated that BK and BKB1R were involved in the pathological onset of EM-associated pain and that they may play an important role in EM-related pain by inducing PGE2 and PGF2alpha.	Dinoprostone	179-183	kininogen 1	Homo sapiens	32-34
34539836-10	2021	Thus, these data indicated that BK and BKB1R were involved in the pathological onset of EM-associated pain and that they may play an important role in EM-related pain by inducing PGE2 and PGF2alpha.	Dinoprost	188-197	kininogen 1	Homo sapiens	32-34
34389655-6	2021	Both dipeptides also enhanced hydrolysis of Nln endogenous substrates neurotensin, angiotensin I and bradykinin, and increased efficiency of the synthetic substrate hydrolysis (Vmax/Km ratio) in a concentration-dependent manner.	Dipeptides	5-15	kininogen 1	Homo sapiens	101-111
34622438-3	2022	Moreover, thanks to the sulfhydryl group, zofenopril has some peculiar properties (higher lipophilicity and tissue penetration, lower bradykinin-dependent effect, higher affinity for, and more persistent binding to, tissue ACE, significant antioxidant effect), which may account for the cardio-protective effects of the drug demonstrated in both pre-clinical studies and randomized clinical trials.	zofenopril	42-52	kininogen 1	Homo sapiens	134-144
34557552-0	2021	Bradykinin Protects Human Endothelial Progenitor Cells from High-Glucose-Induced Senescence through B2 Receptor-Mediated Activation of the Akt/eNOS Signalling Pathway.	Glucose	65-72	kininogen 1	Homo sapiens	0-10
34580391-9	2021	Four proteins with vascular effects were identified (angiotensinogen, kininogen-1, alpha-2-HS-glycoprotein and hemoglobin subunit beta), all upregulated after glucose provocation compared to baseline in all three compartments.	Glucose	159-166	kininogen 1	Homo sapiens	70-81
34580391-10	2021	Glucose provocation is known to cause insulin-induced vasodilation through the nitric oxide pathway, and this study indicates that this is facilitated through the interactions of the RAS (angiotensinogen) and kallikrein-kinin (kininogen-1) systems.	Glucose	0-7	kininogen 1	Homo sapiens	227-238
34580391-10	2021	Glucose provocation is known to cause insulin-induced vasodilation through the nitric oxide pathway, and this study indicates that this is facilitated through the interactions of the RAS (angiotensinogen) and kallikrein-kinin (kininogen-1) systems.	Nitric Oxide	79-91	kininogen 1	Homo sapiens	227-238
34445711-4	2021	Recent updates of studies revealed that these fatty acids are involved in vascular permeability and vasodilation, in addition to bradykinin and histamine-mediated reactions.	Fatty Acids	46-57	kininogen 1	Homo sapiens	129-139
34291395-6	2021	Omeprazole decreased BK-induced phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 and tended to decrease BK-induced nitric oxide production.	Omeprazole	0-10	kininogen 1	Homo sapiens	126-128
34533010-8	2021	RESULTS: Concentration of Bk in serum of patients without DME did not differ from one in controls (12,00 (9,70; 12,40) pg/ml) while all patients with DME had Bk level of 14,69 (13,68; 16,78) pg/ml that was significantly higher (p<0,01).	dme	58-61	kininogen 1	Homo sapiens	26-28
34533010-8	2021	RESULTS: Concentration of Bk in serum of patients without DME did not differ from one in controls (12,00 (9,70; 12,40) pg/ml) while all patients with DME had Bk level of 14,69 (13,68; 16,78) pg/ml that was significantly higher (p<0,01).	dme	150-153	kininogen 1	Homo sapiens	158-160
34533010-10	2021	The Bk/ACE concentrations ratio decreased in patients without DME and increased in those having DME.	dme	62-65	kininogen 1	Homo sapiens	4-6
34533010-10	2021	The Bk/ACE concentrations ratio decreased in patients without DME and increased in those having DME.	dme	96-99	kininogen 1	Homo sapiens	4-6
34533010-11	2021	CONCLUSION: Patients with DME have increased Bk concentration along with nearly normal ACE concentration that indicate predominance of Bk synthesis over its degradation that may lead to the DME development.	dme	26-29	kininogen 1	Homo sapiens	45-47
34533010-11	2021	CONCLUSION: Patients with DME have increased Bk concentration along with nearly normal ACE concentration that indicate predominance of Bk synthesis over its degradation that may lead to the DME development.	dme	26-29	kininogen 1	Homo sapiens	135-137
34533010-11	2021	CONCLUSION: Patients with DME have increased Bk concentration along with nearly normal ACE concentration that indicate predominance of Bk synthesis over its degradation that may lead to the DME development.	dme	190-193	kininogen 1	Homo sapiens	45-47
34533010-11	2021	CONCLUSION: Patients with DME have increased Bk concentration along with nearly normal ACE concentration that indicate predominance of Bk synthesis over its degradation that may lead to the DME development.	dme	190-193	kininogen 1	Homo sapiens	135-137
34533010-12	2021	The Bk/ACE ratio decrease in patients with uncomplicated PDR and increase significantly in ones with DME.	dme	101-104	kininogen 1	Homo sapiens	4-6
34533010-13	2021	It means that determination of Bk in serum of patients with PDR may be used for the prediction of DME development.	dme	98-101	kininogen 1	Homo sapiens	31-33
34265036-5	2022	The effect of ACEIs on the tissue and plasma levels of bradykinin and on nitric oxide production and bioavailability is specific to the mechanism of action of ACEIs; it could account for the different effects of ACEIs and ARBs on endothelial function, atherogenesis and fibrinolysis.	aceis	14-19	kininogen 1	Homo sapiens	55-65
34265036-5	2022	The effect of ACEIs on the tissue and plasma levels of bradykinin and on nitric oxide production and bioavailability is specific to the mechanism of action of ACEIs; it could account for the different effects of ACEIs and ARBs on endothelial function, atherogenesis and fibrinolysis.	aceis	159-164	kininogen 1	Homo sapiens	55-65
34265036-5	2022	The effect of ACEIs on the tissue and plasma levels of bradykinin and on nitric oxide production and bioavailability is specific to the mechanism of action of ACEIs; it could account for the different effects of ACEIs and ARBs on endothelial function, atherogenesis and fibrinolysis.	aceis	212-217	kininogen 1	Homo sapiens	55-65
34291395-6	2021	Omeprazole decreased BK-induced phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 and tended to decrease BK-induced nitric oxide production.	Nitric Oxide	137-149	kininogen 1	Homo sapiens	21-23
34291395-6	2021	Omeprazole decreased BK-induced phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 and tended to decrease BK-induced nitric oxide production.	Nitric Oxide	137-149	kininogen 1	Homo sapiens	126-128
34291395-8	2021	CONCLUSION: Our results are the first to indicate that high doses of omeprazole may suppress both store-operated Ca2+ channels and partially the G protein-coupled receptor/phospholipase C/inositol 1,4,5-triphosphate pathway, and decreased BK-induced, Ca2+-dependent phosphorylation of eNOS(Ser1177).	Omeprazole	69-79	kininogen 1	Homo sapiens	239-241
35634493-7	2022	In-vitro studies in cultured human amnion fibroblasts showed that both BK and DABK increased the expression of prostaglandin-endoperoxide synthase 2 (PTGS2), the rate-limiting enzyme in prostaglandin synthesis, and subsequent PGE2 production.	Prostaglandins	186-199	kininogen 1	Homo sapiens	71-73
34291395-4	2021	METHODS AND RESULTS: Omeprazole (10-1000 muM) suppressed both bradykinin (BK)- and thapsigargin-induced endothelial Ca2+ response in a dose-dependent manner.	Omeprazole	21-31	kininogen 1	Homo sapiens	62-72
34291395-4	2021	METHODS AND RESULTS: Omeprazole (10-1000 muM) suppressed both bradykinin (BK)- and thapsigargin-induced endothelial Ca2+ response in a dose-dependent manner.	Omeprazole	21-31	kininogen 1	Homo sapiens	74-76
34291395-6	2021	Omeprazole decreased BK-induced phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 and tended to decrease BK-induced nitric oxide production.	Omeprazole	0-10	kininogen 1	Homo sapiens	21-23
34074111-3	2021	Even though both drug groups block angiotensin II, ACE inhibitors typically reduce the degradation of bradykinin, which leads to the release of nitric oxide and prostaglandins with subsequent vasodilation.	Nitric Oxide	144-156	kininogen 1	Homo sapiens	102-112
34074111-3	2021	Even though both drug groups block angiotensin II, ACE inhibitors typically reduce the degradation of bradykinin, which leads to the release of nitric oxide and prostaglandins with subsequent vasodilation.	Prostaglandins	161-175	kininogen 1	Homo sapiens	102-112
35612774-12	2022	Comorbid ADNC and mVBI appear to synergistically interact to selectively impair bradykinin-induced vasodilation in WM-penetrating arterioles, which may be related to reduced nitric oxide- and excess reactive oxygen species-mediated vascular endothelial dysfunction.	Nitric Oxide	174-186	kininogen 1	Homo sapiens	80-90
35612774-12	2022	Comorbid ADNC and mVBI appear to synergistically interact to selectively impair bradykinin-induced vasodilation in WM-penetrating arterioles, which may be related to reduced nitric oxide- and excess reactive oxygen species-mediated vascular endothelial dysfunction.	Oxygen	208-214	kininogen 1	Homo sapiens	80-90
35629941-6	2022	Our novel findings were that the carriers of pathogenic or likely pathogenic variants for HCM had significantly increased concentrations of bradykinin (des-arg 9), vanillactate, and dimethylglycine and decreased concentrations of polysaturated fatty acids (PUFAs) and lysophosphatidylcholines compared with the controls without HCM.	des-arg	152-159	kininogen 1	Homo sapiens	140-150
34177089-8	2021	The lower serum 25(OH)D was observed in the following gene/genotypes: KNG1 rs11924390 T/T; ANKH rs2454873 G/G; NPFFR2 rs4129733 T/G; SH2B1 rs4788102 G/A; RAP1A rs494453 T/T and CRHBP rs7728378 T/C.	25(oh)d	16-23	kininogen 1	Homo sapiens	70-74
34719573-7	2021	Berotralstat suppressed bradykinin production in the HUVEC system.	Berotralstat	0-12	kininogen 1	Homo sapiens	24-34
35634493-7	2022	In-vitro studies in cultured human amnion fibroblasts showed that both BK and DABK increased the expression of prostaglandin-endoperoxide synthase 2 (PTGS2), the rate-limiting enzyme in prostaglandin synthesis, and subsequent PGE2 production.	Dinoprostone	226-230	kininogen 1	Homo sapiens	71-73
35634493-10	2022	Induction of BDKRB1 and BDKRB2 expression by LPS and SAA1 enhanced BK- or DABK-induced PTGS2 expression and PGE2 production in human amnion fibroblasts.	Dinoprostone	108-112	kininogen 1	Homo sapiens	67-69
35634493-11	2022	Conclusions: This study demonstrated for the first time that the human amnion is a target tissue of bradykinin peptides and the bradykinin system may be part of the regulatory network of PTGS2 expression and PGE2 production in human amnion fibroblasts at both term and preterm birth, which may be enhanced by infection.	Dinoprostone	208-212	kininogen 1	Homo sapiens	128-138
35105472-1	2022	Tranexamic acid (TXA) is an antifibrinolytic agent which reduces bradykinin production through its blockade of the conversion of plasminogen to plasmin and subsequently pre-kallikrein to kallikrein.	Tranexamic Acid	17-20	kininogen 1	Homo sapiens	65-75
35100351-8	2022	The lysine analog e-aminocaproic acid blocks plasmin-catalyzed bradykinin generation.	Lysine	4-10	kininogen 1	Homo sapiens	63-73
35100351-8	2022	The lysine analog e-aminocaproic acid blocks plasmin-catalyzed bradykinin generation.	Aminocaproic Acid	18-37	kininogen 1	Homo sapiens	63-73
35239284-9	2022	Propofol also stimulated release of pain mediators, namely, reactive oxygen species (ROS) and bradykinin, Our data suggest propofol elicited Ca2+ release and repressed Ca2+ clearance, causing a sustained cytosolic (Ca2+)i elevation.	Propofol	0-8	kininogen 1	Homo sapiens	94-104
35239284-9	2022	Propofol also stimulated release of pain mediators, namely, reactive oxygen species (ROS) and bradykinin, Our data suggest propofol elicited Ca2+ release and repressed Ca2+ clearance, causing a sustained cytosolic (Ca2+)i elevation.	Propofol	123-131	kininogen 1	Homo sapiens	94-104
35412805-1	2022	A high-performance field asymmetric waveform ion mobility spectrometry (FAIMS)-IMS-MS platform was developed and applied to explore the conformational diversity of the singly and doubly charged bradykinin (BK + H+)+ and (BK + 2H+)2+ ions.	Berkelium	206-208	kininogen 1	Homo sapiens	194-204
35412805-1	2022	A high-performance field asymmetric waveform ion mobility spectrometry (FAIMS)-IMS-MS platform was developed and applied to explore the conformational diversity of the singly and doubly charged bradykinin (BK + H+)+ and (BK + 2H+)2+ ions.	Deuterium	226-228	kininogen 1	Homo sapiens	194-204
35259564-0	2022	Contribution of cyclooxygenase-1-dependent prostacyclin synthesis to bradykinin-induced dermal extravasation.	Epoprostenol	43-55	kininogen 1	Homo sapiens	69-79
35105472-1	2022	Tranexamic acid (TXA) is an antifibrinolytic agent which reduces bradykinin production through its blockade of the conversion of plasminogen to plasmin and subsequently pre-kallikrein to kallikrein.	Tranexamic Acid	0-15	kininogen 1	Homo sapiens	65-75
35573493-3	2022	Angiotensin receptor blockers (ARBs) such as losartan, however, are not known to increase bradykinin levels and, therefore, this complication is not as widely recognized.	Losartan	45-53	kininogen 1	Homo sapiens	90-100
35100519-6	2022	Protein-protein interaction analysis of the differentially expressed transcripts regulated by DMB showed 5 hub genes with a strong connectivity of proinflammatory cytokines and chemokines including Kng1, Cxcl1, Cxcl2, CxcL6 and Il6.	3,3-dimethylbutan-1-ol	94-97	kininogen 1	Homo sapiens	198-202
35100519-7	2022	In vitro, TMAO significantly increased the expression of Kng1, Cxcl1, Cxcl2, CxcL6 and Il6 in bone marrow derived macrophage.	trimethyloxamine	10-14	kininogen 1	Homo sapiens	57-61
35259564-10	2022	Moreover, 6-keto-PGF1alpha concentrations were increased after bradykinin treatment in subcutaneous tissue from C57BL/6 as well as in human dermal microvascular endothelial cells and this increase was abolished by diclofenac.	6-Ketoprostaglandin F1 alpha	10-26	kininogen 1	Homo sapiens	63-73
35259564-10	2022	Moreover, 6-keto-PGF1alpha concentrations were increased after bradykinin treatment in subcutaneous tissue from C57BL/6 as well as in human dermal microvascular endothelial cells and this increase was abolished by diclofenac.	Diclofenac	214-224	kininogen 1	Homo sapiens	63-73
35212456-3	2022	Plasma kallikrein is a serine protease essential for the formation of bradykinin.	Serine	23-29	kininogen 1	Homo sapiens	70-80
2480920-5	1989	Third, following initial treatment with BK, PASMC were able to respond to NPY, but not to ATII.	pasmc	44-49	kininogen 1	Homo sapiens	40-42
35278245-12	2022	On-demand administration of KVD900 may provide an opportunity to halt the generation of bradykinin and reverse HAE attacks.	KVD900	28-34	kininogen 1	Homo sapiens	88-98
35250626-5	2022	The coronary arteriole responses to pharmacological agonists bradykinin and acetylcholine were similar in T2D and non-diabetic patients, however, exposure of the isolated arteries to methyl-beta-cyclodextrin (mbetaCD), an agent known to disrupt caveolae, reduced vasodilation to bradykinin selectively in T2D subjects and converted acetylcholine-induced vasoconstriction to dilation similarly in the two groups.	methyl-beta-cyclodextrin	183-207	kininogen 1	Homo sapiens	279-289
35250626-5	2022	The coronary arteriole responses to pharmacological agonists bradykinin and acetylcholine were similar in T2D and non-diabetic patients, however, exposure of the isolated arteries to methyl-beta-cyclodextrin (mbetaCD), an agent known to disrupt caveolae, reduced vasodilation to bradykinin selectively in T2D subjects and converted acetylcholine-induced vasoconstriction to dilation similarly in the two groups.	methyl-beta-cyclodextrin	209-216	kininogen 1	Homo sapiens	61-71
35250626-5	2022	The coronary arteriole responses to pharmacological agonists bradykinin and acetylcholine were similar in T2D and non-diabetic patients, however, exposure of the isolated arteries to methyl-beta-cyclodextrin (mbetaCD), an agent known to disrupt caveolae, reduced vasodilation to bradykinin selectively in T2D subjects and converted acetylcholine-induced vasoconstriction to dilation similarly in the two groups.	Acetylcholine	332-345	kininogen 1	Homo sapiens	61-71
35386662-3	2022	Methods: A validated LC-MS/MS platform of picomolar sensitivity developed for the analysis of eleven bradykinin-related peptides was applied to the plasma of HAE-C1INH and HAE-FXII sampled during remission.	Peptides	120-128	kininogen 1	Homo sapiens	101-111
2557246-0	1989	Histamine and bradykinin stimulate the phosphoinositide turnover in human umbilical vein endothelial cells via different G-proteins.	Phosphatidylinositols	39-55	kininogen 1	Homo sapiens	14-24
2480920-6	1989	Finally, BK and ATII, but not NPY, significantly increased inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) generation.	Inositol 1,4,5-Trisphosphate	59-87	kininogen 1	Homo sapiens	9-11
2480920-6	1989	Finally, BK and ATII, but not NPY, significantly increased inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) generation.	Inositol 1,4,5-Trisphosphate	89-101	kininogen 1	Homo sapiens	9-11
2620324-6	1989	L-NMMA (100 nmol.min-1) stereospecifically inhibited vasodilatation induced by acetylcholine and bradykinin (p less than 0.02) but not that induced by the endothelium independent vasodilator glyceryl trinitrate.	N(G)-monomethylarginine acetate	0-6	kininogen 1	Homo sapiens	97-107
2619053-3	1989	Replicate analyses of different bradykinin/glycerol/water mixtures show this improvement to depend upon the glycerol/bradykinin relationship and not the water/bradykinin relationship in sampling 4 nmol of bradykinin from 1% to 56% aqueous glycerol (2 microL initial sample volumes).	Glycerol	43-51	kininogen 1	Homo sapiens	117-127
2619053-3	1989	Replicate analyses of different bradykinin/glycerol/water mixtures show this improvement to depend upon the glycerol/bradykinin relationship and not the water/bradykinin relationship in sampling 4 nmol of bradykinin from 1% to 56% aqueous glycerol (2 microL initial sample volumes).	Glycerol	43-51	kininogen 1	Homo sapiens	117-127
2619053-3	1989	Replicate analyses of different bradykinin/glycerol/water mixtures show this improvement to depend upon the glycerol/bradykinin relationship and not the water/bradykinin relationship in sampling 4 nmol of bradykinin from 1% to 56% aqueous glycerol (2 microL initial sample volumes).	Glycerol	43-51	kininogen 1	Homo sapiens	117-127
2619053-3	1989	Replicate analyses of different bradykinin/glycerol/water mixtures show this improvement to depend upon the glycerol/bradykinin relationship and not the water/bradykinin relationship in sampling 4 nmol of bradykinin from 1% to 56% aqueous glycerol (2 microL initial sample volumes).	Water	52-57	kininogen 1	Homo sapiens	117-127
2619053-3	1989	Replicate analyses of different bradykinin/glycerol/water mixtures show this improvement to depend upon the glycerol/bradykinin relationship and not the water/bradykinin relationship in sampling 4 nmol of bradykinin from 1% to 56% aqueous glycerol (2 microL initial sample volumes).	Water	52-57	kininogen 1	Homo sapiens	117-127
2619053-3	1989	Replicate analyses of different bradykinin/glycerol/water mixtures show this improvement to depend upon the glycerol/bradykinin relationship and not the water/bradykinin relationship in sampling 4 nmol of bradykinin from 1% to 56% aqueous glycerol (2 microL initial sample volumes).	Water	52-57	kininogen 1	Homo sapiens	117-127
2619053-3	1989	Replicate analyses of different bradykinin/glycerol/water mixtures show this improvement to depend upon the glycerol/bradykinin relationship and not the water/bradykinin relationship in sampling 4 nmol of bradykinin from 1% to 56% aqueous glycerol (2 microL initial sample volumes).	Glycerol	108-116	kininogen 1	Homo sapiens	32-42
2619053-3	1989	Replicate analyses of different bradykinin/glycerol/water mixtures show this improvement to depend upon the glycerol/bradykinin relationship and not the water/bradykinin relationship in sampling 4 nmol of bradykinin from 1% to 56% aqueous glycerol (2 microL initial sample volumes).	Glycerol	108-116	kininogen 1	Homo sapiens	32-42
2592429-9	1989	This was specific for the nucleotide receptor since a response to bradykinin was not affected by the ATP pretreatment, although pretreatment with phorbol ester inhibited responses to both the nucleotides and bradykinin.	Phorbol Esters	146-159	kininogen 1	Homo sapiens	208-218
2619053-1	1989	Fast atom bombardment mass spectrometry (FAB-MS) studies of the nonapeptide bradykinin sampled from aqueous glycerol illustrate the importance of the matrix to analyte ratio in the FAB experiment.	Glycerol	108-116	kininogen 1	Homo sapiens	76-86
2586015-7	1989	This effect of bradykinin appears to be independent of changes in sodium metabolism, of beta adrenoceptors, of histamine-1 receptors, and of prostaglandins.	Prostaglandins	141-155	kininogen 1	Homo sapiens	15-25
2582988-0	1989	Effect of bradykinin on feline gallbladder water transport and prostanoid formation.	Water	43-48	kininogen 1	Homo sapiens	10-20
2582988-3	1989	Bradykinin has been previously implicated in the pathogenesis of cholecystitis and, in the intestine, bradykinin stimulates mucosal fluid secretion by a prostaglandin-mediated mechanism.	Prostaglandins	153-166	kininogen 1	Homo sapiens	102-112
2582988-6	1989	Perfusate and gallbladder tissue prostaglandin E concentrations were significantly increased by bradykinin when compared to control values.	Prostaglandins E	33-48	kininogen 1	Homo sapiens	96-106
2582988-7	1989	Concentrations of 6-keto PGF1 alpha in perfusate solutions and in gallbladder tissue were significantly increased, suggesting bradykinin increased prostacyclin formation.	6-Ketoprostaglandin F1 alpha	18-35	kininogen 1	Homo sapiens	126-136
2582988-7	1989	Concentrations of 6-keto PGF1 alpha in perfusate solutions and in gallbladder tissue were significantly increased, suggesting bradykinin increased prostacyclin formation.	Epoprostenol	147-159	kininogen 1	Homo sapiens	126-136
2509519-4	1989	PGE2 production, stimulated by bradykinin, epidermal growth factor, zymosan, and calcium ionophore, was greater in the small-cell elutriator fraction (SCEF) than in the medium and large cell fractions, which contained mucous, chief, and parietal cells.	Dinoprostone	0-4	kininogen 1	Homo sapiens	31-41
2621777-8	1989	Plasma bradykinin was 14 +/- 3 pg/ml in the SMI group and 15 +/- 3 in the PMI group (N.S), whereas it was 7 +/- 4 in the NL (p less than 0.05).	SMI496	44-47	kininogen 1	Homo sapiens	7-17
2590611-2	1989	Effects of a single intravenous dose of aspirin (600 mg) on bradykinin-stimulated prostaglandin (PG) and on thromboxane (TX) biosynthesis were determined in nine healthy male volunteers.	Aspirin	40-47	kininogen 1	Homo sapiens	60-70
2621777-8	1989	Plasma bradykinin was 14 +/- 3 pg/ml in the SMI group and 15 +/- 3 in the PMI group (N.S), whereas it was 7 +/- 4 in the NL (p less than 0.05).	pmi	74-77	kininogen 1	Homo sapiens	7-17
2590611-2	1989	Effects of a single intravenous dose of aspirin (600 mg) on bradykinin-stimulated prostaglandin (PG) and on thromboxane (TX) biosynthesis were determined in nine healthy male volunteers.	Prostaglandins	82-95	kininogen 1	Homo sapiens	60-70
2590611-2	1989	Effects of a single intravenous dose of aspirin (600 mg) on bradykinin-stimulated prostaglandin (PG) and on thromboxane (TX) biosynthesis were determined in nine healthy male volunteers.	Prostaglandins	97-99	kininogen 1	Homo sapiens	60-70
2557820-0	1989	Bradykinin and thrombin effects on polyphosphoinositide hydrolysis and prostacyclin production in endothelial cells.	Epoprostenol	71-83	kininogen 1	Homo sapiens	0-10
2590611-5	1989	Aspirin inhibited bradykinin stimulated PG and platelet TX biosynthesis 0.5 h after the dose.	Aspirin	0-7	kininogen 1	Homo sapiens	18-28
2557820-2	1989	Bradykinin caused a rapid and transient 3-fold increase in the formation of inositol polyphosphates in BAEC.	inositol polyphosphates	76-99	kininogen 1	Homo sapiens	0-10
2557820-2	1989	Bradykinin caused a rapid and transient 3-fold increase in the formation of inositol polyphosphates in BAEC.	baec	103-107	kininogen 1	Homo sapiens	0-10
2550484-5	1989	Pretreatment with tumor necrosis factor synergistically enhanced prostaglandin synthesis in response to bradykinin, bombesin, thrombin, norepinephrine, and platelet-activating factor.	Prostaglandins	65-78	kininogen 1	Homo sapiens	104-114
2687997-4	1989	We conclude that the hyponatremia may be caused by high secretion of prostagrandin and bradykinin associated with captopril therapy.	Captopril	114-123	kininogen 1	Homo sapiens	87-97
2550484-0	1989	Tumor necrosis factor causes amplification of arachidonic acid metabolism in response to interleukin 1, bradykinin, and other agonists.	Arachidonic Acid	46-62	kininogen 1	Homo sapiens	104-114
2634232-4	1989	In this study we investigated whether flurbiprofen (F) pretreatment inhibited Bk tachyphylaxis.	Flurbiprofen	38-50	kininogen 1	Homo sapiens	78-80
2634232-10	1989	Tachyphylaxis was still present at 6 h, but not in all subjects at 24 h. This study demonstrated that release of protective prostaglandins in the airway after Bk stimulation does not account for the loss of responsiveness following repeated exposure to Bk.	Prostaglandins	124-138	kininogen 1	Homo sapiens	159-161
2561022-2	1989	It has been suggested that the effects of ACE inhibitors are partially mediated by increased prostaglandin synthesis induced by a simultaneous rise in bradykinin.	Prostaglandins	93-106	kininogen 1	Homo sapiens	151-161
2482133-5	1989	In the same experimental conditions, acetylcholine and serotonin failed to relax the human coronary rings (n = 11) while substance P and bradykinin induced relaxations of 72(4)% (n = 11) and 66(7)% (n = 11) of PGF2 alpha response respectively.	Dinoprost	210-214	kininogen 1	Homo sapiens	137-147
2555202-1	1989	Simultaneous addition of bradykinin and thrombin to 3T3 fibroblasts for 5 min resulted in less than additive stimulation of prostaglandin E2 synthesis.	Dinoprostone	124-140	kininogen 1	Homo sapiens	25-35
2555202-4	1989	Bradykinin and thrombin caused increased diacylglycerol accumulation in the cells, and addition of the diacylglycerol kinase inhibitor R59022 dramatically increased the effects of sequential addition of the agonists.	Diglycerides	41-55	kininogen 1	Homo sapiens	0-10
2506191-11	1989	They also confirm that the Ca2+-phosphatidylinositol cascade is present in these cells and suggest that this cascade is modulated by ATP, TRH, and bradykinin.	Phosphatidylinositols	32-52	kininogen 1	Homo sapiens	147-157
2570343-0	1989	Glucagon and hepatic glucose production: modulation by low-dose bradykinin infusion.	Glucagon	0-8	kininogen 1	Homo sapiens	64-74
2570343-1	1989	The effect of a low-dose bradykinin (BK) infusion (30 ng/kg min) on glucagon-induced hepatic glucose production and glucose cycling was studied in five normal volunteers.	Glucagon	68-76	kininogen 1	Homo sapiens	25-35
2570343-1	1989	The effect of a low-dose bradykinin (BK) infusion (30 ng/kg min) on glucagon-induced hepatic glucose production and glucose cycling was studied in five normal volunteers.	Glucagon	68-76	kininogen 1	Homo sapiens	37-39
2570343-1	1989	The effect of a low-dose bradykinin (BK) infusion (30 ng/kg min) on glucagon-induced hepatic glucose production and glucose cycling was studied in five normal volunteers.	Glucose	93-100	kininogen 1	Homo sapiens	25-35
2570343-1	1989	The effect of a low-dose bradykinin (BK) infusion (30 ng/kg min) on glucagon-induced hepatic glucose production and glucose cycling was studied in five normal volunteers.	Glucose	93-100	kininogen 1	Homo sapiens	37-39
2570343-5	1989	In a second set of experiments BK was infused concomitantly with the high dose glucagon.	Glucagon	79-87	kininogen 1	Homo sapiens	31-33
2570343-9	1989	These findings suggest that intravenous BK may interact with mechanisms involved in the down-regulation of hepatic glucagon effects.	Glucagon	115-123	kininogen 1	Homo sapiens	40-42
2765565-2	1989	Addition of either cerebroside sulfate (CS) or phosphatidylinositol (PI), solubilized with the nonionic surfactant C12E8, to BK or its analogue [Gly6]-BK enhances the relative fluorescence intensity of peptide emission at 288 nm.	Phosphatidylinositols	47-67	kininogen 1	Homo sapiens	151-153
2765565-2	1989	Addition of either cerebroside sulfate (CS) or phosphatidylinositol (PI), solubilized with the nonionic surfactant C12E8, to BK or its analogue [Gly6]-BK enhances the relative fluorescence intensity of peptide emission at 288 nm.	gly6]	145-150	kininogen 1	Homo sapiens	151-153
2765565-5	1989	The value of the equilibrium constant, K, for the interaction of either BK or [Gly6]-BK with CS is 1.5.10(4) M-1.	cerebroside sulfate	93-95	kininogen 1	Homo sapiens	72-74
2765565-5	1989	The value of the equilibrium constant, K, for the interaction of either BK or [Gly6]-BK with CS is 1.5.10(4) M-1.	cerebroside sulfate	93-95	kininogen 1	Homo sapiens	85-87
2765565-7	1989	Although electrostatic forces no doubt play a major role in these interactions, measurements on the model peptide Gly-Phe-Gly indicate that the phenylalanine residues of BK are disposed in the hydrophobic environment provided by the lipid-C12E8 mixed micelle.	glycyl-phenylalanyl-glycine	114-125	kininogen 1	Homo sapiens	170-172
2765565-7	1989	Although electrostatic forces no doubt play a major role in these interactions, measurements on the model peptide Gly-Phe-Gly indicate that the phenylalanine residues of BK are disposed in the hydrophobic environment provided by the lipid-C12E8 mixed micelle.	Phenylalanine	144-157	kininogen 1	Homo sapiens	170-172
2765565-7	1989	Although electrostatic forces no doubt play a major role in these interactions, measurements on the model peptide Gly-Phe-Gly indicate that the phenylalanine residues of BK are disposed in the hydrophobic environment provided by the lipid-C12E8 mixed micelle.	dodecyloctaethyleneglycol monoether	239-244	kininogen 1	Homo sapiens	170-172
2765565-9	1989	The increase in the relative fluorescence intensity of BK accompanying its cooperative interaction with sodium dodecyl sulfate (SDS) implicates the role of hydrophobic forces in this interaction as well.	Sodium Dodecyl Sulfate	104-126	kininogen 1	Homo sapiens	55-57
2765565-9	1989	The increase in the relative fluorescence intensity of BK accompanying its cooperative interaction with sodium dodecyl sulfate (SDS) implicates the role of hydrophobic forces in this interaction as well.	Sodium Dodecyl Sulfate	128-131	kininogen 1	Homo sapiens	55-57
2765565-10	1989	These results bear on the interpretation of the changes in circular dichroism (CD) of BK caused by SDS.	Sodium Dodecyl Sulfate	99-102	kininogen 1	Homo sapiens	86-88
2546937-0	1989	Characterization of the bradykinin-stimulated calcium influx pathway of cultured vascular endothelial cells.	Calcium	46-53	kininogen 1	Homo sapiens	24-34
2546937-3	1989	The BK-stimulated influx pathway was characterized with respect to its 1) sensitivity to extracellular Ca2+, 2) inhibition by membrane depolarization, and 3) permeability to Ba2+ and Sr2+.	N-methyl-valyl-amiclenomycin	174-178	kininogen 1	Homo sapiens	4-6
2546937-3	1989	The BK-stimulated influx pathway was characterized with respect to its 1) sensitivity to extracellular Ca2+, 2) inhibition by membrane depolarization, and 3) permeability to Ba2+ and Sr2+.	strontium cation	183-187	kininogen 1	Homo sapiens	4-6
2546937-5	1989	Fura-2 fluorescence was used to compare the profiles for BK-stimulated changes in cytosolic Ca2+, Sr2+, and Ba2+ (Ca2+i, Ba2+i, and Sr2+i).	Fura-2	0-6	kininogen 1	Homo sapiens	57-59
2546937-5	1989	Fura-2 fluorescence was used to compare the profiles for BK-stimulated changes in cytosolic Ca2+, Sr2+, and Ba2+ (Ca2+i, Ba2+i, and Sr2+i).	strontium cation	98-102	kininogen 1	Homo sapiens	57-59
2546937-5	1989	Fura-2 fluorescence was used to compare the profiles for BK-stimulated changes in cytosolic Ca2+, Sr2+, and Ba2+ (Ca2+i, Ba2+i, and Sr2+i).	N-methyl-valyl-amiclenomycin	108-112	kininogen 1	Homo sapiens	57-59
2546937-5	1989	Fura-2 fluorescence was used to compare the profiles for BK-stimulated changes in cytosolic Ca2+, Sr2+, and Ba2+ (Ca2+i, Ba2+i, and Sr2+i).	N-methyl-valyl-amiclenomycin	121-125	kininogen 1	Homo sapiens	57-59
2546937-5	1989	Fura-2 fluorescence was used to compare the profiles for BK-stimulated changes in cytosolic Ca2+, Sr2+, and Ba2+ (Ca2+i, Ba2+i, and Sr2+i).	strontium cation	132-136	kininogen 1	Homo sapiens	57-59
2546937-6	1989	Addition of Ca2+ and Sr2+ to Ca2+-depleted cells in the presence of BK produced a transient increase in Ca2+i and Sr2+i.	strontium cation	21-25	kininogen 1	Homo sapiens	68-70
2546937-6	1989	Addition of Ca2+ and Sr2+ to Ca2+-depleted cells in the presence of BK produced a transient increase in Ca2+i and Sr2+i.	strontium cation	114-118	kininogen 1	Homo sapiens	68-70
2546937-9	1989	Addition of Ba2+ to Ca2+-depleted cells in the presence of BK produced an increase in Ba2+i which continued to rise with time to a steady level.	N-methyl-valyl-amiclenomycin	12-16	kininogen 1	Homo sapiens	59-61
2546937-9	1989	Addition of Ba2+ to Ca2+-depleted cells in the presence of BK produced an increase in Ba2+i which continued to rise with time to a steady level.	N-methyl-valyl-amiclenomycin	86-90	kininogen 1	Homo sapiens	59-61
2546937-13	1989	The results of these experiments demonstrate that BK stimulates a 100- to 150-fold increase in Ca2+ permeability of the BAEC but that the influx pathway turns off or inactivates within 2 min.	baec	120-124	kininogen 1	Homo sapiens	50-52
2475035-4	1989	Bradykinin stimulated inositol phosphate accumulation but, in the presence of indomethacin, did not alter cAMP levels.	Inositol Phosphates	22-40	kininogen 1	Homo sapiens	0-10
2475035-5	1989	Despite the difference in second messenger pathways, both bradykinin and isoproterenol transiently increased [Ca2+]c. Bradykinin stimulated inositol phosphate accumulation and increased [Ca2+]c with similar potencies, suggesting that bradykinin elevated [Ca2+]c by stimulating inositol phosphate production.	Isoproterenol	73-86	kininogen 1	Homo sapiens	234-244
2475035-5	1989	Despite the difference in second messenger pathways, both bradykinin and isoproterenol transiently increased [Ca2+]c. Bradykinin stimulated inositol phosphate accumulation and increased [Ca2+]c with similar potencies, suggesting that bradykinin elevated [Ca2+]c by stimulating inositol phosphate production.	Inositol Phosphates	140-158	kininogen 1	Homo sapiens	58-68
2475035-5	1989	Despite the difference in second messenger pathways, both bradykinin and isoproterenol transiently increased [Ca2+]c. Bradykinin stimulated inositol phosphate accumulation and increased [Ca2+]c with similar potencies, suggesting that bradykinin elevated [Ca2+]c by stimulating inositol phosphate production.	Inositol Phosphates	140-158	kininogen 1	Homo sapiens	118-128
2475035-5	1989	Despite the difference in second messenger pathways, both bradykinin and isoproterenol transiently increased [Ca2+]c. Bradykinin stimulated inositol phosphate accumulation and increased [Ca2+]c with similar potencies, suggesting that bradykinin elevated [Ca2+]c by stimulating inositol phosphate production.	Inositol Phosphates	277-295	kininogen 1	Homo sapiens	58-68
2475035-5	1989	Despite the difference in second messenger pathways, both bradykinin and isoproterenol transiently increased [Ca2+]c. Bradykinin stimulated inositol phosphate accumulation and increased [Ca2+]c with similar potencies, suggesting that bradykinin elevated [Ca2+]c by stimulating inositol phosphate production.	Inositol Phosphates	277-295	kininogen 1	Homo sapiens	118-128
2752143-8	1989	In addition, the antibody inhibits HK-dependent clotting activity of normal human plasma and dextran sulfate-mediated activation of prekallikrein in plasma and retards cleavage of HK in normal plasma after contact activation with dextran sulfate.	Dextran Sulfate	230-245	kininogen 1	Homo sapiens	35-37
2752143-8	1989	In addition, the antibody inhibits HK-dependent clotting activity of normal human plasma and dextran sulfate-mediated activation of prekallikrein in plasma and retards cleavage of HK in normal plasma after contact activation with dextran sulfate.	Dextran Sulfate	230-245	kininogen 1	Homo sapiens	180-182
2752143-11	1989	Decreased levels of kallikrein thus formed may be responsible for the inhibition of HK-dependent clotting activity and the decrease in rate and extent of HK cleavage in normal plasma on contact activation with dextran sulfate.	Dextran Sulfate	210-225	kininogen 1	Homo sapiens	154-156
2562502-8	1989	The migratory response to bradykinin could not be attributed to the release of arachidonic acid metabolites, but stimulated migration could be significantly inhibited by the histamine type 2 receptor antagonist cimetidine.	Arachidonic Acid	79-95	kininogen 1	Homo sapiens	26-36
2562502-8	1989	The migratory response to bradykinin could not be attributed to the release of arachidonic acid metabolites, but stimulated migration could be significantly inhibited by the histamine type 2 receptor antagonist cimetidine.	Cimetidine	211-221	kininogen 1	Homo sapiens	26-36
2545733-1	1989	In cultured foreskin fibroblasts, bradykinin stimulates inositol phosphate generation, arachidonic acid release, and Na+/H+ exchange, with doses of 1-3 nM yielding half-maximal stimulation.	Inositol Phosphates	56-74	kininogen 1	Homo sapiens	34-44
2545733-1	1989	In cultured foreskin fibroblasts, bradykinin stimulates inositol phosphate generation, arachidonic acid release, and Na+/H+ exchange, with doses of 1-3 nM yielding half-maximal stimulation.	Arachidonic Acid	87-103	kininogen 1	Homo sapiens	34-44
2545733-2	1989	Binding of 3H-bradykinin to these cells demonstrates a single receptor site with a Kd of 2.0 nM and a Bmax of 91 fmoles/mg protein.	Tritium	11-13	kininogen 1	Homo sapiens	14-24
2545733-4	1989	GTP synergizes with bradykinin to stimulate phosphatidylinositol turnover in permeabilized fibroblasts and GTP-gamma-S decreases the Bmax of bradykinin binding to fibroblast membranes, indicating that a G-protein couples the receptor to phospholipase C. Pretreatment of fibroblasts with either cholera or pertussis toxin enhances bradykinin stimulation of inositol phosphate accumulation.	Guanosine 5'-O-(3-Thiotriphosphate)	107-118	kininogen 1	Homo sapiens	141-151
2545733-4	1989	GTP synergizes with bradykinin to stimulate phosphatidylinositol turnover in permeabilized fibroblasts and GTP-gamma-S decreases the Bmax of bradykinin binding to fibroblast membranes, indicating that a G-protein couples the receptor to phospholipase C. Pretreatment of fibroblasts with either cholera or pertussis toxin enhances bradykinin stimulation of inositol phosphate accumulation.	Guanosine 5'-O-(3-Thiotriphosphate)	107-118	kininogen 1	Homo sapiens	141-151
2517685-3	1989	Bradykinin-induced relaxation was not inhibited by acetylsalicylic acid (10(-4) M), indomethacin (10(-6) M), and combined treatment with phentolamine (10(-6) M) and propranolol (10(-6) M).	Aspirin	51-71	kininogen 1	Homo sapiens	0-10
2517685-3	1989	Bradykinin-induced relaxation was not inhibited by acetylsalicylic acid (10(-4) M), indomethacin (10(-6) M), and combined treatment with phentolamine (10(-6) M) and propranolol (10(-6) M).	Phentolamine	137-149	kininogen 1	Homo sapiens	0-10
2517685-3	1989	Bradykinin-induced relaxation was not inhibited by acetylsalicylic acid (10(-4) M), indomethacin (10(-6) M), and combined treatment with phentolamine (10(-6) M) and propranolol (10(-6) M).	Propranolol	165-176	kininogen 1	Homo sapiens	0-10
2520217-2	1989	After electrophoresis separation on a polyacrylamide gel, the peptide bradykinin was localized using Coomassie Blue as a staining dye.	polyacrylamide	38-52	kininogen 1	Homo sapiens	70-80
2520217-2	1989	After electrophoresis separation on a polyacrylamide gel, the peptide bradykinin was localized using Coomassie Blue as a staining dye.	Coomassie blue	101-115	kininogen 1	Homo sapiens	70-80
2516453-4	1989	However, arachidonic acid, acetylcholine, bradykinin, and PMA stimulated the release of 15-hydroxyeicosatetraenoic acid (15-HETE) as major and prostaglandin E2 (PGE2) as minor products.	Eicosatetraenoic acid, 15-hydroxy-	88-119	kininogen 1	Homo sapiens	42-52
2516453-4	1989	However, arachidonic acid, acetylcholine, bradykinin, and PMA stimulated the release of 15-hydroxyeicosatetraenoic acid (15-HETE) as major and prostaglandin E2 (PGE2) as minor products.	15-Hete	121-128	kininogen 1	Homo sapiens	42-52
2516453-4	1989	However, arachidonic acid, acetylcholine, bradykinin, and PMA stimulated the release of 15-hydroxyeicosatetraenoic acid (15-HETE) as major and prostaglandin E2 (PGE2) as minor products.	Dinoprostone	143-159	kininogen 1	Homo sapiens	42-52
2516453-4	1989	However, arachidonic acid, acetylcholine, bradykinin, and PMA stimulated the release of 15-hydroxyeicosatetraenoic acid (15-HETE) as major and prostaglandin E2 (PGE2) as minor products.	Dinoprostone	161-165	kininogen 1	Homo sapiens	42-52
2516453-6	1989	Arachidonic acid at 30 microM caused the release of 258 +/- 76 ng and 29 +/- 15 ng (n = 12) of 15-HETE and PGE2, respectively, from 10 x 10(6) epithelial cells, whereas acetylcholine, bradykinin, or PMA caused the release of approximately 2- to 10-fold less 15-HETE and PGE2.	Arachidonic Acid	0-16	kininogen 1	Homo sapiens	184-194
2555202-0	1989	Diacylglycerol in the synergy of bradykinin and thrombin stimulation of prostaglandin synthesis.	Diglycerides	0-14	kininogen 1	Homo sapiens	33-43
2545496-1	1989	Bradykinin and its active metabolites, produced by kallikreins at their sites of action, potently elicit a variety of biological effects: hypotension, bronchoconstriction, gut and uterine contraction, epithelial secretion in airway, gut, and exocrine glands, vascular permeability, pain, connective tissue proliferation, cytokine release, and eicosanoid formation.	Eicosanoids	343-353	kininogen 1	Homo sapiens	0-10
2502590-5	1989	Stimulation of endogenous PGE2 production by bradykinin had a similar effect on glycosaminoglycan synthesis.	Dinoprostone	26-30	kininogen 1	Homo sapiens	45-55
2760947-2	1989	Our purpose was to determine if isoproterenol (ISO) reversed a BRADY-produced accelerated loss of intravascular fluid and protein into the interstitium of skin.	Isoproterenol	32-45	kininogen 1	Homo sapiens	63-68
2760947-2	1989	Our purpose was to determine if isoproterenol (ISO) reversed a BRADY-produced accelerated loss of intravascular fluid and protein into the interstitium of skin.	Isoproterenol	47-50	kininogen 1	Homo sapiens	63-68
2507329-0	1989	Interleukin-1 potentiates bradykinin- and TNF alpha-induced PGE2 release.	Dinoprostone	60-64	kininogen 1	Homo sapiens	26-36
2507329-1	1989	The ability of interleukin-1 (IL-1 alpha), IL-1 beta, tumour necrosis factor alpha (TNF alpha) and bradykinin to cause prostaglandin E2 (PGE2) release from human synovial cells was examined.	Dinoprostone	119-135	kininogen 1	Homo sapiens	99-109
2507329-1	1989	The ability of interleukin-1 (IL-1 alpha), IL-1 beta, tumour necrosis factor alpha (TNF alpha) and bradykinin to cause prostaglandin E2 (PGE2) release from human synovial cells was examined.	Dinoprostone	137-141	kininogen 1	Homo sapiens	99-109
2507329-3	1989	When the cells were pretreated with IL-1 alpha or IL-1 beta for 24 h, their ability to release PGE2 in response to a short incubation (1 h) with bradykinin, TNF alpha or a second dose of IL-1 was potentiated.	Dinoprostone	95-99	kininogen 1	Homo sapiens	145-155
2507329-4	1989	In addition, TNF alpha and bradykinin were shown to increase the level of free arachidonic acid (AA) in the cells.	Arachidonic Acid	79-95	kininogen 1	Homo sapiens	27-37
2507329-7	1989	It seems likely, therefore, that activation of phospholipase A2 which occurs during a short incubation with IL-1, TNF alpha or bradykinin releases substrate, AA, which is more rapidly converted to PGE2 by cells in which CO has been induced.	Dinoprostone	197-201	kininogen 1	Homo sapiens	127-137
2472445-0	1989	Preincubation of human synovial cells with IL-1 modulates prostaglandin E2 release in response to bradykinin.	Dinoprostone	58-74	kininogen 1	Homo sapiens	98-108
2472445-4	1989	However, after a period of preincubation with the cytokine, IL-1, which is itself a stimulus for PGE2 production, synovial cells exhibited a further striking time- and dose-dependent response to bradykinin.	Dinoprostone	97-101	kininogen 1	Homo sapiens	195-205
2472445-5	1989	Maximal release of PGE2 was observed in response to 10(-7) to 10(-6) M bradykinin after first pretreating the cells for 24 h with 5 to 10 U/ml of IL-1.	Dinoprostone	19-23	kininogen 1	Homo sapiens	71-81
2472445-9	1989	The synergistic response in PGE2 production induced by IL-1 and bradykinin was significantly inhibited by pretreatment with 1 microM indomethacin or dexamethasone (96 and 94% inhibition, respectively).	Dinoprostone	28-32	kininogen 1	Homo sapiens	64-74
2472445-9	1989	The synergistic response in PGE2 production induced by IL-1 and bradykinin was significantly inhibited by pretreatment with 1 microM indomethacin or dexamethasone (96 and 94% inhibition, respectively).	Indomethacin	133-145	kininogen 1	Homo sapiens	64-74
2472445-9	1989	The synergistic response in PGE2 production induced by IL-1 and bradykinin was significantly inhibited by pretreatment with 1 microM indomethacin or dexamethasone (96 and 94% inhibition, respectively).	Dexamethasone	149-162	kininogen 1	Homo sapiens	64-74
2702034-4	1989	The cause of the damage to the alveolar-capillary membranes is still unknown and we thought that long-term administration of captopril might have contributed to the damage itself, since like all ACE-inhibitors, captopril is able to bring about tissular storage of both bradykinin and prostaglandins and therefore alter the pulmonary reactivity to phlogistic stimuli.	Captopril	125-134	kininogen 1	Homo sapiens	269-279
2702034-4	1989	The cause of the damage to the alveolar-capillary membranes is still unknown and we thought that long-term administration of captopril might have contributed to the damage itself, since like all ACE-inhibitors, captopril is able to bring about tissular storage of both bradykinin and prostaglandins and therefore alter the pulmonary reactivity to phlogistic stimuli.	Captopril	211-220	kininogen 1	Homo sapiens	269-279
2526132-14	1989	Fibrinogen binding to ADP-stimulated platelets was increased twofold by Zn++ (50 microM) and was inhibited by HMWK.	Adenosine Diphosphate	22-25	kininogen 1	Homo sapiens	110-114
2738152-4	1989	Human neutrophils were found to possess surface membrane-binding sites for HMWK but no internalization was detected at 37 degrees C. 125I-HMWK binding to neutrophils was dependent upon Zn2+.	Zinc	185-189	kininogen 1	Homo sapiens	138-142
2508445-4	1989	The bradykinin treated cells had higher levels of IPs (37-fold) than the controls.	IPS	50-53	kininogen 1	Homo sapiens	4-14
2801307-4	1989	When fibroblasts were incubated with bradykinin, PGE2 synthesis was stimulated.	Dinoprostone	49-53	kininogen 1	Homo sapiens	37-47
2801307-5	1989	Pretreatment with IL-1 or TNF dramatically amplified bradykinin-stimulated PGE2 synthesis.	Dinoprostone	75-79	kininogen 1	Homo sapiens	53-63
2500022-2	1989	The synthesis of these eicosanoids was measured by specific radioimmunoassays after stimulation by arachidonic acid, A23187, bradykinin, melittin, or histamine.	Eicosanoids	23-34	kininogen 1	Homo sapiens	125-135
2547408-0	1989	Bradykinin-induced bronchoconstriction: inhibition by nedocromil sodium and sodium cromoglycate.	Nedocromil	54-71	kininogen 1	Homo sapiens	0-10
2547408-0	1989	Bradykinin-induced bronchoconstriction: inhibition by nedocromil sodium and sodium cromoglycate.	Cromolyn Sodium	76-95	kininogen 1	Homo sapiens	0-10
2547408-10	1989	Both nedocromil sodium (4 mg) and sodium cromoglycate (10 mg) gave significant protection (P less than 0.05) against bradykinin-induced bronchoconstriction (PD40 0.37: 0.19-0.72 mumol after nedocromil sodium and 0.22: 0.11-0.49 after sodium cromoglycate).	Nedocromil	5-22	kininogen 1	Homo sapiens	117-127
2547408-10	1989	Both nedocromil sodium (4 mg) and sodium cromoglycate (10 mg) gave significant protection (P less than 0.05) against bradykinin-induced bronchoconstriction (PD40 0.37: 0.19-0.72 mumol after nedocromil sodium and 0.22: 0.11-0.49 after sodium cromoglycate).	Cromolyn Sodium	34-53	kininogen 1	Homo sapiens	117-127
2547408-12	1989	Since bradykinin-induced bronchoconstriction is probably neurally mediated we conclude that both nedocromil sodium and sodium cromoglycate have an action on neural pathways which may be useful in the control of asthma symptoms.	Nedocromil	97-114	kininogen 1	Homo sapiens	6-16
2547408-12	1989	Since bradykinin-induced bronchoconstriction is probably neurally mediated we conclude that both nedocromil sodium and sodium cromoglycate have an action on neural pathways which may be useful in the control of asthma symptoms.	Cromolyn Sodium	119-138	kininogen 1	Homo sapiens	6-16
2547411-0	1989	The effect of indomethacin and enalapril on the cutaneous response to bradykinin.	Indomethacin	14-26	kininogen 1	Homo sapiens	70-80
2547411-0	1989	The effect of indomethacin and enalapril on the cutaneous response to bradykinin.	Enalapril	31-40	kininogen 1	Homo sapiens	70-80
2547411-2	1989	Both converting enzyme inhibitors and bradykinin stimulate prostaglandin synthesis and prostaglandins enhance the cutaneous response to bradykinin.	Prostaglandins	59-72	kininogen 1	Homo sapiens	38-48
2547411-2	1989	Both converting enzyme inhibitors and bradykinin stimulate prostaglandin synthesis and prostaglandins enhance the cutaneous response to bradykinin.	Prostaglandins	87-101	kininogen 1	Homo sapiens	38-48
2547411-2	1989	Both converting enzyme inhibitors and bradykinin stimulate prostaglandin synthesis and prostaglandins enhance the cutaneous response to bradykinin.	Prostaglandins	87-101	kininogen 1	Homo sapiens	136-146
2547411-3	1989	We examined the possibility that the increased wheal response to intradermal bradykinin in the presence of enalapril was due to the effect of prostaglandins.	Enalapril	107-116	kininogen 1	Homo sapiens	77-87
2547411-3	1989	We examined the possibility that the increased wheal response to intradermal bradykinin in the presence of enalapril was due to the effect of prostaglandins.	Prostaglandins	142-156	kininogen 1	Homo sapiens	77-87
2731571-4	1989	A dose-dependent increase in intracellular calcium was found for the following drugs, which are given with their respective EC50 values: carbachol (15.7 +/- 4 microM), ATP (1.67 +/- 0.4 microM), arginine vasopressin (52 +/- 14 nM), bradykinin (2.4 +/- 0.7 nM), histamine (0.7 +/- 0.1 microM), and angiotensin II (6.4 +/- 1 nM).	Adenosine Triphosphate	168-171	kininogen 1	Homo sapiens	232-242
2731571-4	1989	A dose-dependent increase in intracellular calcium was found for the following drugs, which are given with their respective EC50 values: carbachol (15.7 +/- 4 microM), ATP (1.67 +/- 0.4 microM), arginine vasopressin (52 +/- 14 nM), bradykinin (2.4 +/- 0.7 nM), histamine (0.7 +/- 0.1 microM), and angiotensin II (6.4 +/- 1 nM).	Calcium	43-50	kininogen 1	Homo sapiens	232-242
2674438-4	1989	Interactions involving bradykinin include captopril-indomethacin, in which an attenuation of the antihypertensive effects of captopril is manifest.	Captopril	42-51	kininogen 1	Homo sapiens	23-33
2674438-4	1989	Interactions involving bradykinin include captopril-indomethacin, in which an attenuation of the antihypertensive effects of captopril is manifest.	Indomethacin	52-64	kininogen 1	Homo sapiens	23-33
2674438-4	1989	Interactions involving bradykinin include captopril-indomethacin, in which an attenuation of the antihypertensive effects of captopril is manifest.	Captopril	125-134	kininogen 1	Homo sapiens	23-33
2722798-3	1989	Bradykinin similarly increased [3H]inositol phosphates.	[3h]inositol phosphates	31-54	kininogen 1	Homo sapiens	0-10
2505402-7	1989	Stimulation of the endothelial cells with bradykinin produced an unstable factor(s) that potentiated ADP-induced platelet aggregation, was not affected by hemoglobin or cyclooxygenase inhibitions, and had no platelet aggregatory activity on its own.	Adenosine Diphosphate	101-104	kininogen 1	Homo sapiens	42-52
2557432-11	1989	Enalaprilat increased vasodilatation caused by bradykinin.	Enalaprilat	0-11	kininogen 1	Homo sapiens	47-57
2503838-4	1989	The MTM cells produced increased amounts of PGE2 in response to treatment with bradykinin, platelet activating factor, and A-23187.	Dinoprostone	44-48	kininogen 1	Homo sapiens	79-89
2540174-7	1989	Cd2+ increased [3H]inositol polyphosphates; [3H]inositol trisphosphate increased 4-fold in 15 s. Zn2+ reversibly blocked 45Ca2+ efflux evoked by Cd2+ but not that produced by bradykinin.	Zinc	97-101	kininogen 1	Homo sapiens	175-185
2651524-1	1989	Activation of the Hageman factor-dependent pathways in human plasma leads to the cleavage of high molecular weight kininogen (HMWK) into a disulfide-linked two-chain (heavy and light chain) molecule and release of bradykinin, a vasoactive peptide.	Disulfides	139-148	kininogen 1	Homo sapiens	93-124
2651524-1	1989	Activation of the Hageman factor-dependent pathways in human plasma leads to the cleavage of high molecular weight kininogen (HMWK) into a disulfide-linked two-chain (heavy and light chain) molecule and release of bradykinin, a vasoactive peptide.	Disulfides	139-148	kininogen 1	Homo sapiens	126-130
2540021-6	1989	Internally applied bradykinin produces a frequency-dependent block of the sodium current.	Sodium	74-80	kininogen 1	Homo sapiens	19-29
2495258-5	1989	The release of all three prostanoids was significantly increased by the addition of the calcium ionophore (A23187), human thrombin, bradykinin and histamine.	Prostaglandins	25-36	kininogen 1	Homo sapiens	132-142
2474031-2	1989	Histamine, bradykinin, and thrombin significantly stimulated formation of inositol mono-, bis-, and trisphosphate and 1,2-diacylglycerol within 5 min after addition.	inositol mono-, bis-, and trisphosphate	74-113	kininogen 1	Homo sapiens	11-21
2474031-2	1989	Histamine, bradykinin, and thrombin significantly stimulated formation of inositol mono-, bis-, and trisphosphate and 1,2-diacylglycerol within 5 min after addition.	1,2-diacylglycerol	118-136	kininogen 1	Homo sapiens	11-21
2671341-1	1989	Thrombin and bradykinin stimulate production of prostaglandin E2 (PGE2), and 6-keto-prostaglandin F1 alpha (the stable breakdown product of prostacyclin) in isolated human peripheral blood monocytes in a dose- and time-dependent manner.	6-Ketoprostaglandin F1 alpha	77-106	kininogen 1	Homo sapiens	13-23
2671341-1	1989	Thrombin and bradykinin stimulate production of prostaglandin E2 (PGE2), and 6-keto-prostaglandin F1 alpha (the stable breakdown product of prostacyclin) in isolated human peripheral blood monocytes in a dose- and time-dependent manner.	Epoprostenol	140-152	kininogen 1	Homo sapiens	13-23
2671341-0	1989	Thrombin and bradykinin enhance prostaglandin production in human peripheral blood monocytes.	Prostaglandins	32-45	kininogen 1	Homo sapiens	13-23
2671341-2	1989	Since PGE2 and prostacyclin can affect the activity of immunocompetent cells and bone resorbing osteoclasts, our finding indicates that thrombin and bradykinin, both of which are formed in inflammatory processes as a consequence of activation of the Hageman factor (coagulation factor XII), may have important roles in the modulation of the inflammatory response and the loss of alveolar bone in periodontitis.	Dinoprostone	6-10	kininogen 1	Homo sapiens	149-159
2671341-1	1989	Thrombin and bradykinin stimulate production of prostaglandin E2 (PGE2), and 6-keto-prostaglandin F1 alpha (the stable breakdown product of prostacyclin) in isolated human peripheral blood monocytes in a dose- and time-dependent manner.	Dinoprostone	48-64	kininogen 1	Homo sapiens	13-23
2671341-2	1989	Since PGE2 and prostacyclin can affect the activity of immunocompetent cells and bone resorbing osteoclasts, our finding indicates that thrombin and bradykinin, both of which are formed in inflammatory processes as a consequence of activation of the Hageman factor (coagulation factor XII), may have important roles in the modulation of the inflammatory response and the loss of alveolar bone in periodontitis.	Epoprostenol	15-27	kininogen 1	Homo sapiens	149-159
2671341-1	1989	Thrombin and bradykinin stimulate production of prostaglandin E2 (PGE2), and 6-keto-prostaglandin F1 alpha (the stable breakdown product of prostacyclin) in isolated human peripheral blood monocytes in a dose- and time-dependent manner.	Dinoprostone	66-70	kininogen 1	Homo sapiens	13-23
2538467-0	1989	Bradykinin-induced activation of phospholipase A2 is independent of the activation of polyphosphoinositide-hydrolyzing phospholipase C. This study evaluates the role of phosphatidylinositol 4,5-bisphosphate (PIP2) and its metabolites as possible mediators in the activation of phospholipases A2 in porcine aortic endothelial cells.	Phosphatidylinositol 4,5-Diphosphate	208-212	kininogen 1	Homo sapiens	0-10
2538467-1	1989	We compared the time courses of bradykinin-induced turnover of phosphoinositides and the appearance of unesterified arachidonic acid (uAA) and eicosanoids.	Phosphatidylinositols	63-80	kininogen 1	Homo sapiens	32-42
2538467-1	1989	We compared the time courses of bradykinin-induced turnover of phosphoinositides and the appearance of unesterified arachidonic acid (uAA) and eicosanoids.	6-Carboxymethyluracil	134-137	kininogen 1	Homo sapiens	32-42
2538467-3	1989	At 37 degrees C, bradykinin induced a rapid rise in lysophosphatidylinositol (lyso-PI) and inositol 1,4,5-trisphosphate (IP3) as well as a decrease in PIP2.	lysophosphatidylinositol	52-76	kininogen 1	Homo sapiens	17-27
2538467-3	1989	At 37 degrees C, bradykinin induced a rapid rise in lysophosphatidylinositol (lyso-PI) and inositol 1,4,5-trisphosphate (IP3) as well as a decrease in PIP2.	lysophosphatidylinositol	78-85	kininogen 1	Homo sapiens	17-27
2538467-3	1989	At 37 degrees C, bradykinin induced a rapid rise in lysophosphatidylinositol (lyso-PI) and inositol 1,4,5-trisphosphate (IP3) as well as a decrease in PIP2.	Inositol 1,4,5-Trisphosphate	91-119	kininogen 1	Homo sapiens	17-27
2538467-3	1989	At 37 degrees C, bradykinin induced a rapid rise in lysophosphatidylinositol (lyso-PI) and inositol 1,4,5-trisphosphate (IP3) as well as a decrease in PIP2.	Inositol 1,4,5-Trisphosphate	121-124	kininogen 1	Homo sapiens	17-27
2538467-3	1989	At 37 degrees C, bradykinin induced a rapid rise in lysophosphatidylinositol (lyso-PI) and inositol 1,4,5-trisphosphate (IP3) as well as a decrease in PIP2.	Phosphatidylinositol 4,5-Diphosphate	151-155	kininogen 1	Homo sapiens	17-27
2538467-9	1989	Bradykinin stimulated the intracellular accumulation of uAA, detectable at 5 s, earlier than that of 1,2-diacylglycerol and phosphatidic acid.	6-Carboxymethyluracil	56-59	kininogen 1	Homo sapiens	0-10
2538467-10	1989	Such immediate formation of uAA further supports the notion that activation of phospholipase A2 is a very early event during the interaction of bradykinin with porcine endothelial cells, and that PIP2 hydrolysis is not prerequisite for the initial activation of phospholipase A2.	6-Carboxymethyluracil	28-31	kininogen 1	Homo sapiens	144-154
2539165-3	1989	Angiotensin-converting enzyme was an effective kininase in mixtures with carboxypeptidase N at physiologic concentration and digested bradykinin to the dipeptides Phe- Arg and Ser-Pro plus the pentapeptide Arg-Pro-Pro-Gly-Phe.	Dipeptides	152-162	kininogen 1	Homo sapiens	134-144
2539165-3	1989	Angiotensin-converting enzyme was an effective kininase in mixtures with carboxypeptidase N at physiologic concentration and digested bradykinin to the dipeptides Phe- Arg and Ser-Pro plus the pentapeptide Arg-Pro-Pro-Gly-Phe.	phenylalanylarginine	163-171	kininogen 1	Homo sapiens	134-144
2539165-5	1989	In serum, however, the C-terminal Arg was removed from bradykinin about five times faster than was accounted for by the activity of carboxypeptidase N. The primary substrate of ACE in serum, therefore, was des-Arg9-bradykinin and not bradykinin.	Arginine	34-37	kininogen 1	Homo sapiens	215-225
2539165-3	1989	Angiotensin-converting enzyme was an effective kininase in mixtures with carboxypeptidase N at physiologic concentration and digested bradykinin to the dipeptides Phe- Arg and Ser-Pro plus the pentapeptide Arg-Pro-Pro-Gly-Phe.	seryl-proline	176-183	kininogen 1	Homo sapiens	134-144
2539165-3	1989	Angiotensin-converting enzyme was an effective kininase in mixtures with carboxypeptidase N at physiologic concentration and digested bradykinin to the dipeptides Phe- Arg and Ser-Pro plus the pentapeptide Arg-Pro-Pro-Gly-Phe.	Arginine	168-171	kininogen 1	Homo sapiens	134-144
2539165-8	1989	Our studies indicate that the final products of bradykinin degradation were the tripeptide Arg-Pro-Pro, one mole each of Ser, Pro, Gly, and Arg, and two moles of phenylalanine.	tripeptide K-26	80-90	kininogen 1	Homo sapiens	48-58
2539165-3	1989	Angiotensin-converting enzyme was an effective kininase in mixtures with carboxypeptidase N at physiologic concentration and digested bradykinin to the dipeptides Phe- Arg and Ser-Pro plus the pentapeptide Arg-Pro-Pro-Gly-Phe.	Glycine	218-221	kininogen 1	Homo sapiens	134-144
2539165-3	1989	Angiotensin-converting enzyme was an effective kininase in mixtures with carboxypeptidase N at physiologic concentration and digested bradykinin to the dipeptides Phe- Arg and Ser-Pro plus the pentapeptide Arg-Pro-Pro-Gly-Phe.	Phenylalanine	163-166	kininogen 1	Homo sapiens	134-144
2539165-8	1989	Our studies indicate that the final products of bradykinin degradation were the tripeptide Arg-Pro-Pro, one mole each of Ser, Pro, Gly, and Arg, and two moles of phenylalanine.	arginyl-prolyl-proline	91-102	kininogen 1	Homo sapiens	48-58
2539165-4	1989	Carboxypeptidase N slowly removed the C-terminal Arg from bradykinin to yield des-Arg9-bradykinin (DBK); the latter was digested by ACE to yield the aforementioned pentapeptide and the tripeptide Ser-Pro-Phe.	Arginine	49-52	kininogen 1	Homo sapiens	58-68
2539165-8	1989	Our studies indicate that the final products of bradykinin degradation were the tripeptide Arg-Pro-Pro, one mole each of Ser, Pro, Gly, and Arg, and two moles of phenylalanine.	Serine	121-124	kininogen 1	Homo sapiens	48-58
2539165-4	1989	Carboxypeptidase N slowly removed the C-terminal Arg from bradykinin to yield des-Arg9-bradykinin (DBK); the latter was digested by ACE to yield the aforementioned pentapeptide and the tripeptide Ser-Pro-Phe.	Arginine	49-52	kininogen 1	Homo sapiens	87-97
2539165-8	1989	Our studies indicate that the final products of bradykinin degradation were the tripeptide Arg-Pro-Pro, one mole each of Ser, Pro, Gly, and Arg, and two moles of phenylalanine.	Proline	95-98	kininogen 1	Homo sapiens	48-58
2539165-5	1989	In serum, however, the C-terminal Arg was removed from bradykinin about five times faster than was accounted for by the activity of carboxypeptidase N. The primary substrate of ACE in serum, therefore, was des-Arg9-bradykinin and not bradykinin.	Arginine	34-37	kininogen 1	Homo sapiens	55-65
2539165-5	1989	In serum, however, the C-terminal Arg was removed from bradykinin about five times faster than was accounted for by the activity of carboxypeptidase N. The primary substrate of ACE in serum, therefore, was des-Arg9-bradykinin and not bradykinin.	Arginine	34-37	kininogen 1	Homo sapiens	215-225
2539165-8	1989	Our studies indicate that the final products of bradykinin degradation were the tripeptide Arg-Pro-Pro, one mole each of Ser, Pro, Gly, and Arg, and two moles of phenylalanine.	Glycine	131-134	kininogen 1	Homo sapiens	48-58
2783692-8	1989	The Ca2+ ionophore ionomycin, and two other Ca2+-mobilizing hormones, bradykinin and histamine, mimic the effects of carbachol.	Carbachol	117-126	kininogen 1	Homo sapiens	70-80
2539165-8	1989	Our studies indicate that the final products of bradykinin degradation were the tripeptide Arg-Pro-Pro, one mole each of Ser, Pro, Gly, and Arg, and two moles of phenylalanine.	Arginine	91-94	kininogen 1	Homo sapiens	48-58
2539165-8	1989	Our studies indicate that the final products of bradykinin degradation were the tripeptide Arg-Pro-Pro, one mole each of Ser, Pro, Gly, and Arg, and two moles of phenylalanine.	Phenylalanine	162-175	kininogen 1	Homo sapiens	48-58
2917978-5	1989	Experiments conducted with cells in a Ca2+-free buffer indicated that t-butyl-hydroperoxide inhibited bradykinin-stimulated Ca2+ influx from the extracellular space and had little effect on agonist-induced release of Ca2+ from internal stores.	tert-Butylhydroperoxide	70-91	kininogen 1	Homo sapiens	102-112
2640560-0	1989	Edematous response caused by [Thi5,8,D-Phe7]bradykinin, a B2 receptor antagonist, is due to mast cell degranulation.	[thi5	29-34	kininogen 1	Homo sapiens	44-54
2640560-0	1989	Edematous response caused by [Thi5,8,D-Phe7]bradykinin, a B2 receptor antagonist, is due to mast cell degranulation.	Deuterium	36-38	kininogen 1	Homo sapiens	44-54
2640560-2	1989	Pretreatment with diphenhydramine/methysergide or compound 48/80 completely suppressed the edematous response caused by [Thi5,8,D-Phe7]bradykinin, whereas bradykinin-induced hind-paw swelling was only partially inhibited by diphenhydramine and methysergide pretreatment; the residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin.	Diphenhydramine	18-33	kininogen 1	Homo sapiens	135-145
2640560-2	1989	Pretreatment with diphenhydramine/methysergide or compound 48/80 completely suppressed the edematous response caused by [Thi5,8,D-Phe7]bradykinin, whereas bradykinin-induced hind-paw swelling was only partially inhibited by diphenhydramine and methysergide pretreatment; the residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin.	Diphenhydramine	18-33	kininogen 1	Homo sapiens	155-165
2640560-2	1989	Pretreatment with diphenhydramine/methysergide or compound 48/80 completely suppressed the edematous response caused by [Thi5,8,D-Phe7]bradykinin, whereas bradykinin-induced hind-paw swelling was only partially inhibited by diphenhydramine and methysergide pretreatment; the residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin.	Diphenhydramine	18-33	kininogen 1	Homo sapiens	155-165
2640560-2	1989	Pretreatment with diphenhydramine/methysergide or compound 48/80 completely suppressed the edematous response caused by [Thi5,8,D-Phe7]bradykinin, whereas bradykinin-induced hind-paw swelling was only partially inhibited by diphenhydramine and methysergide pretreatment; the residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin.	Methysergide	34-46	kininogen 1	Homo sapiens	135-145
2640560-2	1989	Pretreatment with diphenhydramine/methysergide or compound 48/80 completely suppressed the edematous response caused by [Thi5,8,D-Phe7]bradykinin, whereas bradykinin-induced hind-paw swelling was only partially inhibited by diphenhydramine and methysergide pretreatment; the residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin.	Methysergide	34-46	kininogen 1	Homo sapiens	155-165
2640560-2	1989	Pretreatment with diphenhydramine/methysergide or compound 48/80 completely suppressed the edematous response caused by [Thi5,8,D-Phe7]bradykinin, whereas bradykinin-induced hind-paw swelling was only partially inhibited by diphenhydramine and methysergide pretreatment; the residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin.	Methysergide	34-46	kininogen 1	Homo sapiens	155-165
2640560-2	1989	Pretreatment with diphenhydramine/methysergide or compound 48/80 completely suppressed the edematous response caused by [Thi5,8,D-Phe7]bradykinin, whereas bradykinin-induced hind-paw swelling was only partially inhibited by diphenhydramine and methysergide pretreatment; the residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin.	Diphenhydramine	224-239	kininogen 1	Homo sapiens	155-165
2640560-2	1989	Pretreatment with diphenhydramine/methysergide or compound 48/80 completely suppressed the edematous response caused by [Thi5,8,D-Phe7]bradykinin, whereas bradykinin-induced hind-paw swelling was only partially inhibited by diphenhydramine and methysergide pretreatment; the residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin.	Diphenhydramine	224-239	kininogen 1	Homo sapiens	155-165
2640560-2	1989	Pretreatment with diphenhydramine/methysergide or compound 48/80 completely suppressed the edematous response caused by [Thi5,8,D-Phe7]bradykinin, whereas bradykinin-induced hind-paw swelling was only partially inhibited by diphenhydramine and methysergide pretreatment; the residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin.	Methysergide	244-256	kininogen 1	Homo sapiens	155-165
2640560-2	1989	Pretreatment with diphenhydramine/methysergide or compound 48/80 completely suppressed the edematous response caused by [Thi5,8,D-Phe7]bradykinin, whereas bradykinin-induced hind-paw swelling was only partially inhibited by diphenhydramine and methysergide pretreatment; the residual response was significantly further depressed by [Thi5,8,D-Phe7]bradykinin.	Methysergide	244-256	kininogen 1	Homo sapiens	155-165
2640560-4	1989	The mast cell degranulation caused by [Thi5,8,D-Phe7]bradykinin and bradykinin was inhibited by gangliosides but not by heparin.	Gangliosides	96-108	kininogen 1	Homo sapiens	53-63
2640560-4	1989	The mast cell degranulation caused by [Thi5,8,D-Phe7]bradykinin and bradykinin was inhibited by gangliosides but not by heparin.	Gangliosides	96-108	kininogen 1	Homo sapiens	68-78
2643439-6	1989	Exposure of human umbilical vein endothelial cells to bradykinin, thrombin or interleukin-1 resulted in negligible release of either hexosaminidase or lactate dehydrogenase (LDH), in contrast to phorbol myristate acetate, which caused a parallel, dose-dependent release of both enzymes.	Tetradecanoylphorbol Acetate	195-220	kininogen 1	Homo sapiens	54-64
2917978-0	1989	Effect of t-butyl-hydroperoxide on bradykinin-stimulated changes in cytosolic calcium in vascular endothelial cells.	tert-Butylhydroperoxide	10-31	kininogen 1	Homo sapiens	35-45
2917978-0	1989	Effect of t-butyl-hydroperoxide on bradykinin-stimulated changes in cytosolic calcium in vascular endothelial cells.	Calcium	78-85	kininogen 1	Homo sapiens	35-45
2917978-3	1989	Bradykinin-stimulated changes in (Ca2+i) were measured in cells exposed to the hydroperoxide for 0, 30, 60, 120, and 180 min.	Hydrogen Peroxide	79-92	kininogen 1	Homo sapiens	0-10
2917978-4	1989	Incubation of cells with the oxidant initially (within 30 min) diminished the peak rise in (Ca2+i) that occurs after stimulation with bradykinin.	ca2+i	92-97	kininogen 1	Homo sapiens	134-144
2785834-4	1989	rIL-1 beta, bradykinin (Bk) and arachidonic acid (AA) significantly stimulated PGE2 release from HSF incubated overnight in the presence of either <protein-id="3562">interleukin.	Dinoprostone	79-83	kininogen 1	Homo sapiens	12-22
2785834-4	1989	rIL-1 beta, bradykinin (Bk) and arachidonic acid (AA) significantly stimulated PGE2 release from HSF incubated overnight in the presence of either <protein-id="3562">interleukin.	Dinoprostone	79-83	kininogen 1	Homo sapiens	24-26
2665169-3	1989	No differences between the rates of prostacyclin production were seen between the two groups, either basally or when prostacyclin release was stimulated with thrombin or bradykinin.	Epoprostenol	117-129	kininogen 1	Homo sapiens	170-180
2543830-5	1989	The calcium content of endothelial cells calculated using 45Ca flux techniques is increased in response to bradykinin and thrombin.	Calcium	4-11	kininogen 1	Homo sapiens	107-117
2738422-0	1989	[Hydroxyproline analogues of bradykinin: its structure and function].	Hydroxyproline	1-15	kininogen 1	Homo sapiens	29-39
2543821-3	1989	It was shown that in EC the release of inositol phosphates can be stimulated by histamine, thrombin, serotonin, acetylcholine, carbachol, bradykinin, vasopressin, angiotensin II, platelet-activating factor (PAF), the thromboxane A2 mimetic, U46619, and prostaglandin E2.	Inositol Phosphates	39-58	kininogen 1	Homo sapiens	138-148
2910866-5	1989	Prior stimulation of the cells with bradykinin prevented Na+o removal from increasing [Ca2+]i and vice versa.	10-N-nonylacridinium orange	57-61	kininogen 1	Homo sapiens	36-46
2678848-7	1989	Magnesium deficiency can predispose to increased contractility of the arteries and its excess can modulate smooth muscle contractility caused by bradykinin, angiotensin II, serotonin, prostaglandins and catecholamines.	Magnesium	0-9	kininogen 1	Homo sapiens	145-155
2913861-5	1989	Protamine inhibited the hydrolysis of FA-Ala-Lys by CPN, (IC50 = 3.2 X 10(-7) M); added human serum albumin (30 mg/ml) increased the IC50 to 7 X 10(-6) M. When plasma was the source of CPN, the IC50 was 2 X 10(-6) M. Protamine more effectively inhibited the hydrolysis of bradykinin and C3a8.	furylacryloylalanyllysine	38-48	kininogen 1	Homo sapiens	272-282
2560344-2	1989	The evidence suggests that in the mammalian renal tubule bradykinin and parathyroid hormone interact with cell surface receptors to initiate the hydrolysis of PIP2 leading to the formation of I 1,4,5P3 and diacylglycerol in the distal and proximal tubule, respectively.	Phosphatidylinositol 4,5-Diphosphate	159-163	kininogen 1	Homo sapiens	57-67
2560344-2	1989	The evidence suggests that in the mammalian renal tubule bradykinin and parathyroid hormone interact with cell surface receptors to initiate the hydrolysis of PIP2 leading to the formation of I 1,4,5P3 and diacylglycerol in the distal and proximal tubule, respectively.	Diglycerides	206-220	kininogen 1	Homo sapiens	57-67
2603793-4	1989	The rank order of potency of several kinin analogues on the pain response was BK much much greater than sigma-cyclo-(Lys1-Gly6)-BK = sigma-cyclo-kallidin greater than des-Arg9-BK.	(lys1-gly6)	116-127	kininogen 1	Homo sapiens	128-130
2603793-4	1989	The rank order of potency of several kinin analogues on the pain response was BK much much greater than sigma-cyclo-(Lys1-Gly6)-BK = sigma-cyclo-kallidin greater than des-Arg9-BK.	(lys1-gly6)	116-127	kininogen 1	Homo sapiens	128-130
2603793-7	1989	The B2-receptor antagonists, D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg-TFA and D-Pro-Phe-Arg-heptylamide produced significant antagonism of the bradykinin-induced pain responses at doses which had no effect against 5-hydroxytryptamine or potassium chloride.	d-arg-arg-pro-hyp-gly-thi-ser-d-phe-thi-arg-tfa	29-76	kininogen 1	Homo sapiens	146-156
2603793-7	1989	The B2-receptor antagonists, D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg-TFA and D-Pro-Phe-Arg-heptylamide produced significant antagonism of the bradykinin-induced pain responses at doses which had no effect against 5-hydroxytryptamine or potassium chloride.	d-pro-phe-arg-heptylamide	81-106	kininogen 1	Homo sapiens	146-156
2640567-8	1989	Sequence analysis of peak A showed that the proline at the third amino acid residue of bradykinin was replaced by hydroxyproline.	Proline	44-51	kininogen 1	Homo sapiens	87-97
2640567-8	1989	Sequence analysis of peak A showed that the proline at the third amino acid residue of bradykinin was replaced by hydroxyproline.	Hydroxyproline	114-128	kininogen 1	Homo sapiens	87-97
2481386-0	1989	Bradykinin analog induce histamine release from human skin mast cells.	Histamine	25-34	kininogen 1	Homo sapiens	0-10
2513708-0	1989	Bradykinin infusion in long term postoperative parenteral nutrition improves nitrogen balance and protein synthesis.	Nitrogen	77-85	kininogen 1	Homo sapiens	0-10
2558508-2	1989	Each kininase activity was determined by measuring the hydrolysis of bradykinin in the presence of specific inhibitors of kininase I (2-mercaptomethyl-3-guanidinoethylthiopropanoic acid), kininase II (captopril) and NEP (phosphoramidon) in 8 normal subjects.	2-mercaptomethyl-3-guanidinoethylthiopropionic acid	134-185	kininogen 1	Homo sapiens	69-79
2558508-2	1989	Each kininase activity was determined by measuring the hydrolysis of bradykinin in the presence of specific inhibitors of kininase I (2-mercaptomethyl-3-guanidinoethylthiopropanoic acid), kininase II (captopril) and NEP (phosphoramidon) in 8 normal subjects.	Captopril	201-210	kininogen 1	Homo sapiens	69-79
2558508-2	1989	Each kininase activity was determined by measuring the hydrolysis of bradykinin in the presence of specific inhibitors of kininase I (2-mercaptomethyl-3-guanidinoethylthiopropanoic acid), kininase II (captopril) and NEP (phosphoramidon) in 8 normal subjects.	phosphoramidon	221-235	kininogen 1	Homo sapiens	69-79
2643280-8	1989	Captopril significantly increased plasma bradykinin, prostaglandin E2, and 6-keto-prostaglandin F1 alpha (p less than 0.05 for each).	Captopril	0-9	kininogen 1	Homo sapiens	41-51
2536234-5	1989	Bradykinin stimulates chloride ion secretion by the guinea pig and rabbit ileum, rabbit colon, rat colon and monolayers of human HCA-7 cells.	Chlorides	22-30	kininogen 1	Homo sapiens	0-10
2547571-5	1989	Both sulphur dioxide (SO2) and bradykinin cause bronchoconstriction in asthmatic patients, which is likely to be due to a neural mechanism since SO2 activates C-fibre sensory nerve endings in airways.	Sulfur Dioxide	145-148	kininogen 1	Homo sapiens	31-41
2547571-6	1989	Inhaled nedocromil sodium is effective in inhibiting both SO2- and bradykinin-induced bronchoconstriction, and furthermore reduces the sensation of dyspnoea, indicating a possible action on sensory nerve endings in airways.	Nedocromil	8-25	kininogen 1	Homo sapiens	67-77
2532136-0	1989	Effect of captopril on skin blood flow following intradermal bradykinin measured by laser Doppler flowmetry.	Captopril	10-19	kininogen 1	Homo sapiens	61-71
2532136-1	1989	The effect of captopril on skin response to intradermal injection of bradykinin was investigated by laser Doppler flowmetry (LDF) and weal and flare measurements in this randomised, double-blind, placebo-controlled, cross-over balanced study.	Captopril	14-23	kininogen 1	Homo sapiens	69-79
2532136-6	1989	Pre-treatment with captopril significantly increased LDF output following intradermal bradykinin at t1 but not at t2.	Captopril	19-28	kininogen 1	Homo sapiens	86-96
2532136-10	1989	This study showed that captopril potentiated the effects of intradermal bradykinin both with respect to blood flow changes and weal formation.	Captopril	23-32	kininogen 1	Homo sapiens	72-82
2612455-5	1989	Catalytic actions of NME-I and NME-II upon bradykinin were identical; the Gly4-Phe5 and Pro7-Phe8 bonds of bradykinin were cleaved with the final hydrolytic products for each enzyme being the tetrapeptide, Arg-Pro-Pro-Gly, the tripeptide, Phe-Ser-Pro, and the dipeptide, Phe-Arg.	gly4-phe5	74-83	kininogen 1	Homo sapiens	107-117
2612455-5	1989	Catalytic actions of NME-I and NME-II upon bradykinin were identical; the Gly4-Phe5 and Pro7-Phe8 bonds of bradykinin were cleaved with the final hydrolytic products for each enzyme being the tetrapeptide, Arg-Pro-Pro-Gly, the tripeptide, Phe-Ser-Pro, and the dipeptide, Phe-Arg.	arg-pro-pro-gly	206-221	kininogen 1	Homo sapiens	107-117
2612455-5	1989	Catalytic actions of NME-I and NME-II upon bradykinin were identical; the Gly4-Phe5 and Pro7-Phe8 bonds of bradykinin were cleaved with the final hydrolytic products for each enzyme being the tetrapeptide, Arg-Pro-Pro-Gly, the tripeptide, Phe-Ser-Pro, and the dipeptide, Phe-Arg.	tripeptide K-26	227-237	kininogen 1	Homo sapiens	107-117
2612455-5	1989	Catalytic actions of NME-I and NME-II upon bradykinin were identical; the Gly4-Phe5 and Pro7-Phe8 bonds of bradykinin were cleaved with the final hydrolytic products for each enzyme being the tetrapeptide, Arg-Pro-Pro-Gly, the tripeptide, Phe-Ser-Pro, and the dipeptide, Phe-Arg.	Phe-Ser-Pro	239-250	kininogen 1	Homo sapiens	107-117
2612455-5	1989	Catalytic actions of NME-I and NME-II upon bradykinin were identical; the Gly4-Phe5 and Pro7-Phe8 bonds of bradykinin were cleaved with the final hydrolytic products for each enzyme being the tetrapeptide, Arg-Pro-Pro-Gly, the tripeptide, Phe-Ser-Pro, and the dipeptide, Phe-Arg.	Dipeptides	260-269	kininogen 1	Homo sapiens	107-117
2612455-5	1989	Catalytic actions of NME-I and NME-II upon bradykinin were identical; the Gly4-Phe5 and Pro7-Phe8 bonds of bradykinin were cleaved with the final hydrolytic products for each enzyme being the tetrapeptide, Arg-Pro-Pro-Gly, the tripeptide, Phe-Ser-Pro, and the dipeptide, Phe-Arg.	phenylalanylarginine	271-278	kininogen 1	Homo sapiens	107-117
2544772-4	1989	Both acetylcholine and bradykinin elicited endothelium-dependent relaxation which was not inhibited by indomethacin, but by methylene blue, an inhibitor of soluble guanylate cyclase.	Indomethacin	103-115	kininogen 1	Homo sapiens	23-33
2544772-4	1989	Both acetylcholine and bradykinin elicited endothelium-dependent relaxation which was not inhibited by indomethacin, but by methylene blue, an inhibitor of soluble guanylate cyclase.	Methylene Blue	124-138	kininogen 1	Homo sapiens	23-33
2544772-6	1989	The endothelium dependent vasodilator peptides such as bradykinin contain L-arginine in their sequence.	Arginine	74-84	kininogen 1	Homo sapiens	55-65
2536466-4	1989	In these neuronal hybrids, we have found that bradykinin induces sequential elevation in the concentrations of several second messengers involved in neuronal activation, including inositol trisphosphate (6.5-fold), intracellular calcium (2.7-fold), and cyclic GMP (20.5-fold).	inositol 1,2,3-trisphosphate	180-202	kininogen 1	Homo sapiens	46-56
2536466-4	1989	In these neuronal hybrids, we have found that bradykinin induces sequential elevation in the concentrations of several second messengers involved in neuronal activation, including inositol trisphosphate (6.5-fold), intracellular calcium (2.7-fold), and cyclic GMP (20.5-fold).	Calcium	229-236	kininogen 1	Homo sapiens	46-56
2536466-6	1989	The same relative rank order of potency of inhibition of bradykinin-induced second messenger production was achieved in the inositol trisphosphate, calcium, and cyclic GMP assay systems, suggesting strongly that all three messenger systems are being activated by the same bradykinin receptor.	inositol 1,2,3-trisphosphate	124-146	kininogen 1	Homo sapiens	57-67
2536466-6	1989	The same relative rank order of potency of inhibition of bradykinin-induced second messenger production was achieved in the inositol trisphosphate, calcium, and cyclic GMP assay systems, suggesting strongly that all three messenger systems are being activated by the same bradykinin receptor.	Calcium	148-155	kininogen 1	Homo sapiens	57-67
2536466-7	1989	The most potent antagonist was D-Arg0-Hyp3-Thi5,8-D-Phe7-bradykinin, which inhibited in a competitive manner, with pA2 values, upon Schild plot analysis, in the nanomolar range.	d-arg0-hyp3-thi5	31-47	kininogen 1	Homo sapiens	57-67
2508121-5	1989	Bradykinin, thrombin, platelet activating factor, and serum were found to be effective stimulators of PG production by HTM cells, whereas calcium ionophore produced only a minor effect.	pg	102-104	kininogen 1	Homo sapiens	0-10
2538844-0	1989	Bradykinin and bradykinin antagonists effects on endothelial cell phosphoinositide metabolism; implications for septic shock.	Phosphatidylinositols	66-82	kininogen 1	Homo sapiens	0-10
2538844-0	1989	Bradykinin and bradykinin antagonists effects on endothelial cell phosphoinositide metabolism; implications for septic shock.	Phosphatidylinositols	66-82	kininogen 1	Homo sapiens	15-25
2629164-10	1989	The dose-dependence of morphological changes was compared and contrasted to the dose-dependent effect of phorbol esters on bradykinin-stimulated phosphoinositide turnover.	Phorbol Esters	105-119	kininogen 1	Homo sapiens	123-133
2629164-10	1989	The dose-dependence of morphological changes was compared and contrasted to the dose-dependent effect of phorbol esters on bradykinin-stimulated phosphoinositide turnover.	Phosphatidylinositols	145-161	kininogen 1	Homo sapiens	123-133
2711742-5	1989	The cholinergic neurones are shown to participate in producing small-intestinal responses to 5-hydroxytryptamine, histamine, bradykinin, the responses being, for this reason, dependent on the level of catecholamines, stimulating excitatory beta-adrenoreceptors.	Catecholamines	201-215	kininogen 1	Homo sapiens	125-135
3214176-7	1988	It also hydrolyzes biologically active peptides such as bradykinin (Km = 6 microM, kcat = 43 min-1), Arg6-Met5-enkephalin (Km = 103 microM, kcat = 438 min-1), and Lys6-Met5-enkephalin (Km = 848 microM, kcat = 449 min-1).	lys6-met5-enkephalin	163-183	kininogen 1	Homo sapiens	56-66
3271542-0	1988	High-field NMR and circular dichroism solvent-dependent conformational studies of the bradykinin C-terminal tetrapeptide Ser-Pro-Phe-Arg.	ser-pro-phe-arg	121-136	kininogen 1	Homo sapiens	86-96
2464345-0	1989	Induction of histamine release from human skin mast cells by bradykinin analogs.	Histamine	13-22	kininogen 1	Homo sapiens	61-71
3143746-6	1988	Increased release of 15-HETE in the presence of elevated glucose in response to A23187, bradykinin, and thrombin was confirmed by RIA.	15-Hete	21-28	kininogen 1	Homo sapiens	88-98
2464345-2	1989	We examined the ability of bradykinin, lysylbradykinin and a series of kinin analogs to cause histamine release from human basophils, human lung mast cells and human skin mast cells.	Histamine	94-103	kininogen 1	Homo sapiens	27-37
2464345-4	1989	Lysylbradykinin was also without effect on basophils and lung mast cells, but was a weak secretagogue for human skin mast cells, inducing 5.5 +/- 3% (mean +/- SD) of total cellular histamine release at a concentration of 10(-5) M. Similarly, when sixteen recently developed bradykinin antagonists were examined, these compounds had no effect on basophils or lung mast cells but all sixteen induced dose-dependent histamine release from skin mast cells.	Histamine	181-190	kininogen 1	Homo sapiens	5-15
2464345-4	1989	Lysylbradykinin was also without effect on basophils and lung mast cells, but was a weak secretagogue for human skin mast cells, inducing 5.5 +/- 3% (mean +/- SD) of total cellular histamine release at a concentration of 10(-5) M. Similarly, when sixteen recently developed bradykinin antagonists were examined, these compounds had no effect on basophils or lung mast cells but all sixteen induced dose-dependent histamine release from skin mast cells.	Histamine	413-422	kininogen 1	Homo sapiens	5-15
2464345-6	1989	Although preincubation of cells with 10(-3) M bradykinin or des(Arg9) bradykinin significantly inhibited antagonist-induced histamine release, the requirement for such high concentrations of these peptides to cause inhibition suggested that histamine release is not mediated by either B1 or B2 kinin receptors.	Histamine	124-133	kininogen 1	Homo sapiens	46-56
2464345-6	1989	Although preincubation of cells with 10(-3) M bradykinin or des(Arg9) bradykinin significantly inhibited antagonist-induced histamine release, the requirement for such high concentrations of these peptides to cause inhibition suggested that histamine release is not mediated by either B1 or B2 kinin receptors.	Histamine	124-133	kininogen 1	Homo sapiens	70-80
2464345-6	1989	Although preincubation of cells with 10(-3) M bradykinin or des(Arg9) bradykinin significantly inhibited antagonist-induced histamine release, the requirement for such high concentrations of these peptides to cause inhibition suggested that histamine release is not mediated by either B1 or B2 kinin receptors.	Histamine	241-250	kininogen 1	Homo sapiens	46-56
2464345-6	1989	Although preincubation of cells with 10(-3) M bradykinin or des(Arg9) bradykinin significantly inhibited antagonist-induced histamine release, the requirement for such high concentrations of these peptides to cause inhibition suggested that histamine release is not mediated by either B1 or B2 kinin receptors.	Histamine	241-250	kininogen 1	Homo sapiens	70-80
2464345-8	1989	Replacement of proline7 in the bradykinin sequence with D-phenylalanine is the essential change used to convert kinin analogs into antagonists, and 10(-5) M [DPhe7]-bradykinin induced 8-10% histamine release.	proline7	15-23	kininogen 1	Homo sapiens	31-41
2464345-8	1989	Replacement of proline7 in the bradykinin sequence with D-phenylalanine is the essential change used to convert kinin analogs into antagonists, and 10(-5) M [DPhe7]-bradykinin induced 8-10% histamine release.	proline7	15-23	kininogen 1	Homo sapiens	165-175
2464345-8	1989	Replacement of proline7 in the bradykinin sequence with D-phenylalanine is the essential change used to convert kinin analogs into antagonists, and 10(-5) M [DPhe7]-bradykinin induced 8-10% histamine release.	D-phenylalanine	56-71	kininogen 1	Homo sapiens	31-41
2464345-8	1989	Replacement of proline7 in the bradykinin sequence with D-phenylalanine is the essential change used to convert kinin analogs into antagonists, and 10(-5) M [DPhe7]-bradykinin induced 8-10% histamine release.	D-phenylalanine	56-71	kininogen 1	Homo sapiens	165-175
2464345-8	1989	Replacement of proline7 in the bradykinin sequence with D-phenylalanine is the essential change used to convert kinin analogs into antagonists, and 10(-5) M [DPhe7]-bradykinin induced 8-10% histamine release.	dphe7	158-163	kininogen 1	Homo sapiens	31-41
2464345-8	1989	Replacement of proline7 in the bradykinin sequence with D-phenylalanine is the essential change used to convert kinin analogs into antagonists, and 10(-5) M [DPhe7]-bradykinin induced 8-10% histamine release.	dphe7	158-163	kininogen 1	Homo sapiens	165-175
2464345-8	1989	Replacement of proline7 in the bradykinin sequence with D-phenylalanine is the essential change used to convert kinin analogs into antagonists, and 10(-5) M [DPhe7]-bradykinin induced 8-10% histamine release.	Histamine	190-199	kininogen 1	Homo sapiens	31-41
2464345-8	1989	Replacement of proline7 in the bradykinin sequence with D-phenylalanine is the essential change used to convert kinin analogs into antagonists, and 10(-5) M [DPhe7]-bradykinin induced 8-10% histamine release.	Histamine	190-199	kininogen 1	Homo sapiens	165-175
3143746-6	1988	Increased release of 15-HETE in the presence of elevated glucose in response to A23187, bradykinin, and thrombin was confirmed by RIA.	Glucose	57-64	kininogen 1	Homo sapiens	88-98
2852237-2	1988	In a dose of 5 micrograms/min enalaprilat inhibits arteriolar vasoconstriction in response to angiotensin I (Ang I) and enhances vasodilation in response to bradykinin.	Enalaprilat	30-41	kininogen 1	Homo sapiens	157-167
2464345-9	1989	Other analogs, devoid of antagonist activity, however, such as [DPhe6]-bradykinin and [LPhe7]-bradykinin were able to induce equivalent levels of histamine release.	Histamine	146-155	kininogen 1	Homo sapiens	71-81
2464345-9	1989	Other analogs, devoid of antagonist activity, however, such as [DPhe6]-bradykinin and [LPhe7]-bradykinin were able to induce equivalent levels of histamine release.	Histamine	146-155	kininogen 1	Homo sapiens	94-104
3196332-4	1988	The isolation of [Hyp3]-BK and [Hyp3]-Lys-BK suggests that a novel kininogen containing hydroxyproline in the third position of the bradykinin sequence in human plasma protein, possibly undergone post-translational modifications.	Hydroxyproline	88-102	kininogen 1	Homo sapiens	42-44
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	Histamine	22-31	kininogen 1	Homo sapiens	111-121
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	Histamine	22-31	kininogen 1	Homo sapiens	134-144
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	Histamine	22-31	kininogen 1	Homo sapiens	134-144
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	dtrp6	104-109	kininogen 1	Homo sapiens	111-121
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	dtrp7	127-132	kininogen 1	Homo sapiens	134-144
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	dtrp7	127-132	kininogen 1	Homo sapiens	134-144
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	Histamine	172-181	kininogen 1	Homo sapiens	111-121
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	Histamine	172-181	kininogen 1	Homo sapiens	134-144
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	Histamine	172-181	kininogen 1	Homo sapiens	134-144
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	Histamine	172-181	kininogen 1	Homo sapiens	111-121
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	Histamine	172-181	kininogen 1	Homo sapiens	134-144
2464345-10	1989	The ability to induce histamine release appears to be related, at least in part, to aromaticity, since [DTrp6]-bradykinin and [DTrp7]-bradykinin induced greater amounts of histamine release than equivalent [DPhe]-analogs, causing approximately 20% histamine release at 10(-5) M. By contrast, [DAla7]-bradykinin was an ineffective stimulus.	Histamine	172-181	kininogen 1	Homo sapiens	134-144
3196332-4	1988	The isolation of [Hyp3]-BK and [Hyp3]-Lys-BK suggests that a novel kininogen containing hydroxyproline in the third position of the bradykinin sequence in human plasma protein, possibly undergone post-translational modifications.	Hydroxyproline	88-102	kininogen 1	Homo sapiens	132-142
3263854-0	1988	Defective formation of inositol 1,4,5-trisphosphate in bradykinin-stimulated fibroblasts from progressive systemic sclerotic patients.	Inositol 1,4,5-Trisphosphate	23-51	kininogen 1	Homo sapiens	55-65
3263854-1	1988	The effect of bradykinin on inositol 1,4,5-trisphosphate (1,4,5-IP3) formation was investigated in fibroblasts from normal subjects and patients with progressive systemic sclerosis (PSS).	Inositol 1,4,5-Trisphosphate	28-56	kininogen 1	Homo sapiens	14-24
3263854-1	1988	The effect of bradykinin on inositol 1,4,5-trisphosphate (1,4,5-IP3) formation was investigated in fibroblasts from normal subjects and patients with progressive systemic sclerosis (PSS).	Inositol 1,4,5-Trisphosphate	58-67	kininogen 1	Homo sapiens	14-24
3263854-2	1988	1,4,5-IP3 in both PSS and normal fibroblasts reached peak levels at 15 sec after stimulation with bradykinin, though this level was significantly lower in PSS fibroblasts than in normal cells.	Inositol 1,4,5-Trisphosphate	0-9	kininogen 1	Homo sapiens	98-108
3263854-4	1988	These findings suggest that bradykinin stimulates phosphoinositide hydrolysis by phospholipase C in human fibroblasts via IAP-insensitive pathway, and that PSS fibroblasts appear to be defective in the pathway.	Phosphatidylinositols	50-66	kininogen 1	Homo sapiens	28-38
3182782-5	1988	Sequence analysis of fraction I showed that the proline at the third amino acid residue of bradykinin was replaced by hydroxyproline.	Proline	48-55	kininogen 1	Homo sapiens	91-101
3182782-5	1988	Sequence analysis of fraction I showed that the proline at the third amino acid residue of bradykinin was replaced by hydroxyproline.	Hydroxyproline	118-132	kininogen 1	Homo sapiens	91-101
3211715-0	1988	Desensitization of the bradykinin-induced rise in intracellular free calcium in cultured endothelial cells.	Calcium	69-76	kininogen 1	Homo sapiens	23-33
2460446-5	1988	[35S]Methionine-labeled HUVEC in culture synthesize a 120-kDa protein immunoisolated using an anti-kininogen antibody, and a 3500-nucleotide message for human HMWK was detected by Northern blot in RNA extracted from HUVEC.	Sulfur-35	1-4	kininogen 1	Homo sapiens	159-163
2460446-5	1988	[35S]Methionine-labeled HUVEC in culture synthesize a 120-kDa protein immunoisolated using an anti-kininogen antibody, and a 3500-nucleotide message for human HMWK was detected by Northern blot in RNA extracted from HUVEC.	Methionine	5-15	kininogen 1	Homo sapiens	159-163
2460446-7	1988	125I-HMWK specifically binds to HUVEC in a reaction requiring Zn2+.	Zinc	62-66	kininogen 1	Homo sapiens	5-9
2460446-13	1988	Both added and cell-bound 125I-HMWK migrate at 120 kDa on sodium dodecyl sulfate gel electrophoresis, suggesting that the protein remains uncleaved upon binding to the HUVEC surface.	Sodium Dodecyl Sulfate	58-80	kininogen 1	Homo sapiens	31-35
2460446-15	1988	By synthesizing and localizing HMWK to the cell surface, endothelial cells may contribute to the activation of plasma"s contact serine zymogens and regulation of tissue cysteine proteases.	Serine	128-134	kininogen 1	Homo sapiens	31-35
2853304-6	1988	When cells were pulsed with 32Pi for 60 min and stimulated by veratridine plus scorpion venom for an additional 30 min, uptake of 32Pi into phosphatidylinositol was reduced; stimulating cells with bradykinin, a receptor agonist which activates the inositol cycle, promoted a 3.8 fold increase.	32pi	28-32	kininogen 1	Homo sapiens	197-207
2853304-6	1988	When cells were pulsed with 32Pi for 60 min and stimulated by veratridine plus scorpion venom for an additional 30 min, uptake of 32Pi into phosphatidylinositol was reduced; stimulating cells with bradykinin, a receptor agonist which activates the inositol cycle, promoted a 3.8 fold increase.	Veratridine	62-73	kininogen 1	Homo sapiens	197-207
2853304-6	1988	When cells were pulsed with 32Pi for 60 min and stimulated by veratridine plus scorpion venom for an additional 30 min, uptake of 32Pi into phosphatidylinositol was reduced; stimulating cells with bradykinin, a receptor agonist which activates the inositol cycle, promoted a 3.8 fold increase.	32pi	130-134	kininogen 1	Homo sapiens	197-207
2853304-6	1988	When cells were pulsed with 32Pi for 60 min and stimulated by veratridine plus scorpion venom for an additional 30 min, uptake of 32Pi into phosphatidylinositol was reduced; stimulating cells with bradykinin, a receptor agonist which activates the inositol cycle, promoted a 3.8 fold increase.	Phosphatidylinositols	140-160	kininogen 1	Homo sapiens	197-207
2853304-7	1988	Polyphosphoinositide turnover was not affected by Na+-channel activation, but was stimulated by bradykinin.	Phosphatidylinositol Phosphates	0-20	kininogen 1	Homo sapiens	96-106
2851881-2	1988	Because nedocromil has previously been shown to inhibit reflex bronchoconstriction provoked by inhaled sulphur dioxide and inhaled bradykinin, the results suggest that inhaled capsaicin acts on different nerve fibres.	Nedocromil	8-18	kininogen 1	Homo sapiens	131-141
2851881-2	1988	Because nedocromil has previously been shown to inhibit reflex bronchoconstriction provoked by inhaled sulphur dioxide and inhaled bradykinin, the results suggest that inhaled capsaicin acts on different nerve fibres.	Capsaicin	176-185	kininogen 1	Homo sapiens	131-141
3211715-5	1988	The initial peak of [Cai2+] after stimulation with bradykinin or ATP was not affected by removal of extracellular calcium ions, indicating mobilization of Ca2+ from intracellular stores.	cai2+	21-26	kininogen 1	Homo sapiens	51-61
3211715-2	1988	Bradykinin (10 nmol/l) evoked a rise in the intracellular free calcium concentration [( Cai2+]), measured with the fluorescent probe indo-1, from 137 +/- 30 (+/- SEM) to 623 +/- 101 nmol/l.	Calcium	63-70	kininogen 1	Homo sapiens	0-10
3211715-2	1988	Bradykinin (10 nmol/l) evoked a rise in the intracellular free calcium concentration [( Cai2+]), measured with the fluorescent probe indo-1, from 137 +/- 30 (+/- SEM) to 623 +/- 101 nmol/l.	cai2+	88-93	kininogen 1	Homo sapiens	0-10
3211715-2	1988	Bradykinin (10 nmol/l) evoked a rise in the intracellular free calcium concentration [( Cai2+]), measured with the fluorescent probe indo-1, from 137 +/- 30 (+/- SEM) to 623 +/- 101 nmol/l.	Indomethacin	133-137	kininogen 1	Homo sapiens	0-10
3211715-4	1988	However, purinergic stimulation with ATP (10 mumol/l) elicited the same increase in [Cai2+] in endothelial cells desensitized to bradykinin as in cells never exposed to bradykinin.	Adenosine Triphosphate	37-40	kininogen 1	Homo sapiens	129-139
3211715-4	1988	However, purinergic stimulation with ATP (10 mumol/l) elicited the same increase in [Cai2+] in endothelial cells desensitized to bradykinin as in cells never exposed to bradykinin.	Adenosine Triphosphate	37-40	kininogen 1	Homo sapiens	169-179
3211715-4	1988	However, purinergic stimulation with ATP (10 mumol/l) elicited the same increase in [Cai2+] in endothelial cells desensitized to bradykinin as in cells never exposed to bradykinin.	cai2+	85-90	kininogen 1	Homo sapiens	129-139
3185968-0	1988	Bradykinin-induced stimulation of afferent fibres is mediated through protein kinase C. In an in vitro preparation of the neonatal spinal cord with the tail attached, brief administration of bradykinin or capsaicin in the tail superfusate containing a normal calcium concentration, activated peripheral fibres and produced a depolarization recorded at a spinal ventral root (L3-L5).	Capsaicin	205-214	kininogen 1	Homo sapiens	0-10
3139453-5	1988	Hydroxyproline in hydroxyprolyl3-bradykinin was assigned as trans-4-hydroxyproline by comparison of the retention times on reversed-phase HPLC with isomers of hydroxyproline after derivatization with 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole chloride.	Hydroxyproline	0-14	kininogen 1	Homo sapiens	33-43
3139453-5	1988	Hydroxyproline in hydroxyprolyl3-bradykinin was assigned as trans-4-hydroxyproline by comparison of the retention times on reversed-phase HPLC with isomers of hydroxyproline after derivatization with 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole chloride.	Hydroxyproline	60-82	kininogen 1	Homo sapiens	33-43
3139453-5	1988	Hydroxyproline in hydroxyprolyl3-bradykinin was assigned as trans-4-hydroxyproline by comparison of the retention times on reversed-phase HPLC with isomers of hydroxyproline after derivatization with 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole chloride.	Hydroxyproline	68-82	kininogen 1	Homo sapiens	33-43
3139453-5	1988	Hydroxyproline in hydroxyprolyl3-bradykinin was assigned as trans-4-hydroxyproline by comparison of the retention times on reversed-phase HPLC with isomers of hydroxyproline after derivatization with 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole chloride.	7-chloro-4-nitrobenzo-2-oxa-1,3-diazole chloride	200-248	kininogen 1	Homo sapiens	33-43
2464382-3	1988	In contrast, eledoisin, physalaemin, neurokinin A, neurokinin B, calcitonin gene-related peptide (CGRP), neurotensin, bradykinin and Lys-bradykinin induced negligible histamine release.	Histamine	167-176	kininogen 1	Homo sapiens	137-147
2843748-0	1988	Mechanism of enhanced sensitivity to bradykinin in pertussis toxin-treated fibroblasts: toxin increases bradykinin-stimulated prostaglandin formation.	Prostaglandins	126-139	kininogen 1	Homo sapiens	37-47
2843748-0	1988	Mechanism of enhanced sensitivity to bradykinin in pertussis toxin-treated fibroblasts: toxin increases bradykinin-stimulated prostaglandin formation.	Prostaglandins	126-139	kininogen 1	Homo sapiens	104-114
2843748-4	1988	Bradykinin increased prostaglandin accumulation to a greater extent in toxin-treated than in control fibroblasts.	Prostaglandins	21-34	kininogen 1	Homo sapiens	0-10
2843748-5	1988	Agents such as cholera toxin, which elevated cAMP, also increased bradykinin-induced prostaglandin production.	Cyclic AMP	45-49	kininogen 1	Homo sapiens	66-76
2843748-5	1988	Agents such as cholera toxin, which elevated cAMP, also increased bradykinin-induced prostaglandin production.	Prostaglandins	85-98	kininogen 1	Homo sapiens	66-76
2843748-6	1988	These data are consistent with the hypothesis that the enhanced sensitivity to bradykinin after pertussis toxin treatment results from modification of Gi alpha and increased cAMP, leading to enhanced formation of prostaglandins in response to bradykinin.	Cyclic AMP	174-178	kininogen 1	Homo sapiens	79-89
2843748-6	1988	These data are consistent with the hypothesis that the enhanced sensitivity to bradykinin after pertussis toxin treatment results from modification of Gi alpha and increased cAMP, leading to enhanced formation of prostaglandins in response to bradykinin.	Cyclic AMP	174-178	kininogen 1	Homo sapiens	243-253
2843748-6	1988	These data are consistent with the hypothesis that the enhanced sensitivity to bradykinin after pertussis toxin treatment results from modification of Gi alpha and increased cAMP, leading to enhanced formation of prostaglandins in response to bradykinin.	Prostaglandins	213-227	kininogen 1	Homo sapiens	79-89
2843748-6	1988	These data are consistent with the hypothesis that the enhanced sensitivity to bradykinin after pertussis toxin treatment results from modification of Gi alpha and increased cAMP, leading to enhanced formation of prostaglandins in response to bradykinin.	Prostaglandins	213-227	kininogen 1	Homo sapiens	243-253
2901097-4	1988	In contrast to IL-1, bradykinin stimulation of prostaglandin E2 synthesis is rapid; its effect is maximal by 5 min.	Dinoprostone	47-63	kininogen 1	Homo sapiens	21-31
2901097-5	1988	In cells that had been pretreated with IL-1 for 24 hr, prostaglandin E2 synthesis in response to bradykinin was amplified more than 10-fold.	Dinoprostone	55-71	kininogen 1	Homo sapiens	97-107
2901097-9	1988	It also enhanced bradykinin-stimulated GTPase activity, suggesting possible induction of the GTP-binding regulatory protein coupled to the bradykinin receptor.	Guanosine Triphosphate	39-42	kininogen 1	Homo sapiens	17-27
2901097-10	1988	Thus, IL-1 enhanced receptor-mediated release of prostaglandin E2 in response to bradykinin, bombesin, and thrombin by increasing the cellular levels of phospholipase A2, cyclooxygenase, and GTP-binding regulatory protein(s).	Dinoprostone	49-65	kininogen 1	Homo sapiens	81-91
3061568-9	1988	These data are compatible with the suggestion that the prostaglandin products mediating BK and NE hyperalgesia differ, BK hyperalgesia being mediated by PGE2 and NE hyperalgesia by PGI2.	Prostaglandins	55-68	kininogen 1	Homo sapiens	88-90
3395372-3	1988	Purified microvessels contained a membrane-bound carboxypeptidase which hydrolyzed the C-terminal Phe-Arg bond of both kallidin and bradykinin.	Phenylalanine	98-101	kininogen 1	Homo sapiens	132-142
3395372-3	1988	Purified microvessels contained a membrane-bound carboxypeptidase which hydrolyzed the C-terminal Phe-Arg bond of both kallidin and bradykinin.	Arginine	102-105	kininogen 1	Homo sapiens	132-142
3137235-3	1988	We now report that histamine, bradykinin, and the calcium ionophore A23187 exhibit the same fatty acid specificity as does thrombin.	Fatty Acids	92-102	kininogen 1	Homo sapiens	30-40
3137235-6	1988	These results suggest that histamine, bradykinin, and A23187 activate a common calcium-dependent phospholipase A2.	Calcium	79-86	kininogen 1	Homo sapiens	38-48
3228488-3	1988	Two kinds of kinin, bradykinin and Met-Lys-bradykinin, were found to be released from L-kininogen by the synergistic action of PMN elastase and plasma kallikrein.	l-kininogen	86-97	kininogen 1	Homo sapiens	20-30
3228488-3	1988	Two kinds of kinin, bradykinin and Met-Lys-bradykinin, were found to be released from L-kininogen by the synergistic action of PMN elastase and plasma kallikrein.	l-kininogen	86-97	kininogen 1	Homo sapiens	43-53
3185968-0	1988	Bradykinin-induced stimulation of afferent fibres is mediated through protein kinase C. In an in vitro preparation of the neonatal spinal cord with the tail attached, brief administration of bradykinin or capsaicin in the tail superfusate containing a normal calcium concentration, activated peripheral fibres and produced a depolarization recorded at a spinal ventral root (L3-L5).	Calcium	259-266	kininogen 1	Homo sapiens	0-10
3185968-5	1988	Inactivation of protein kinase C with the inhibitor staurosporine (10-100 nM) attenuated the effect of bradykinin and PDBu but not that of capsaicin.	Staurosporine	52-65	kininogen 1	Homo sapiens	103-113
3185968-7	1988	These data suggest that a phorbol ester and bradykinin stimulate capsaicin-sensitive C-fibres by a mechanism which involves the activation of protein kinase C.	Capsaicin	65-74	kininogen 1	Homo sapiens	44-54
3260776-7	1988	Our data provide convincing evidence that under basal, BK and ATP-stimulated conditions 1. endothelial cells release nitric oxide as free radical, 2.	Nitric Oxide	117-129	kininogen 1	Homo sapiens	55-57
2456360-6	1988	A similar sequence of cleavage of plasma HMWK occurs when the soluble activator dextran sulfate is used to stimulate the system.	Dextran Sulfate	80-95	kininogen 1	Homo sapiens	41-45
2906145-3	1988	The neural peptide bradykinin stimulates a rapid production of identified inositol phosphate isomers and an intracellular Ca2+ discharge followed by a persistent plasma membrane influx.	Inositol Phosphates	74-92	kininogen 1	Homo sapiens	19-29
3391275-1	1988	We recently demonstrated that diacylglycerol induced arachidonate release and prostaglandin E2 synthesis in 3T3 fibroblasts, and greatly augmented prostaglandin E2 synthesis in response to submaximal and maximal concentrations of bradykinin.	Diglycerides	30-44	kininogen 1	Homo sapiens	230-240
3391275-1	1988	We recently demonstrated that diacylglycerol induced arachidonate release and prostaglandin E2 synthesis in 3T3 fibroblasts, and greatly augmented prostaglandin E2 synthesis in response to submaximal and maximal concentrations of bradykinin.	Dinoprostone	147-163	kininogen 1	Homo sapiens	230-240
3133127-0	1988	Characteristics of bradykinin and TPA increases in the PGE2 levels of human urothelial cells.	Dinoprostone	55-59	kininogen 1	Homo sapiens	19-29
3133127-6	1988	In contrast to TPA, the bradykinin-increased PGE2 levels were maximal at 5 min (the earliest time-point assessed) and were not inhibited by cycloheximide.	Dinoprostone	45-49	kininogen 1	Homo sapiens	24-34
3133127-7	1988	Increases in PGE2 levels by both TPA and bradykinin required calcium.	Dinoprostone	13-17	kininogen 1	Homo sapiens	41-51
3133127-7	1988	Increases in PGE2 levels by both TPA and bradykinin required calcium.	Calcium	61-68	kininogen 1	Homo sapiens	41-51
3133127-9	1988	Combination of TPA with bradykinin produced at least an additive effect on PGE2 levels.	Dinoprostone	75-79	kininogen 1	Homo sapiens	24-34
3133127-11	1988	Bradykinin and TPA appear to increase PGE2 levels by enhancing arachidonic acid availability through separate phospholipase pathways.	Dinoprostone	38-42	kininogen 1	Homo sapiens	0-10
3133127-11	1988	Bradykinin and TPA appear to increase PGE2 levels by enhancing arachidonic acid availability through separate phospholipase pathways.	Arachidonic Acid	63-79	kininogen 1	Homo sapiens	0-10
3133127-12	1988	Thus, human urothelial cells exhibit similar, but yet distinct profiles for prostaglandin stimulation by TPA and bradykinin.	Prostaglandins	76-89	kininogen 1	Homo sapiens	113-123
3131684-4	1988	Release of NO from the endothelial cells induced by bradykinin and the calcium ionophore A23187 was reversibly enhanced by infusions of L-arginine and L-citrulline, but not D-arginine or other close structural analogues.	Arginine	136-146	kininogen 1	Homo sapiens	52-62
3131684-4	1988	Release of NO from the endothelial cells induced by bradykinin and the calcium ionophore A23187 was reversibly enhanced by infusions of L-arginine and L-citrulline, but not D-arginine or other close structural analogues.	Citrulline	151-163	kininogen 1	Homo sapiens	52-62
3138977-9	1988	Treatment of the cells with 12-O-tetradecanoylphorbol 13-acetate completely abolishes the response to EGF and to sub-optimal doses of bradykinin, suggesting a negative-feedback function of protein kinase C. Pretreatment of the cells with pertussis toxin has no effect on inositol phosphate formation induced by either EGF or bradykinin.	Tetradecanoylphorbol Acetate	28-64	kininogen 1	Homo sapiens	134-144
3138977-9	1988	Treatment of the cells with 12-O-tetradecanoylphorbol 13-acetate completely abolishes the response to EGF and to sub-optimal doses of bradykinin, suggesting a negative-feedback function of protein kinase C. Pretreatment of the cells with pertussis toxin has no effect on inositol phosphate formation induced by either EGF or bradykinin.	Tetradecanoylphorbol Acetate	28-64	kininogen 1	Homo sapiens	325-335
3138977-9	1988	Treatment of the cells with 12-O-tetradecanoylphorbol 13-acetate completely abolishes the response to EGF and to sub-optimal doses of bradykinin, suggesting a negative-feedback function of protein kinase C. Pretreatment of the cells with pertussis toxin has no effect on inositol phosphate formation induced by either EGF or bradykinin.	Inositol Phosphates	271-289	kininogen 1	Homo sapiens	134-144
2837913-3	1988	In contrast, BK produced a sustained vasodilator response after treatment with captopril.	Captopril	79-88	kininogen 1	Homo sapiens	13-15
2837913-8	1988	The FITC-D L/P was markedly increased in the groups of animals in which the tracer was injected intravenously at the start or 8 min after the start of the prolonged BK infusion.	Fluorescein-5-isothiocyanate	4-8	kininogen 1	Homo sapiens	165-167
2837913-10	1988	Pretreatment with both captopril and propranolol dramatically potentiated the magnitude of the increase in protein clearance, the filtration rate, and edema formation produced by BK but failed to affect the duration of the transient increase in vascular permeability.	Captopril	23-32	kininogen 1	Homo sapiens	179-181
2837913-10	1988	Pretreatment with both captopril and propranolol dramatically potentiated the magnitude of the increase in protein clearance, the filtration rate, and edema formation produced by BK but failed to affect the duration of the transient increase in vascular permeability.	Propranolol	37-48	kininogen 1	Homo sapiens	179-181
3377072-5	1988	Bradykinin and 9,11-dideoxy-9 alpha, 11 alpha-epoxymethanoprostaglandin F2 alpha (a stable thromboxane agonist) caused a dose-related increase in perfusion pressure.	Thromboxanes	91-102	kininogen 1	Homo sapiens	0-10
3377072-7	1988	Bradykinin increased thromboxane B2 production by 62.0%.	Thromboxane B2	21-35	kininogen 1	Homo sapiens	0-10
3377072-11	1988	SQ29548, a specific thromboxane antagonist, caused a 61.6% inhibition of the bradykinin pressor response but did not change angiotensin II responsiveness.	SQ 29548	0-7	kininogen 1	Homo sapiens	77-87
3377072-11	1988	SQ29548, a specific thromboxane antagonist, caused a 61.6% inhibition of the bradykinin pressor response but did not change angiotensin II responsiveness.	Thromboxanes	20-31	kininogen 1	Homo sapiens	77-87
3377072-12	1988	The data demonstrate that thromboxane is an important mediator of bradykinin-induced vasoconstriction in the isolated perfused human placenta.	Thromboxanes	26-37	kininogen 1	Homo sapiens	66-76
2849459-3	1988	After ultra centrifugation, the enzyme was purified by gel filtration on Sepharose 6B CL and ion exchange chromatography followed by affinity chromatography of EDTA-inhibited enzyme on bradykinin-Sepharose.	Edetic Acid	160-164	kininogen 1	Homo sapiens	185-195
3216463-0	1988	[Fentanyl reduces the inhibition of dorsal horn lamina V type neuronal activity induced by bradykinin injection into the femoral artery contralateral to the recording site].	Fentanyl	1-9	kininogen 1	Homo sapiens	91-101
3366244-0	1988	Isolation and identification of hydroxyproline analogues of bradykinin in human urine.	Hydroxyproline	32-46	kininogen 1	Homo sapiens	60-70
3366244-1	1988	Hydroxyproline (Hyp) analogues of bradykinin and lysyl-bradykinin, in which the third residue of bradykinin, proline, is replaced by hydroxyproline, were isolated from human urine.	Hydroxyproline	0-14	kininogen 1	Homo sapiens	34-44
3366244-1	1988	Hydroxyproline (Hyp) analogues of bradykinin and lysyl-bradykinin, in which the third residue of bradykinin, proline, is replaced by hydroxyproline, were isolated from human urine.	Hydroxyproline	0-14	kininogen 1	Homo sapiens	55-65
3366244-1	1988	Hydroxyproline (Hyp) analogues of bradykinin and lysyl-bradykinin, in which the third residue of bradykinin, proline, is replaced by hydroxyproline, were isolated from human urine.	Hydroxyproline	0-14	kininogen 1	Homo sapiens	55-65
3366244-1	1988	Hydroxyproline (Hyp) analogues of bradykinin and lysyl-bradykinin, in which the third residue of bradykinin, proline, is replaced by hydroxyproline, were isolated from human urine.	Proline	7-14	kininogen 1	Homo sapiens	34-44
3366244-1	1988	Hydroxyproline (Hyp) analogues of bradykinin and lysyl-bradykinin, in which the third residue of bradykinin, proline, is replaced by hydroxyproline, were isolated from human urine.	Proline	7-14	kininogen 1	Homo sapiens	55-65
3366244-1	1988	Hydroxyproline (Hyp) analogues of bradykinin and lysyl-bradykinin, in which the third residue of bradykinin, proline, is replaced by hydroxyproline, were isolated from human urine.	Proline	7-14	kininogen 1	Homo sapiens	55-65
2451949-4	1988	Digestion of purified HMWK with plasma kallikrein yielded, on reduced sodium dodecyl sulfate gels, two LC forms, at 62 and 49 kd, respectively.	Sodium Dodecyl Sulfate	70-92	kininogen 1	Homo sapiens	22-26
3260776-7	1988	Our data provide convincing evidence that under basal, BK and ATP-stimulated conditions 1. endothelial cells release nitric oxide as free radical, 2.	Free Radicals	133-145	kininogen 1	Homo sapiens	55-57
2901369-3	1988	The blockade of beta-adrenoreceptors with propranolol reduced contractile responses to exogenous (i. a. administration) and endogenous (electrical stimulation of the n. vagus" efferent fibers) acetylcholine, histamine and bradykinin.	Propranolol	42-53	kininogen 1	Homo sapiens	222-232
3398992-4	1988	3,4-Diaminopyridine, serum, N-formyl-methionyl-leucyl-phenylalanine and bradykinin increased cytosolic free calcium transiently although the rate of the increase was slower and the magnitude of the rise was less in cells from aged and Alzheimer donors when compared to young donors.	Calcium	108-115	kininogen 1	Homo sapiens	72-82
3411774-0	1988	[Thiamylal reduces the inhibition of dorsal horn lamina V type neuronal activity induced by bradykinin injection into the femoral artery contralateral to the recording site].	Thiamylal	1-10	kininogen 1	Homo sapiens	92-102
3259133-0	1988	Bradykinin induces the bi-phasic production of lysophosphatidyl inositol and diacylglycerol in a dorsal root ganglion X neurotumor hybrid cell line, F-11.	lysophosphatidylinositol	47-72	kininogen 1	Homo sapiens	0-10
3259133-0	1988	Bradykinin induces the bi-phasic production of lysophosphatidyl inositol and diacylglycerol in a dorsal root ganglion X neurotumor hybrid cell line, F-11.	Diglycerides	77-91	kininogen 1	Homo sapiens	0-10
3259133-1	1988	Bradykinin acts on the dorsal root ganglion X neuroblastoma hybrid cell line F-11 to stimulate the rapid elevation of inositol trisphosphate (IP3) and intracellular calcium.	inositol 1,2,3-trisphosphate	118-140	kininogen 1	Homo sapiens	0-10
3259133-1	1988	Bradykinin acts on the dorsal root ganglion X neuroblastoma hybrid cell line F-11 to stimulate the rapid elevation of inositol trisphosphate (IP3) and intracellular calcium.	Inositol 1,4,5-Trisphosphate	142-145	kininogen 1	Homo sapiens	0-10
3259133-1	1988	Bradykinin acts on the dorsal root ganglion X neuroblastoma hybrid cell line F-11 to stimulate the rapid elevation of inositol trisphosphate (IP3) and intracellular calcium.	Calcium	165-172	kininogen 1	Homo sapiens	0-10
3259133-9	1988	Bradykinin also induced an equally rapid increase in lysophosphatidyl inositol (lyso-PI) with a peak around 10-30 seconds, and a second more sustained peak after 10 minutes.	lysophosphatidylinositol	53-78	kininogen 1	Homo sapiens	0-10
3259133-9	1988	Bradykinin also induced an equally rapid increase in lysophosphatidyl inositol (lyso-PI) with a peak around 10-30 seconds, and a second more sustained peak after 10 minutes.	lysophosphatidylinositol	80-87	kininogen 1	Homo sapiens	0-10
3398992-5	1988	Four minutes after N-formyl-methionyl-leucyl-phenylalanine or bradykinin treatment cytosolic free calcium returned to resting levels in all six cell lines.	Calcium	98-105	kininogen 1	Homo sapiens	62-72
3398992-7	1988	Bradykinin and serum were effective in the absence of extracellular calcium but 3,4-diaminopyridine and N-formyl-methionyl-leucyl-phenylalanine were not.	Calcium	68-75	kininogen 1	Homo sapiens	0-10
2898111-0	1988	Bradykinin-induced accumulation of [3H]inositol-1-phosphate in human embryonic pituitary tumour cells by activation of a B2-receptor.	[3h]inositol-1-phosphate	35-59	kininogen 1	Homo sapiens	0-10
2898111-2	1988	Stimulation of Flow 9000 cells, prelabelled with [3H]inositol, with the nonapeptide bradykinin (BK), or its analogues and fragments produced a differential accumulation of [3H]IP1.	[3h]inositol	49-61	kininogen 1	Homo sapiens	84-94
2898111-2	1988	Stimulation of Flow 9000 cells, prelabelled with [3H]inositol, with the nonapeptide bradykinin (BK), or its analogues and fragments produced a differential accumulation of [3H]IP1.	[3h]inositol	49-61	kininogen 1	Homo sapiens	96-98
2898111-2	1988	Stimulation of Flow 9000 cells, prelabelled with [3H]inositol, with the nonapeptide bradykinin (BK), or its analogues and fragments produced a differential accumulation of [3H]IP1.	Tritium	50-52	kininogen 1	Homo sapiens	84-94
2898111-2	1988	Stimulation of Flow 9000 cells, prelabelled with [3H]inositol, with the nonapeptide bradykinin (BK), or its analogues and fragments produced a differential accumulation of [3H]IP1.	Tritium	50-52	kininogen 1	Homo sapiens	96-98
2898111-3	1988	BK-related peptides exhibited the following rank order of potency in this assay: BK = [Lys]BK greater than [Met-Lys]Bk much greater than [Des-Arg9]BK much greater than BK(1-6) = BK(2-7) = BK(2-9).	Lysine	87-90	kininogen 1	Homo sapiens	0-2
2898111-3	1988	BK-related peptides exhibited the following rank order of potency in this assay: BK = [Lys]BK greater than [Met-Lys]Bk much greater than [Des-Arg9]BK much greater than BK(1-6) = BK(2-7) = BK(2-9).	Lysine	87-90	kininogen 1	Homo sapiens	81-83
2898111-3	1988	BK-related peptides exhibited the following rank order of potency in this assay: BK = [Lys]BK greater than [Met-Lys]Bk much greater than [Des-Arg9]BK much greater than BK(1-6) = BK(2-7) = BK(2-9).	Lysine	87-90	kininogen 1	Homo sapiens	81-83
2898111-3	1988	BK-related peptides exhibited the following rank order of potency in this assay: BK = [Lys]BK greater than [Met-Lys]Bk much greater than [Des-Arg9]BK much greater than BK(1-6) = BK(2-7) = BK(2-9).	Lysine	87-90	kininogen 1	Homo sapiens	81-83
2898111-3	1988	BK-related peptides exhibited the following rank order of potency in this assay: BK = [Lys]BK greater than [Met-Lys]Bk much greater than [Des-Arg9]BK much greater than BK(1-6) = BK(2-7) = BK(2-9).	Lysine	87-90	kininogen 1	Homo sapiens	81-83
2898111-3	1988	BK-related peptides exhibited the following rank order of potency in this assay: BK = [Lys]BK greater than [Met-Lys]Bk much greater than [Des-Arg9]BK much greater than BK(1-6) = BK(2-7) = BK(2-9).	Lysine	87-90	kininogen 1	Homo sapiens	81-83
2898111-3	1988	BK-related peptides exhibited the following rank order of potency in this assay: BK = [Lys]BK greater than [Met-Lys]Bk much greater than [Des-Arg9]BK much greater than BK(1-6) = BK(2-7) = BK(2-9).	Lysine	87-90	kininogen 1	Homo sapiens	81-83
2898111-3	1988	BK-related peptides exhibited the following rank order of potency in this assay: BK = [Lys]BK greater than [Met-Lys]Bk much greater than [Des-Arg9]BK much greater than BK(1-6) = BK(2-7) = BK(2-9).	des-arg9	138-146	kininogen 1	Homo sapiens	0-2
2898111-5	1988	[3H]BK receptor binding studies showed that BK and [Des-Arg9]BK produced a concentration-dependent inhibition of [3H]BK binding with Ki values of 4.8 +/- 1.9 nM (n = 3) and 6.8 +/- 0.7 microM (n = 3) respectively.	Tritium	1-3	kininogen 1	Homo sapiens	4-6
2898111-5	1988	[3H]BK receptor binding studies showed that BK and [Des-Arg9]BK produced a concentration-dependent inhibition of [3H]BK binding with Ki values of 4.8 +/- 1.9 nM (n = 3) and 6.8 +/- 0.7 microM (n = 3) respectively.	Tritium	1-3	kininogen 1	Homo sapiens	44-46
2898111-5	1988	[3H]BK receptor binding studies showed that BK and [Des-Arg9]BK produced a concentration-dependent inhibition of [3H]BK binding with Ki values of 4.8 +/- 1.9 nM (n = 3) and 6.8 +/- 0.7 microM (n = 3) respectively.	Tritium	1-3	kininogen 1	Homo sapiens	44-46
2898111-5	1988	[3H]BK receptor binding studies showed that BK and [Des-Arg9]BK produced a concentration-dependent inhibition of [3H]BK binding with Ki values of 4.8 +/- 1.9 nM (n = 3) and 6.8 +/- 0.7 microM (n = 3) respectively.	Tritium	1-3	kininogen 1	Homo sapiens	44-46
2898111-6	1988	These studies suggest the presence of B2-bradykinin receptors on the human embryonic pituitary tumour cell-line which appear to be coupled to the phosphatidyl inositol turnover signal transduction mechanism.	Phosphatidylinositols	146-167	kininogen 1	Homo sapiens	41-51
3162455-0	1988	Phorbol esters and diacylglycerols amplify bradykinin-stimulated prostaglandin synthesis in Swiss 3T3 fibroblasts.	Phorbol Esters	0-14	kininogen 1	Homo sapiens	43-53
3162455-0	1988	Phorbol esters and diacylglycerols amplify bradykinin-stimulated prostaglandin synthesis in Swiss 3T3 fibroblasts.	Diglycerides	19-34	kininogen 1	Homo sapiens	43-53
3162455-0	1988	Phorbol esters and diacylglycerols amplify bradykinin-stimulated prostaglandin synthesis in Swiss 3T3 fibroblasts.	Prostaglandins	65-78	kininogen 1	Homo sapiens	43-53
3162455-1	1988	Possible independence from protein kinase C. When Swiss 3T3 fibroblasts were incubated with bradykinin, prostaglandin E2 (PGE2) synthesis was stimulated.	Dinoprostone	104-120	kininogen 1	Homo sapiens	92-102
3162455-1	1988	Possible independence from protein kinase C. When Swiss 3T3 fibroblasts were incubated with bradykinin, prostaglandin E2 (PGE2) synthesis was stimulated.	Dinoprostone	122-126	kininogen 1	Homo sapiens	92-102
3162455-3	1988	However, when cells were preincubated with phorbol esters or OAG, bradykinin-stimulated PGE2 synthesis was potentiated markedly.	Phorbol Esters	43-57	kininogen 1	Homo sapiens	66-76
3162455-3	1988	However, when cells were preincubated with phorbol esters or OAG, bradykinin-stimulated PGE2 synthesis was potentiated markedly.	Dinoprostone	88-92	kininogen 1	Homo sapiens	66-76
3162455-4	1988	When phorbol esters and OAG were added together, bradykinin-stimulated PGE2 synthesis was potentiated in an additive manner.	Phorbol Esters	5-19	kininogen 1	Homo sapiens	49-59
3162455-4	1988	When phorbol esters and OAG were added together, bradykinin-stimulated PGE2 synthesis was potentiated in an additive manner.	1-oleoyl-2-acetylglycerol	24-27	kininogen 1	Homo sapiens	49-59
3162455-4	1988	When phorbol esters and OAG were added together, bradykinin-stimulated PGE2 synthesis was potentiated in an additive manner.	Dinoprostone	71-75	kininogen 1	Homo sapiens	49-59
3162455-5	1988	When cells were preincubated for 48 h with phorbol esters, then bradykinin added, amplification of bradykinin-stimulated PGE2 synthesis by phorbol ester or OAG was still apparent, even though prolonged pretreatment with phorbol esters abolished protein kinase C (Ca2+/phospholipid-dependent enzyme) activity in cell-free preparations.	Phorbol Esters	43-57	kininogen 1	Homo sapiens	99-109
3162455-5	1988	When cells were preincubated for 48 h with phorbol esters, then bradykinin added, amplification of bradykinin-stimulated PGE2 synthesis by phorbol ester or OAG was still apparent, even though prolonged pretreatment with phorbol esters abolished protein kinase C (Ca2+/phospholipid-dependent enzyme) activity in cell-free preparations.	Dinoprostone	121-125	kininogen 1	Homo sapiens	64-74
3162455-5	1988	When cells were preincubated for 48 h with phorbol esters, then bradykinin added, amplification of bradykinin-stimulated PGE2 synthesis by phorbol ester or OAG was still apparent, even though prolonged pretreatment with phorbol esters abolished protein kinase C (Ca2+/phospholipid-dependent enzyme) activity in cell-free preparations.	Dinoprostone	121-125	kininogen 1	Homo sapiens	99-109
3162455-5	1988	When cells were preincubated for 48 h with phorbol esters, then bradykinin added, amplification of bradykinin-stimulated PGE2 synthesis by phorbol ester or OAG was still apparent, even though prolonged pretreatment with phorbol esters abolished protein kinase C (Ca2+/phospholipid-dependent enzyme) activity in cell-free preparations.	Phorbol Esters	43-56	kininogen 1	Homo sapiens	99-109
3162455-5	1988	When cells were preincubated for 48 h with phorbol esters, then bradykinin added, amplification of bradykinin-stimulated PGE2 synthesis by phorbol ester or OAG was still apparent, even though prolonged pretreatment with phorbol esters abolished protein kinase C (Ca2+/phospholipid-dependent enzyme) activity in cell-free preparations.	1-oleoyl-2-acetylglycerol	156-159	kininogen 1	Homo sapiens	64-74
3162455-5	1988	When cells were preincubated for 48 h with phorbol esters, then bradykinin added, amplification of bradykinin-stimulated PGE2 synthesis by phorbol ester or OAG was still apparent, even though prolonged pretreatment with phorbol esters abolished protein kinase C (Ca2+/phospholipid-dependent enzyme) activity in cell-free preparations.	1-oleoyl-2-acetylglycerol	156-159	kininogen 1	Homo sapiens	99-109
3162455-5	1988	When cells were preincubated for 48 h with phorbol esters, then bradykinin added, amplification of bradykinin-stimulated PGE2 synthesis by phorbol ester or OAG was still apparent, even though prolonged pretreatment with phorbol esters abolished protein kinase C (Ca2+/phospholipid-dependent enzyme) activity in cell-free preparations.	Phorbol Esters	220-234	kininogen 1	Homo sapiens	64-74
3162455-5	1988	When cells were preincubated for 48 h with phorbol esters, then bradykinin added, amplification of bradykinin-stimulated PGE2 synthesis by phorbol ester or OAG was still apparent, even though prolonged pretreatment with phorbol esters abolished protein kinase C (Ca2+/phospholipid-dependent enzyme) activity in cell-free preparations.	Phorbol Esters	220-234	kininogen 1	Homo sapiens	99-109
3162455-5	1988	When cells were preincubated for 48 h with phorbol esters, then bradykinin added, amplification of bradykinin-stimulated PGE2 synthesis by phorbol ester or OAG was still apparent, even though prolonged pretreatment with phorbol esters abolished protein kinase C (Ca2+/phospholipid-dependent enzyme) activity in cell-free preparations.	Phospholipids	268-280	kininogen 1	Homo sapiens	64-74
3162455-5	1988	When cells were preincubated for 48 h with phorbol esters, then bradykinin added, amplification of bradykinin-stimulated PGE2 synthesis by phorbol ester or OAG was still apparent, even though prolonged pretreatment with phorbol esters abolished protein kinase C (Ca2+/phospholipid-dependent enzyme) activity in cell-free preparations.	Phospholipids	268-280	kininogen 1	Homo sapiens	99-109
3162455-6	1988	Further, the protein kinase C antagonist, H-7, only slightly inhibited phorbol ester or OAG amplification of bradykinin-stimulated PGE2 synthesis.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	42-45	kininogen 1	Homo sapiens	109-119
3162455-6	1988	Further, the protein kinase C antagonist, H-7, only slightly inhibited phorbol ester or OAG amplification of bradykinin-stimulated PGE2 synthesis.	Dinoprostone	131-135	kininogen 1	Homo sapiens	109-119
3162455-8	1988	Since desensitization or inhibition of protein kinase C only partially reduced the amplification of bradykinin-stimulated PGE2 synthesis by phorbol esters or OAG, the possibility is raised that diacylglycerol mimetics may have actions in addition to activation of protein kinase C.	Dinoprostone	122-126	kininogen 1	Homo sapiens	100-110
3162455-8	1988	Since desensitization or inhibition of protein kinase C only partially reduced the amplification of bradykinin-stimulated PGE2 synthesis by phorbol esters or OAG, the possibility is raised that diacylglycerol mimetics may have actions in addition to activation of protein kinase C.	Phorbol Esters	140-154	kininogen 1	Homo sapiens	100-110
3162455-8	1988	Since desensitization or inhibition of protein kinase C only partially reduced the amplification of bradykinin-stimulated PGE2 synthesis by phorbol esters or OAG, the possibility is raised that diacylglycerol mimetics may have actions in addition to activation of protein kinase C.	1-oleoyl-2-acetylglycerol	158-161	kininogen 1	Homo sapiens	100-110
3162455-8	1988	Since desensitization or inhibition of protein kinase C only partially reduced the amplification of bradykinin-stimulated PGE2 synthesis by phorbol esters or OAG, the possibility is raised that diacylglycerol mimetics may have actions in addition to activation of protein kinase C.	Diglycerides	194-208	kininogen 1	Homo sapiens	100-110
3382440-1	1988	A certain resemblance of three-dimensional molecular organizations of the known peptide bioregulator bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) and the tentative cytophilic centre of the human IgE igercin (Arg-Ala-Val-Ser-Val-Asn-Pro-Gly-Lys) existing along with their pronounced structural similarity was shown by means of energy calculations.	Arginine	113-116	kininogen 1	Homo sapiens	101-111
3061568-0	1988	Characterization of the arachidonic acid metabolites mediating bradykinin and noradrenaline hyperalgesia.	Arachidonic Acid	24-40	kininogen 1	Homo sapiens	63-73
3061568-1	1988	It has been suggested that bradykinin (BK) and norepinephrine (NE) induce hyperalgesia, indirectly, by stimulating the production of prostaglandin products of the cyclo-oxygenase pathway of arachidonic acid metabolism.	Prostaglandins	133-146	kininogen 1	Homo sapiens	27-37
3061568-1	1988	It has been suggested that bradykinin (BK) and norepinephrine (NE) induce hyperalgesia, indirectly, by stimulating the production of prostaglandin products of the cyclo-oxygenase pathway of arachidonic acid metabolism.	Prostaglandins	133-146	kininogen 1	Homo sapiens	39-41
3061568-1	1988	It has been suggested that bradykinin (BK) and norepinephrine (NE) induce hyperalgesia, indirectly, by stimulating the production of prostaglandin products of the cyclo-oxygenase pathway of arachidonic acid metabolism.	Arachidonic Acid	190-206	kininogen 1	Homo sapiens	27-37
3061568-1	1988	It has been suggested that bradykinin (BK) and norepinephrine (NE) induce hyperalgesia, indirectly, by stimulating the production of prostaglandin products of the cyclo-oxygenase pathway of arachidonic acid metabolism.	Arachidonic Acid	190-206	kininogen 1	Homo sapiens	39-41
3392680-11	1988	Some of the low-threshold receptors (particularly the CS units) showed a desensitization under the influence of bradykinin.	Cesium	54-56	kininogen 1	Homo sapiens	112-122
2893800-2	1988	This effect was observed in a prostaglandin E2-producing cell line (HSDM1C1) by deprivation of exogenous arachidonate for 24-48 h. Icosanoid production by the cells upon bradykinin stimulation was impaired despite no change in the concentration of arachidonate within the cell and no change in the activity of cyclooxygenase, phospholipases, acyltransferases, or fatty acyl-CoA hydrolase.	Dinoprostone	30-46	kininogen 1	Homo sapiens	170-180
2893800-2	1988	This effect was observed in a prostaglandin E2-producing cell line (HSDM1C1) by deprivation of exogenous arachidonate for 24-48 h. Icosanoid production by the cells upon bradykinin stimulation was impaired despite no change in the concentration of arachidonate within the cell and no change in the activity of cyclooxygenase, phospholipases, acyltransferases, or fatty acyl-CoA hydrolase.	Arachidonic Acid	105-117	kininogen 1	Homo sapiens	170-180
2893800-2	1988	This effect was observed in a prostaglandin E2-producing cell line (HSDM1C1) by deprivation of exogenous arachidonate for 24-48 h. Icosanoid production by the cells upon bradykinin stimulation was impaired despite no change in the concentration of arachidonate within the cell and no change in the activity of cyclooxygenase, phospholipases, acyltransferases, or fatty acyl-CoA hydrolase.	Eicosanoids	131-140	kininogen 1	Homo sapiens	170-180
2893800-2	1988	This effect was observed in a prostaglandin E2-producing cell line (HSDM1C1) by deprivation of exogenous arachidonate for 24-48 h. Icosanoid production by the cells upon bradykinin stimulation was impaired despite no change in the concentration of arachidonate within the cell and no change in the activity of cyclooxygenase, phospholipases, acyltransferases, or fatty acyl-CoA hydrolase.	Arachidonic Acid	248-260	kininogen 1	Homo sapiens	170-180
3382440-1	1988	A certain resemblance of three-dimensional molecular organizations of the known peptide bioregulator bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) and the tentative cytophilic centre of the human IgE igercin (Arg-Ala-Val-Ser-Val-Asn-Pro-Gly-Lys) existing along with their pronounced structural similarity was shown by means of energy calculations.	ala-val-ser-val-asn-pro-gly-lys	216-247	kininogen 1	Homo sapiens	101-111
3131319-4	1988	These results were given support by data observed in experiments with des-Arg1 and des-Arg9 bradykinin; the Vmax/Km for des-Arg9 bradykinin was 3 times that for des-Arg1 bradykinin.	des-arg9	83-91	kininogen 1	Homo sapiens	92-102
2833432-0	1988	Source of endogenous arachidonate and 5-lipoxygenase products in human neutrophils stimulated by bradykinin and A23187.	Arachidonic Acid	21-33	kininogen 1	Homo sapiens	97-107
2833432-4	1988	The results of the study indicate that stimulation of 1-14C-AA-prelabelled PMNs with BK liberates AA mainly from phosphatidylinositol, while A23187 causes release of AA from phosphatidylcholine, phosphatidylethanolamine, and possibly phosphatidylserine.	Phosphatidylinositols	113-133	kininogen 1	Homo sapiens	85-87
2833432-4	1988	The results of the study indicate that stimulation of 1-14C-AA-prelabelled PMNs with BK liberates AA mainly from phosphatidylinositol, while A23187 causes release of AA from phosphatidylcholine, phosphatidylethanolamine, and possibly phosphatidylserine.	phosphatidylethanolamine	195-219	kininogen 1	Homo sapiens	85-87
2833432-4	1988	The results of the study indicate that stimulation of 1-14C-AA-prelabelled PMNs with BK liberates AA mainly from phosphatidylinositol, while A23187 causes release of AA from phosphatidylcholine, phosphatidylethanolamine, and possibly phosphatidylserine.	Phosphatidylserines	234-252	kininogen 1	Homo sapiens	85-87
2833432-5	1988	Furthermore BK (10(-9)-10(-6)M) dose-dependently stimulated the formation of 5-HETE and LTB4, reaching a maximum at 10(-7)M, while 5-HT (10(-8)-10(-4)M) released only negligible amounts of eicosanoids, similar to those observed in control experiments.	Eicosanoids	189-200	kininogen 1	Homo sapiens	12-14
3131319-4	1988	These results were given support by data observed in experiments with des-Arg1 and des-Arg9 bradykinin; the Vmax/Km for des-Arg9 bradykinin was 3 times that for des-Arg1 bradykinin.	des-arg9	83-91	kininogen 1	Homo sapiens	129-139
3131319-4	1988	These results were given support by data observed in experiments with des-Arg1 and des-Arg9 bradykinin; the Vmax/Km for des-Arg9 bradykinin was 3 times that for des-Arg1 bradykinin.	des-arg9	83-91	kininogen 1	Homo sapiens	129-139
3346337-1	1988	Mitogenic stimulation of quiescent human fibroblasts (HSWP) with serum or a mixture of growth factors (consisting of vasopressin, bradykinin, EGF, and insulin) stimulates the release of inositol phosphates, mobilization of intracellular Ca, activation of Na/H exchange and subsequent incorporation of [3H]-thymidine.	Inositol Phosphates	186-205	kininogen 1	Homo sapiens	130-140
3131319-4	1988	These results were given support by data observed in experiments with des-Arg1 and des-Arg9 bradykinin; the Vmax/Km for des-Arg9 bradykinin was 3 times that for des-Arg1 bradykinin.	des-arg9	120-128	kininogen 1	Homo sapiens	92-102
3131319-4	1988	These results were given support by data observed in experiments with des-Arg1 and des-Arg9 bradykinin; the Vmax/Km for des-Arg9 bradykinin was 3 times that for des-Arg1 bradykinin.	des-arg9	120-128	kininogen 1	Homo sapiens	129-139
3131319-4	1988	These results were given support by data observed in experiments with des-Arg1 and des-Arg9 bradykinin; the Vmax/Km for des-Arg9 bradykinin was 3 times that for des-Arg1 bradykinin.	des-arg9	120-128	kininogen 1	Homo sapiens	129-139
3131319-13	1988	(1987) in The 8th International Symposium on ADP-Ribosylation, Texas, abstract p. 13), bradykinin functioning in the contraction of smooth muscle may be modified in this way in vivo.	Adenosine Diphosphate	45-48	kininogen 1	Homo sapiens	87-97
2830937-7	1988	Bradykinin (BK) was broken down and A I converted to A II by CSF, both effects being inhibited by captopril.	Captopril	98-107	kininogen 1	Homo sapiens	0-10
3123876-0	1988	Low-dose bradykinin infusion reduces endogenous glucose production in surgical patients.	Glucose	48-55	kininogen 1	Homo sapiens	9-19
3123876-1	1988	The systemic effect of low-dose bradykinin infusion on total body glucose production and arterial substrate concentrations was examined during D5W infusion (1.0 mg/kg/min) in five normal-weight postsurgical subjects and compared to the response in four saline infused control patients, well matched for age, weight, and degree of postoperative stress.	Glucose	66-73	kininogen 1	Homo sapiens	32-42
3123876-1	1988	The systemic effect of low-dose bradykinin infusion on total body glucose production and arterial substrate concentrations was examined during D5W infusion (1.0 mg/kg/min) in five normal-weight postsurgical subjects and compared to the response in four saline infused control patients, well matched for age, weight, and degree of postoperative stress.	Glucose	143-146	kininogen 1	Homo sapiens	32-42
3123876-4	1988	After 75 minutes of bradykinin, endogenous glucose production was significantly reduced as compared to basal values (1.63 +/- 0.21 mg/kg/min, P less than .0125 v 2.20 +/- 0.35 basal).	Glucose	43-50	kininogen 1	Homo sapiens	20-30
3123876-9	1988	These results demonstrate the inhibitory effect of low-dose bradykinin on glucose production in surgically stressed patients.	Glucose	74-81	kininogen 1	Homo sapiens	60-70
3123876-10	1988	The stimulation of hepatic prostaglandin synthesis by bradykinin may explain the results since prostaglandins are known to exert an inhibitory effect on hormone stimulated gluconeogenesis and glycogenolysis in liver tissue.	Prostaglandins	27-40	kininogen 1	Homo sapiens	54-64
3123876-10	1988	The stimulation of hepatic prostaglandin synthesis by bradykinin may explain the results since prostaglandins are known to exert an inhibitory effect on hormone stimulated gluconeogenesis and glycogenolysis in liver tissue.	Prostaglandins	95-109	kininogen 1	Homo sapiens	54-64
2830937-7	1988	Bradykinin (BK) was broken down and A I converted to A II by CSF, both effects being inhibited by captopril.	Captopril	98-107	kininogen 1	Homo sapiens	12-14
3059981-10	1988	Indeed, endo-oligopeptidase A, an enzyme, known to hydrolyze the Phe5-Ser6 bond of bradykinin and the Arg8-Arg9 bond of neurotensin, has been shown to produce, by a single cleavage, [Leu] enkephalin or [Met] enkephalin from small enkephalin-containing peptides, (Camargo et al., 1987, J. Neurochem.	Leucine	183-186	kininogen 1	Homo sapiens	83-93
3146318-9	1988	The nociceptive peptide bradykinin (BK) normally initiates a cascade involving receptor-mediated phospholipase C activation and release of arachidonate and prostanoids from cultured skin fibroblasts.	Arachidonic Acid	139-151	kininogen 1	Homo sapiens	24-34
3146318-9	1988	The nociceptive peptide bradykinin (BK) normally initiates a cascade involving receptor-mediated phospholipase C activation and release of arachidonate and prostanoids from cultured skin fibroblasts.	Arachidonic Acid	139-151	kininogen 1	Homo sapiens	36-38
3146318-9	1988	The nociceptive peptide bradykinin (BK) normally initiates a cascade involving receptor-mediated phospholipase C activation and release of arachidonate and prostanoids from cultured skin fibroblasts.	Prostaglandins	156-167	kininogen 1	Homo sapiens	24-34
3146318-9	1988	The nociceptive peptide bradykinin (BK) normally initiates a cascade involving receptor-mediated phospholipase C activation and release of arachidonate and prostanoids from cultured skin fibroblasts.	Prostaglandins	156-167	kininogen 1	Homo sapiens	36-38
3146318-10	1988	Release of [3H]arachidonate by BK was deficient in NCL fibroblasts, suggesting that the primary defect in NCL could involve the deficiency of a specific phospholipase A2 activity.	Tritium	12-14	kininogen 1	Homo sapiens	31-33
3146318-10	1988	Release of [3H]arachidonate by BK was deficient in NCL fibroblasts, suggesting that the primary defect in NCL could involve the deficiency of a specific phospholipase A2 activity.	Arachidonic Acid	15-27	kininogen 1	Homo sapiens	31-33
3057634-1	1988	cGMP appears to be the intracellular messenger involved in smooth muscle relaxant effects of three major groups of vasodilators, the ANFs, the nitrovasodilators (such as nitroglycerin, sodium nitroprusside, sodium nitrite, isosorbide dinitrate), and the endothelium-dependent vasodilators (such as ACh, histamine, bradykinin, adenosine triphosphate, A23187).	Cyclic GMP	0-4	kininogen 1	Homo sapiens	314-324
2844549-4	1988	In addition the degree of inhibition caused by local salbutamol on the wheal volume due to intradermal prostaglandin E and bradykinin, was compared following ketotifen and placebo.	Albuterol	53-63	kininogen 1	Homo sapiens	123-133
2844549-6	1988	Local salbutamol significantly decreased the wheal volume induced by intradermal prostaglandin E and bradykinin.	Albuterol	6-16	kininogen 1	Homo sapiens	101-111
3124291-7	1987	Histamine, bradykinin and thrombin stimulated PGI2 synthesis in both coronary endothelial cells and human umbilical cells, but only bradykinin stimulated PGI2 synthesis in bovine aortic cells.	Epoprostenol	46-50	kininogen 1	Homo sapiens	11-21
3124291-7	1987	Histamine, bradykinin and thrombin stimulated PGI2 synthesis in both coronary endothelial cells and human umbilical cells, but only bradykinin stimulated PGI2 synthesis in bovine aortic cells.	Epoprostenol	154-158	kininogen 1	Homo sapiens	132-142
3501619-4	1987	Based on this principle, we developed an assay for HK using the chromogenic substrate pyroGlu-Pro-Arg-p-nitroanilide (S-2366, KabiVitrum), which is hydrolyzed by factor XIa.	pyroglu-pro-arg-p-nitroanilide	86-116	kininogen 1	Homo sapiens	51-53
3501619-4	1987	Based on this principle, we developed an assay for HK using the chromogenic substrate pyroGlu-Pro-Arg-p-nitroanilide (S-2366, KabiVitrum), which is hydrolyzed by factor XIa.	S 2366	118-124	kininogen 1	Homo sapiens	51-53
3322463-4	1987	3 Bradykinin induced a ten fold greater release of prostacyclin than CGRP, but did not activate adenylate cyclase.	Epoprostenol	51-63	kininogen 1	Homo sapiens	2-12
3444481-7	1987	The rank order of potency of several kinin analogues on the pain response was BK much much greater than sigma-cyclo-(Lys1-Gly6)-BK = sigma-cyclo-kallidin greater than des-Arg9-BK.	(lys1-gly6)	116-127	kininogen 1	Homo sapiens	128-130
3444481-7	1987	The rank order of potency of several kinin analogues on the pain response was BK much much greater than sigma-cyclo-(Lys1-Gly6)-BK = sigma-cyclo-kallidin greater than des-Arg9-BK.	(lys1-gly6)	116-127	kininogen 1	Homo sapiens	128-130
3444481-12	1987	The B2 receptor antagonists, D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg-TEA and D-Pro-Phe-Arg-heptylamide produced significant antagonism of the bradykinin-induced pain responses at doses which had no effect against 5-hydroxytryptamine or potassium chloride.	d-arg-arg-pro-hyp-gly-thi-ser-d-phe-thi-arg-tea	29-76	kininogen 1	Homo sapiens	146-156
3444481-12	1987	The B2 receptor antagonists, D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg-TEA and D-Pro-Phe-Arg-heptylamide produced significant antagonism of the bradykinin-induced pain responses at doses which had no effect against 5-hydroxytryptamine or potassium chloride.	d-pro-phe-arg-heptylamide	81-106	kininogen 1	Homo sapiens	146-156
2825688-4	1987	This effect of bradykinin was unaffected by aspirin, and was accounted for by the amounts of NO released by the endothelial cells.	Aspirin	44-51	kininogen 1	Homo sapiens	15-25
2889967-3	1987	The inhibitory action of both bradykinin and nitric oxide was abolished by haemoglobin, but not by aspirin, and was potentiated by superoxide dismutase to a similar degree.	Aspirin	99-106	kininogen 1	Homo sapiens	30-40
2889967-4	1987	It is suggested that the effect of bradykinin is mediated by the release of nitric oxide from the endothelial cells, and that nitric oxide release contributes to the non-adhesive properties of vascular endothelium.	Nitric Oxide	76-88	kininogen 1	Homo sapiens	35-45
3322462-6	1987	In the absence of indomethacin, stimulation of the cells with bradykinin (1-3 nM) released small amounts of prostacyclin and EDRF which synergistically inhibited platelet aggregation.	Epoprostenol	108-120	kininogen 1	Homo sapiens	62-72
3661696-7	1987	Moreover, a B1-receptor antagonist, Des-Arg9, [Leu8]-bradykinin, did not significantly affect the increase of cytosolic Ca2+ elicited by bradykinin.	des-arg9	36-44	kininogen 1	Homo sapiens	53-63
3661696-8	1987	On the other hand, the bradykinin-elicited increase of Ca2+ was almost completely inhibited by a novel B2-receptor antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7]-bradykinin.	D-Arginine	127-132	kininogen 1	Homo sapiens	23-33
3661696-8	1987	On the other hand, the bradykinin-elicited increase of Ca2+ was almost completely inhibited by a novel B2-receptor antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7]-bradykinin.	D-Arginine	127-132	kininogen 1	Homo sapiens	156-166
3661696-8	1987	On the other hand, the bradykinin-elicited increase of Ca2+ was almost completely inhibited by a novel B2-receptor antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7]-bradykinin.	[hyp3,	133-139	kininogen 1	Homo sapiens	23-33
3661696-8	1987	On the other hand, the bradykinin-elicited increase of Ca2+ was almost completely inhibited by a novel B2-receptor antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7]-bradykinin.	[hyp3,	133-139	kininogen 1	Homo sapiens	156-166
3661696-8	1987	On the other hand, the bradykinin-elicited increase of Ca2+ was almost completely inhibited by a novel B2-receptor antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7]-bradykinin.	thi5	140-144	kininogen 1	Homo sapiens	23-33
3661696-13	1987	The absence of extracellular Ca2+ during the interim period, or the pretreatment of cells with ionomycin in the absence of extracellular Ca2+, prevented the response of the cells to a second dose of bradykinin.	Ionomycin	95-104	kininogen 1	Homo sapiens	199-209
3310903-9	1987	ME cleaves only the Phe5-Ser6 bond of bradykinin (BK); however, all three ME activities were inhibited by BK.	methionylglutamic acid	0-2	kininogen 1	Homo sapiens	38-48
3310903-9	1987	ME cleaves only the Phe5-Ser6 bond of bradykinin (BK); however, all three ME activities were inhibited by BK.	methionylglutamic acid	0-2	kininogen 1	Homo sapiens	50-52
3310903-9	1987	ME cleaves only the Phe5-Ser6 bond of bradykinin (BK); however, all three ME activities were inhibited by BK.	methionylglutamic acid	74-76	kininogen 1	Homo sapiens	106-108
3322322-2	1987	Also, bradykinin, a vasoactive product of kallikrein"s action upon kininogen substrates, increases glucose uptake when infused into the human forearm.	Glucose	99-106	kininogen 1	Homo sapiens	6-16
3322322-8	1987	These studies suggest that the previously observed in vivo effects of bradykinin on peripheral glucose uptake are probably mediated by changes in tissue perfusion rather than direct kinin effects on skeletal muscle, and that the putative membrane serine protease involved in the insulin-effector system is not tissue kallikrein.	Glucose	95-102	kininogen 1	Homo sapiens	70-80
3121350-1	1987	Bradykinin infusion has been shown to improve glucose metabolism in non-insulin-dependent diabetic subjects (NIDD).	Glucose	46-53	kininogen 1	Homo sapiens	0-10
3121350-2	1987	Therefore, we tested the following hypothesis: inhibition of Kininase II, the bradykinin (BK) degrading enzyme, by captopril may also improve glucose metabolism in NIDD.	Captopril	115-124	kininogen 1	Homo sapiens	78-88
3121350-2	1987	Therefore, we tested the following hypothesis: inhibition of Kininase II, the bradykinin (BK) degrading enzyme, by captopril may also improve glucose metabolism in NIDD.	Glucose	142-149	kininogen 1	Homo sapiens	78-88
3121350-9	1987	Because of the described insulin-like activity of bradykinin, the concomitant accumulation of local kinins by captopril-induced inhibition of kininase II may represent an attractive hypothesis to explain the generated data sufficiently.	Captopril	110-119	kininogen 1	Homo sapiens	50-60
3436959-2	1987	The sulfatide-mediated activation of factor XII and prekallikrein in the presence of high-molecular-weight (HMW) kininogen was remarkably accelerated by 10(-5) M zinc ions.	Sulfoglycosphingolipids	4-13	kininogen 1	Homo sapiens	85-122
3436959-6	1987	In the presence of 5 x 10(-4) M zinc ions, typical difference spectra due to a red shift of tryptophan and/or tyrosine residues were observed for HMW kininogen and its derivatives but not low-molecular-weight (LMW) kininogen.	Tryptophan	92-102	kininogen 1	Homo sapiens	146-159
3436959-6	1987	In the presence of 5 x 10(-4) M zinc ions, typical difference spectra due to a red shift of tryptophan and/or tyrosine residues were observed for HMW kininogen and its derivatives but not low-molecular-weight (LMW) kininogen.	Tyrosine	110-118	kininogen 1	Homo sapiens	146-159
2820797-5	1987	Substances known to activate protein kinase C such as phorbol 12-myristate 13-acetate, or to stimulate phosphoinositide turnover such as thrombin and bradykinin are also effective in raising fructose 2,6-bisphosphate.	Phosphatidylinositols	103-119	kininogen 1	Homo sapiens	150-160
2820797-5	1987	Substances known to activate protein kinase C such as phorbol 12-myristate 13-acetate, or to stimulate phosphoinositide turnover such as thrombin and bradykinin are also effective in raising fructose 2,6-bisphosphate.	fructose 2,6-diphosphate	191-216	kininogen 1	Homo sapiens	150-160
3040751-4	1987	Bradykinin was hydrolyzed at a high rate at the Phe-Ser bond.	Phenylalanine	48-51	kininogen 1	Homo sapiens	0-10
3040751-4	1987	Bradykinin was hydrolyzed at a high rate at the Phe-Ser bond.	Serine	52-55	kininogen 1	Homo sapiens	0-10
3662526-11	1987	In contrast to the effect of the trappers on PG synthesis, BSA and alpha-cyclodextrin are observed to potentiate BK- and ionophore-stimulated incorporation of [3H]acetate into PAF in the endothelial cells.	alpha-cyclodextrin	67-85	kininogen 1	Homo sapiens	113-115
3662526-11	1987	In contrast to the effect of the trappers on PG synthesis, BSA and alpha-cyclodextrin are observed to potentiate BK- and ionophore-stimulated incorporation of [3H]acetate into PAF in the endothelial cells.	[3h]acetate	159-170	kininogen 1	Homo sapiens	113-115
2444995-0	1987	Interference with the distribution and release of arachidonic acid in human keratinocytes by bradykinin, histamine and phosphatidic acid.	Arachidonic Acid	50-66	kininogen 1	Homo sapiens	93-103
2444995-2	1987	Bradykinin, histamine, and phosphatidic acid were found to liberate 14C-arachidonic acid from membrane phospholipids, whereas leukotrienes B4 and C4 were ineffective in this respect.	14c-arachidonic acid	68-88	kininogen 1	Homo sapiens	0-10
2444995-2	1987	Bradykinin, histamine, and phosphatidic acid were found to liberate 14C-arachidonic acid from membrane phospholipids, whereas leukotrienes B4 and C4 were ineffective in this respect.	Phospholipids	103-116	kininogen 1	Homo sapiens	0-10
2444995-4	1987	The present study suggests that bradykinin, histamine, and phosphatidic acid may interfere with the distribution and release of arachidonic acid in human keratinocytes in culture.	Arachidonic Acid	128-144	kininogen 1	Homo sapiens	32-42
2888113-0	1987	Dissociation of bradykinin-induced prostaglandin formation from phosphatidylinositol turnover in Swiss 3T3 fibroblasts: evidence for G protein regulation of phospholipase A2.	Prostaglandins	35-48	kininogen 1	Homo sapiens	16-26
2888113-1	1987	In Swiss 3T3 fibroblasts bradykinin stimulated inositol phosphate (InsP) formation and prostaglandin E2 (PGE2) synthesis.	Inositol Phosphates	47-65	kininogen 1	Homo sapiens	25-35
2888113-1	1987	In Swiss 3T3 fibroblasts bradykinin stimulated inositol phosphate (InsP) formation and prostaglandin E2 (PGE2) synthesis.	Dinoprostone	87-103	kininogen 1	Homo sapiens	25-35
2888113-1	1987	In Swiss 3T3 fibroblasts bradykinin stimulated inositol phosphate (InsP) formation and prostaglandin E2 (PGE2) synthesis.	Dinoprostone	105-109	kininogen 1	Homo sapiens	25-35
2888113-2	1987	The EC50 values for stimulation of PGE2 synthesis and InsP formation by bradykinin were similar, 200 pM and 275 pM, respectively.	Dinoprostone	35-39	kininogen 1	Homo sapiens	72-82
3037217-2	1987	In astrocytes, norepinephrine (NE) produced the greatest stimulation with significant increase also observed with bradykinin.	Norepinephrine	15-29	kininogen 1	Homo sapiens	114-124
3037217-3	1987	In oligodendrocytes, the greatest stimulation was produced by carbachol with significant increase also produced by bradykinin, histamine and NE.	Carbachol	62-71	kininogen 1	Homo sapiens	115-125
3037886-8	1987	Captopril may also influence prostaglandin synthesis by reducing inactivation of bradykinin.	Captopril	0-9	kininogen 1	Homo sapiens	81-91
3037886-8	1987	Captopril may also influence prostaglandin synthesis by reducing inactivation of bradykinin.	Prostaglandins	29-42	kininogen 1	Homo sapiens	81-91
3365237-7	1988	Amino acid sequencing and composition analysis indicated that the structure of the new kinin was [Hyp3]-Lys-bradykinin (Lys-Arg-Pro-Hyp-Gly-Phe-Ser-Pro-Phe-Arg) and not [Ala3]-Lys-bradykinin.	Serine	144-147	kininogen 1	Homo sapiens	108-118
3365237-7	1988	Amino acid sequencing and composition analysis indicated that the structure of the new kinin was [Hyp3]-Lys-bradykinin (Lys-Arg-Pro-Hyp-Gly-Phe-Ser-Pro-Phe-Arg) and not [Ala3]-Lys-bradykinin.	Pro-Phe-Arg	148-159	kininogen 1	Homo sapiens	108-118
3365237-8	1988	We conclude that an important proportion of human kininogens contain hydroxyproline instead of proline in position three of the bradykinin moiety.	Hydroxyproline	69-83	kininogen 1	Homo sapiens	128-138
3166432-4	1988	Most experiments were performed on umbilical arteries and showed that 5 x 10(-4) M or 5 x 10(-3) M TAME significantly inhibited contractions elicited by prostaglandin F2 alpha, bradykinin, serotonin, and histamine.	Tosylarginine Methyl Ester	99-103	kininogen 1	Homo sapiens	177-187
20501240-4	1988	Peptides like substance P, neurotensin, bradykinin inhibited the cleavage of the Ser-Phe bond of atrial natriuretic peptide.	Serine	81-84	kininogen 1	Homo sapiens	40-50
20501240-4	1988	Peptides like substance P, neurotensin, bradykinin inhibited the cleavage of the Ser-Phe bond of atrial natriuretic peptide.	Phenylalanine	85-88	kininogen 1	Homo sapiens	40-50
2888113-3	1987	Guanosine-5"-[gamma-thio]triphosphate stimulated PGE2 synthesis and InsP formation, and guanosine-5"-[beta-thio]diphosphate inhibited both PGE2 synthesis and InsP formation stimulated by bradykinin.	6-thioguanosine 5'-diphosphate	88-123	kininogen 1	Homo sapiens	187-197
2888113-5	1987	Phorbol ester, dexamethasone, and cycloheximide distinguished between bradykinin-stimulated PGE2 synthesis and InsP formation.	Phorbol Esters	0-13	kininogen 1	Homo sapiens	70-80
2888113-5	1987	Phorbol ester, dexamethasone, and cycloheximide distinguished between bradykinin-stimulated PGE2 synthesis and InsP formation.	Dexamethasone	15-28	kininogen 1	Homo sapiens	70-80
2888113-5	1987	Phorbol ester, dexamethasone, and cycloheximide distinguished between bradykinin-stimulated PGE2 synthesis and InsP formation.	Cycloheximide	34-47	kininogen 1	Homo sapiens	70-80
2888113-5	1987	Phorbol ester, dexamethasone, and cycloheximide distinguished between bradykinin-stimulated PGE2 synthesis and InsP formation.	Dinoprostone	92-96	kininogen 1	Homo sapiens	70-80
2888113-6	1987	Phorbol 12-myristate 13-acetate enhanced bradykinin-stimulated PGE2 synthesis but inhibited bradykinin-stimulated InsP formation.	Tetradecanoylphorbol Acetate	0-31	kininogen 1	Homo sapiens	41-51
2888113-6	1987	Phorbol 12-myristate 13-acetate enhanced bradykinin-stimulated PGE2 synthesis but inhibited bradykinin-stimulated InsP formation.	Tetradecanoylphorbol Acetate	0-31	kininogen 1	Homo sapiens	92-102
2888113-6	1987	Phorbol 12-myristate 13-acetate enhanced bradykinin-stimulated PGE2 synthesis but inhibited bradykinin-stimulated InsP formation.	Dinoprostone	63-67	kininogen 1	Homo sapiens	41-51
2888113-7	1987	Pretreatment of cells with dexamethasone for 24 hr inhibited bradykinin-stimulated PGE2 synthesis but was without effect on bradykinin-stimulated InsP formation.	Dexamethasone	27-40	kininogen 1	Homo sapiens	61-71
2888113-7	1987	Pretreatment of cells with dexamethasone for 24 hr inhibited bradykinin-stimulated PGE2 synthesis but was without effect on bradykinin-stimulated InsP formation.	Dinoprostone	83-87	kininogen 1	Homo sapiens	61-71
2888113-8	1987	Cycloheximide inhibited bradykinin-stimulated PGE2 synthesis but was without effect on bradykinin-stimulated InsP formation.	Cycloheximide	0-13	kininogen 1	Homo sapiens	24-34
2888113-8	1987	Cycloheximide inhibited bradykinin-stimulated PGE2 synthesis but was without effect on bradykinin-stimulated InsP formation.	Dinoprostone	46-50	kininogen 1	Homo sapiens	24-34
2888113-9	1987	When bradykinin was added to cells prelabeled with [3H]choline, the phospholipase A2 products lysophosphatidylcholine and glycerophosphocholine were generated.	[3h]choline	51-62	kininogen 1	Homo sapiens	5-15
2888113-9	1987	When bradykinin was added to cells prelabeled with [3H]choline, the phospholipase A2 products lysophosphatidylcholine and glycerophosphocholine were generated.	Lysophosphatidylcholines	94-117	kininogen 1	Homo sapiens	5-15
2888113-9	1987	When bradykinin was added to cells prelabeled with [3H]choline, the phospholipase A2 products lysophosphatidylcholine and glycerophosphocholine were generated.	Glycerylphosphorylcholine	122-143	kininogen 1	Homo sapiens	5-15
2888113-10	1987	In cells pretreated with dexamethasone, lysophosphatidylcholine and glycerophosphocholine formation induced by bradykinin were inhibited.	Dexamethasone	25-38	kininogen 1	Homo sapiens	111-121
2888113-10	1987	In cells pretreated with dexamethasone, lysophosphatidylcholine and glycerophosphocholine formation induced by bradykinin were inhibited.	Lysophosphatidylcholines	40-63	kininogen 1	Homo sapiens	111-121
2888113-10	1987	In cells pretreated with dexamethasone, lysophosphatidylcholine and glycerophosphocholine formation induced by bradykinin were inhibited.	Glycerylphosphorylcholine	68-89	kininogen 1	Homo sapiens	111-121
2888113-11	1987	Treatment of cells with phorbol ester enhanced bradykinin-induced formation of these metabolites.	Phorbol Esters	24-37	kininogen 1	Homo sapiens	47-57
2888113-12	1987	The data suggest that bradykinin receptors are coupled by GTP-binding proteins to both phospholipase C and phospholipase A2 and that phospholipase A2 is the enzyme that catalyzes release of arachidonate for prostaglandin synthesis.	Guanosine Triphosphate	58-61	kininogen 1	Homo sapiens	22-32
2888113-12	1987	The data suggest that bradykinin receptors are coupled by GTP-binding proteins to both phospholipase C and phospholipase A2 and that phospholipase A2 is the enzyme that catalyzes release of arachidonate for prostaglandin synthesis.	Arachidonic Acid	190-202	kininogen 1	Homo sapiens	22-32
2888113-12	1987	The data suggest that bradykinin receptors are coupled by GTP-binding proteins to both phospholipase C and phospholipase A2 and that phospholipase A2 is the enzyme that catalyzes release of arachidonate for prostaglandin synthesis.	Prostaglandins	207-220	kininogen 1	Homo sapiens	22-32
3113307-4	1987	Radicals from the PGH synthase pathway are produced in vivo during topical application of arachidonate or bradykinin, a polypeptide that releases endogenous arachidonate from tissues.	Arachidonic Acid	157-169	kininogen 1	Homo sapiens	106-116
3496338-13	1987	Stimulation of 32P-labeled serum-deprived fibroblasts with serum, individual growth factors (bradykinin, vasopressin, and epidermal growth factor), or Ca2+ ionophores resulted in a rapid 2- to 10-fold increase in the phosphorylation of Mr 100,000 as determined by immunoprecipitation using polyclonal antibodies.	Phosphorus-32	15-18	kininogen 1	Homo sapiens	93-103
3496879-0	1987	Bradykinin-stimulated changes in inositol phosphate mass in renal papillary collecting tubule cells.	Inositol Phosphates	33-51	kininogen 1	Homo sapiens	0-10
3496879-1	1987	The effect of bradykinin on changes in the chemical levels of myo-inositol polyphosphates in renal papillary collecting tubules was investigated.	myo-inositol polyphosphates	62-89	kininogen 1	Homo sapiens	14-24
3496879-3	1987	Bradykinin induced increases in myo-inositol mono-, bis-, and trisphosphate which were both time and concentration dependent.	myo-inositol mono-, bis-, and trisphosphate	32-75	kininogen 1	Homo sapiens	0-10
3496879-6	1987	This study also confirms, in freshly isolated renal tubules, observations regarding bradykinin-induced phosphatidylinositol bisphosphate hydrolysis made previously in radiolabeled cultures.	phosphatidylinositol bisphosphate	103-136	kininogen 1	Homo sapiens	84-94
3300283-2	1987	Work using classical paper chromatographic techniques for detecting free amino acids indicated that the octapeptide, des-(Arg9)-bradykinin, enters these cells and its amino-terminal arginine residue is released by cytosolic aminopeptidase-P.	Arginine	182-190	kininogen 1	Homo sapiens	128-138
3300283-3	1987	We have used 1H NMR to monitor directly the release of arginine from bradykinin.	Hydrogen	13-15	kininogen 1	Homo sapiens	69-79
3300283-3	1987	We have used 1H NMR to monitor directly the release of arginine from bradykinin.	Arginine	55-63	kininogen 1	Homo sapiens	69-79
3663107-0	1987	Inositol phosphate metabolism in bradykinin-stimulated human A431 carcinoma cells.	Inositol Phosphates	0-18	kininogen 1	Homo sapiens	33-43
3663107-2	1987	Stimulation of human A431 epidermoid carcinoma cells by bradykinin causes a very rapid release of inositol phosphates and a transient rise in cytoplasmic free Ca2+ concentration ([Ca2+]i).	Inositol Phosphates	98-117	kininogen 1	Homo sapiens	56-66
3663107-3	1987	Bradykinin-induced inositol phosphate formation is half-maximal at a concentration of 4 nM and is not affected by pertussis toxin.	Inositol Phosphates	19-37	kininogen 1	Homo sapiens	0-10
3663107-7	1987	After a lag period, bradykinin also induces a massive accumulation of Ins(1,3,4)P3 and inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4].	Ins(1,3,4)P3	70-82	kininogen 1	Homo sapiens	20-30
3663107-7	1987	After a lag period, bradykinin also induces a massive accumulation of Ins(1,3,4)P3 and inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4].	inositol-1,3,4,5-tetrakisphosphate	87-121	kininogen 1	Homo sapiens	20-30
3663107-7	1987	After a lag period, bradykinin also induces a massive accumulation of Ins(1,3,4)P3 and inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4].	inositol-1,3,4,5-tetrakisphosphate	123-137	kininogen 1	Homo sapiens	20-30
3474045-0	1987	Identification of 13,14-dihydro-15-oxo-prostaglandin F2 alpha in the circulation during infusions of bradykinin and prostaglandin E2 in man.	13,14-dihydro-15-oxo-prostaglandin f2	18-55	kininogen 1	Homo sapiens	101-111
3474045-2	1987	13,14-Dihydro-15-oxo-PGF2 alpha was identified in plasma samples obtained during intravenous infusions of bradykinin and PGE2 but not during infusions of PGD2 or saline.	13,14-dihydro-15-oxo-pgf2	0-25	kininogen 1	Homo sapiens	106-116
3474045-4	1987	Bradykinin increased plasma concentrations of 13,14-dihydro-15-oxo-PGF2 alpha from baseline values in the range less than 5-10 pg ml-1 to 28-403 pg ml-1.	13,14-dihydro-15-oxo-pgf2	46-71	kininogen 1	Homo sapiens	0-10
3474045-7	1987	We conclude that bradykinin-stimulated 13,14-dihydro-15-oxo-PGF2 alpha may be derived from PGE2 or PGF2 alpha.	13,14-dihydro-15-oxo-pgf2	39-64	kininogen 1	Homo sapiens	17-27
3474045-7	1987	We conclude that bradykinin-stimulated 13,14-dihydro-15-oxo-PGF2 alpha may be derived from PGE2 or PGF2 alpha.	Dinoprostone	91-95	kininogen 1	Homo sapiens	17-27
3474045-7	1987	We conclude that bradykinin-stimulated 13,14-dihydro-15-oxo-PGF2 alpha may be derived from PGE2 or PGF2 alpha.	Dinoprost	60-64	kininogen 1	Homo sapiens	17-27
3474045-8	1987	The possibility that these prostaglandins are synthesized by stimulation of microvascular endothelium during bradykinin infusion is discussed.	Prostaglandins	27-41	kininogen 1	Homo sapiens	109-119
2435852-9	1987	Bradykinin stimulated the synthesis of inositol-1,4-bisphosphate and inositol-1,4,5-trisphosphate.	inositol 1,4-bis(phosphate)	39-64	kininogen 1	Homo sapiens	0-10
2435852-9	1987	Bradykinin stimulated the synthesis of inositol-1,4-bisphosphate and inositol-1,4,5-trisphosphate.	Inositol 1,4,5-Trisphosphate	69-97	kininogen 1	Homo sapiens	0-10
3596900-6	1987	Bradykinin and [AIB7]-BK adopt similar hydrogen bonded conformations in TFE, apparently with a contribution from a beta-turn involving their common Arg1-Pro2-Pro3-Gly4 moiety.	Polytetrafluoroethylene	72-75	kininogen 1	Homo sapiens	0-10
3039382-6	1987	1,10-phenanthroline did attenuate breakdown of bradykinin but this was found not to be significant compared with controls.	1,10-phenanthroline	0-19	kininogen 1	Homo sapiens	47-57
3552749-4	1987	Bradykinin stimulated sperm motility and velocity at 22 degrees C and at 33 degrees C. However, it did not stimulate sperm motility at 37 degrees C. With 1.10 phenantroline, the effect of bradykinin on sperm motility was detected.	1,10-phenanthroline	159-172	kininogen 1	Homo sapiens	188-198
3596900-1	1987	study of the solution conformation of bradykinin analogs containing alpha-aminoisobutyric acid.	2-aminoisobutyric acid	68-94	kininogen 1	Homo sapiens	38-48
3596900-2	1987	The conformation in aqueous solution of several alpha-aminoisobutyric acid (AIB)-containing analogs of bradykinin (BK) has been probed by complementary CD and 1H n.m.r.	2-aminoisobutyric acid	48-74	kininogen 1	Homo sapiens	103-113
3596900-2	1987	The conformation in aqueous solution of several alpha-aminoisobutyric acid (AIB)-containing analogs of bradykinin (BK) has been probed by complementary CD and 1H n.m.r.	2-aminoisobutyric acid	48-74	kininogen 1	Homo sapiens	115-117
3596900-2	1987	The conformation in aqueous solution of several alpha-aminoisobutyric acid (AIB)-containing analogs of bradykinin (BK) has been probed by complementary CD and 1H n.m.r.	2-aminoisobutyric acid	76-79	kininogen 1	Homo sapiens	103-113
3596900-2	1987	The conformation in aqueous solution of several alpha-aminoisobutyric acid (AIB)-containing analogs of bradykinin (BK) has been probed by complementary CD and 1H n.m.r.	2-aminoisobutyric acid	76-79	kininogen 1	Homo sapiens	115-117
3596900-2	1987	The conformation in aqueous solution of several alpha-aminoisobutyric acid (AIB)-containing analogs of bradykinin (BK) has been probed by complementary CD and 1H n.m.r.	Cadmium	152-154	kininogen 1	Homo sapiens	103-113
3596900-2	1987	The conformation in aqueous solution of several alpha-aminoisobutyric acid (AIB)-containing analogs of bradykinin (BK) has been probed by complementary CD and 1H n.m.r.	Cadmium	152-154	kininogen 1	Homo sapiens	115-117
3596900-2	1987	The conformation in aqueous solution of several alpha-aminoisobutyric acid (AIB)-containing analogs of bradykinin (BK) has been probed by complementary CD and 1H n.m.r.	Hydrogen	159-161	kininogen 1	Homo sapiens	103-113
3596900-2	1987	The conformation in aqueous solution of several alpha-aminoisobutyric acid (AIB)-containing analogs of bradykinin (BK) has been probed by complementary CD and 1H n.m.r.	Hydrogen	159-161	kininogen 1	Homo sapiens	115-117
3596900-6	1987	Bradykinin and [AIB7]-BK adopt similar hydrogen bonded conformations in TFE, apparently with a contribution from a beta-turn involving their common Arg1-Pro2-Pro3-Gly4 moiety.	Hydrogen	39-47	kininogen 1	Homo sapiens	0-10
3596900-6	1987	Bradykinin and [AIB7]-BK adopt similar hydrogen bonded conformations in TFE, apparently with a contribution from a beta-turn involving their common Arg1-Pro2-Pro3-Gly4 moiety.	Hydrogen	39-47	kininogen 1	Homo sapiens	22-24
3596900-6	1987	Bradykinin and [AIB7]-BK adopt similar hydrogen bonded conformations in TFE, apparently with a contribution from a beta-turn involving their common Arg1-Pro2-Pro3-Gly4 moiety.	Polytetrafluoroethylene	72-75	kininogen 1	Homo sapiens	22-24
3596900-6	1987	Bradykinin and [AIB7]-BK adopt similar hydrogen bonded conformations in TFE, apparently with a contribution from a beta-turn involving their common Arg1-Pro2-Pro3-Gly4 moiety.	glycyl-glycyl-glycyl-glycine	163-167	kininogen 1	Homo sapiens	0-10
3596900-6	1987	Bradykinin and [AIB7]-BK adopt similar hydrogen bonded conformations in TFE, apparently with a contribution from a beta-turn involving their common Arg1-Pro2-Pro3-Gly4 moiety.	glycyl-glycyl-glycyl-glycine	163-167	kininogen 1	Homo sapiens	22-24
3037391-4	1987	The B2-receptor antagonist Thi5,8, D-Phe7-BK but not the B1-receptor antagonist des-Arg9-Leu8-BK selectively blocked BK-induced relaxations of the human basilar artery.	thi5	27-31	kininogen 1	Homo sapiens	42-44
3101745-6	1987	Production of prostaglandins from endogenous arachidonic acid, released by either bradykinin or the ionophore A23187, was also inhibited by H2O2 exposure, however, full recovery of this stimulated synthesis occurred within 3 h. Cycloheximide pre-treatment completely inhibited recovery of bradykinin-induced prostaglandin I2 synthesis.	Prostaglandins	14-28	kininogen 1	Homo sapiens	82-92
3102480-1	1987	Exposure of A431 human epidermoid carcinoma cells to epidermal growth factor (EGF), bradykinin, and histamine resulted in a time- and concentration-dependent accumulation of the inositol phosphates (InsP) inositol monophosphate, inositol bisphosphate, and inositol trisphosphate (InsP3).	Inositol Phosphates	178-197	kininogen 1	Homo sapiens	84-94
3102480-1	1987	Exposure of A431 human epidermoid carcinoma cells to epidermal growth factor (EGF), bradykinin, and histamine resulted in a time- and concentration-dependent accumulation of the inositol phosphates (InsP) inositol monophosphate, inositol bisphosphate, and inositol trisphosphate (InsP3).	insp) inositol monophosphate	199-227	kininogen 1	Homo sapiens	84-94
3102480-1	1987	Exposure of A431 human epidermoid carcinoma cells to epidermal growth factor (EGF), bradykinin, and histamine resulted in a time- and concentration-dependent accumulation of the inositol phosphates (InsP) inositol monophosphate, inositol bisphosphate, and inositol trisphosphate (InsP3).	inositol bisphosphate	229-250	kininogen 1	Homo sapiens	84-94
3102480-1	1987	Exposure of A431 human epidermoid carcinoma cells to epidermal growth factor (EGF), bradykinin, and histamine resulted in a time- and concentration-dependent accumulation of the inositol phosphates (InsP) inositol monophosphate, inositol bisphosphate, and inositol trisphosphate (InsP3).	inositol 1,2,3-trisphosphate	256-278	kininogen 1	Homo sapiens	84-94
3102480-2	1987	Maximal concentrations of EGF (316 ng/ml; approximately 50 nM), bradykinin (1 microM), and histamine (1 mM) resulted in 3-, 6-, and 3-fold increases, respectively, in the amounts of inositol phosphates formed over a 10-min period.	Inositol Phosphates	182-201	kininogen 1	Homo sapiens	64-74
3102480-4	1987	EGF and bradykinin stimulated the rapid accumulation of the two isomers of InsP3, Ins(1,3,4)P3, and Ins(1,4,5)P3 as determined by high performance liquid chromatography analysis; maximal accumulation of Ins(1,4,5)P3 occurred within 15 s. EGF and bradykinin also stimulated a rapid (maximal levels attained within 30 s after addition of hormone) and a sustained 4- and 6-fold rise, respectively, in cytosolic free Ca2+ levels as measured by Fura-2 fluorescence.	Fura-2	440-446	kininogen 1	Homo sapiens	8-18
3102480-5	1987	EGF and bradykinin also produced a rapid, although transient, 3- and 5-fold increase, respectively, in cytosolic free Ca2+ after chelation of extracellular Ca2+ with 3 mM EGTA.	Egtazic Acid	171-175	kininogen 1	Homo sapiens	8-18
3643926-2	1987	Sequencing of the NH2-terminal region of the light chain reported herein identified the third kallikrein cleavage site of high molecular weight kininogen as Arg-437.	Arginine	157-160	kininogen 1	Homo sapiens	122-153
3643926-10	1987	These studies indicate that histidines participate in surface binding and that free carboxyl groups and tryptophan side chains are involved in binding of high molecular weight kininogen to other clotting factors.	Tryptophan	104-114	kininogen 1	Homo sapiens	154-185
3101745-6	1987	Production of prostaglandins from endogenous arachidonic acid, released by either bradykinin or the ionophore A23187, was also inhibited by H2O2 exposure, however, full recovery of this stimulated synthesis occurred within 3 h. Cycloheximide pre-treatment completely inhibited recovery of bradykinin-induced prostaglandin I2 synthesis.	Prostaglandins	14-28	kininogen 1	Homo sapiens	289-299
3101745-6	1987	Production of prostaglandins from endogenous arachidonic acid, released by either bradykinin or the ionophore A23187, was also inhibited by H2O2 exposure, however, full recovery of this stimulated synthesis occurred within 3 h. Cycloheximide pre-treatment completely inhibited recovery of bradykinin-induced prostaglandin I2 synthesis.	Arachidonic Acid	45-61	kininogen 1	Homo sapiens	82-92
3101745-6	1987	Production of prostaglandins from endogenous arachidonic acid, released by either bradykinin or the ionophore A23187, was also inhibited by H2O2 exposure, however, full recovery of this stimulated synthesis occurred within 3 h. Cycloheximide pre-treatment completely inhibited recovery of bradykinin-induced prostaglandin I2 synthesis.	Arachidonic Acid	45-61	kininogen 1	Homo sapiens	289-299
3101745-6	1987	Production of prostaglandins from endogenous arachidonic acid, released by either bradykinin or the ionophore A23187, was also inhibited by H2O2 exposure, however, full recovery of this stimulated synthesis occurred within 3 h. Cycloheximide pre-treatment completely inhibited recovery of bradykinin-induced prostaglandin I2 synthesis.	Hydrogen Peroxide	140-144	kininogen 1	Homo sapiens	82-92
3101745-6	1987	Production of prostaglandins from endogenous arachidonic acid, released by either bradykinin or the ionophore A23187, was also inhibited by H2O2 exposure, however, full recovery of this stimulated synthesis occurred within 3 h. Cycloheximide pre-treatment completely inhibited recovery of bradykinin-induced prostaglandin I2 synthesis.	Hydrogen Peroxide	140-144	kininogen 1	Homo sapiens	289-299
2437774-4	1987	Dimethyl sulfoxide was also active in inhibiting histamine release induced by other polyamines such as bradykinin, polymyxin B and protamine, by concanavalin A and dextran, by ionophore A23187 and by three anthracyclines, doxorubicin, daunomycin and epirubicin.	Dimethyl Sulfoxide	0-18	kininogen 1	Homo sapiens	103-113
3588345-6	1987	CGRP, bradykinin, and SP regularly dilated, in a concentration-dependent way, both arteries and veins precontracted with prostaglandin F2 alpha or uridine triphosphate.	Dinoprost	121-143	kininogen 1	Homo sapiens	6-16
3588345-6	1987	CGRP, bradykinin, and SP regularly dilated, in a concentration-dependent way, both arteries and veins precontracted with prostaglandin F2 alpha or uridine triphosphate.	Uridine Triphosphate	147-167	kininogen 1	Homo sapiens	6-16
2437774-4	1987	Dimethyl sulfoxide was also active in inhibiting histamine release induced by other polyamines such as bradykinin, polymyxin B and protamine, by concanavalin A and dextran, by ionophore A23187 and by three anthracyclines, doxorubicin, daunomycin and epirubicin.	Histamine	49-58	kininogen 1	Homo sapiens	103-113
2438581-0	1987	Muscarinic M1 receptors in the lateral septal area mediate cardiovascular responses to cholinergic agonists and bradykinin: supersensitivity induced by chronic treatment with atropine.	Atropine	175-183	kininogen 1	Homo sapiens	112-122
3030335-1	1987	Bradykinin is degraded in human plasma by a carboxypeptidase to yield desArg9-bradykinin (DBK) which is then digested by angiotensin-converting enzyme (ACE) to the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	Arginine	73-76	kininogen 1	Homo sapiens	0-10
3030335-1	1987	Bradykinin is degraded in human plasma by a carboxypeptidase to yield desArg9-bradykinin (DBK) which is then digested by angiotensin-converting enzyme (ACE) to the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	Arginine	73-76	kininogen 1	Homo sapiens	78-88
3030335-1	1987	Bradykinin is degraded in human plasma by a carboxypeptidase to yield desArg9-bradykinin (DBK) which is then digested by angiotensin-converting enzyme (ACE) to the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	pro-pro-gly-phe	181-196	kininogen 1	Homo sapiens	0-10
3030335-1	1987	Bradykinin is degraded in human plasma by a carboxypeptidase to yield desArg9-bradykinin (DBK) which is then digested by angiotensin-converting enzyme (ACE) to the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	pro-pro-gly-phe	181-196	kininogen 1	Homo sapiens	78-88
3030335-1	1987	Bradykinin is degraded in human plasma by a carboxypeptidase to yield desArg9-bradykinin (DBK) which is then digested by angiotensin-converting enzyme (ACE) to the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	Serine	216-219	kininogen 1	Homo sapiens	0-10
3030335-1	1987	Bradykinin is degraded in human plasma by a carboxypeptidase to yield desArg9-bradykinin (DBK) which is then digested by angiotensin-converting enzyme (ACE) to the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	Serine	216-219	kininogen 1	Homo sapiens	78-88
3030335-1	1987	Bradykinin is degraded in human plasma by a carboxypeptidase to yield desArg9-bradykinin (DBK) which is then digested by angiotensin-converting enzyme (ACE) to the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	H-Pro-Phe-OH	220-227	kininogen 1	Homo sapiens	0-10
3030335-1	1987	Bradykinin is degraded in human plasma by a carboxypeptidase to yield desArg9-bradykinin (DBK) which is then digested by angiotensin-converting enzyme (ACE) to the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	H-Pro-Phe-OH	220-227	kininogen 1	Homo sapiens	78-88
2438581-5	1987	Pirenzepine, a M1 muscarinic blocking agent, inhibited completely the effect of both muscarinic agonists and bradykinin on cardiovascular activity.	Pirenzepine	0-11	kininogen 1	Homo sapiens	109-119
3104868-1	1987	In human skin fibroblasts, exposed during 24 h to molsidomine and SIN-1, the functional status of prostaglandin synthesis is altered in so far, that the bradykinin stimulation of thromboxane is inhibited whereas the production of other PG"s is not different from control.	Molsidomine	50-61	kininogen 1	Homo sapiens	153-163
3104868-1	1987	In human skin fibroblasts, exposed during 24 h to molsidomine and SIN-1, the functional status of prostaglandin synthesis is altered in so far, that the bradykinin stimulation of thromboxane is inhibited whereas the production of other PG"s is not different from control.	Prostaglandins	98-111	kininogen 1	Homo sapiens	153-163
3104868-1	1987	In human skin fibroblasts, exposed during 24 h to molsidomine and SIN-1, the functional status of prostaglandin synthesis is altered in so far, that the bradykinin stimulation of thromboxane is inhibited whereas the production of other PG"s is not different from control.	Thromboxanes	179-190	kininogen 1	Homo sapiens	153-163
2829599-2	1987	In case of cultured EC, AI and bradykinin (BK) increased PGI2 generation and at the same time ACE released from EC, however angiotensin II (AII) did not show any effect on both of them.	Epoprostenol	57-61	kininogen 1	Homo sapiens	31-41
2829599-2	1987	In case of cultured EC, AI and bradykinin (BK) increased PGI2 generation and at the same time ACE released from EC, however angiotensin II (AII) did not show any effect on both of them.	Epoprostenol	57-61	kininogen 1	Homo sapiens	43-45
2829599-3	1987	When the EC were pretreated by captopril both of basal PGI2 production and ACE activity were reduced but the enhancing effects on PGI2 generation by AI or BK were preserved.	Captopril	31-40	kininogen 1	Homo sapiens	155-157
2829599-9	1987	(3) It was speculated that the enhanced PGI2 generation by AI or BK might be modulated through their activating effect on ACE as an autoregulatory mechanism.	Epoprostenol	40-44	kininogen 1	Homo sapiens	65-67
3541715-4	1987	Bradykinin was approximately 10 times more potent than histamine and methacholine, and there was a significant correlation between the subjects" sensitivity to histamine and bradykinin.	Histamine	160-169	kininogen 1	Homo sapiens	0-10
3304302-3	1987	Bradykinin stimulation of cells that had been preexposed to the drug induced a continuous increase in PG-production as compared to controls, despite the absence of the drug.	Prostaglandins	102-105	kininogen 1	Homo sapiens	0-10
3304302-4	1987	In addition, an acute 5-min exposure to dipyridamole produced an increased thromboxane production, but no consistent changes of PGI2 or PGE2, and it inhibited significantly and dose-dependently the comcomitant bradykinin stimulated production of all the examined PG"s.	Dipyridamole	40-52	kininogen 1	Homo sapiens	210-220
3028457-0	1987	Effect of enalapril on the skin response to bradykinin in man.	Enalapril	10-19	kininogen 1	Homo sapiens	44-54
3028457-3	1987	Three hours later bradykinin was injected into the skin of the back in doses increasing from 10(-11) to 10(-9) M. Enalapril increased the bradykinin-induced wheal.	Enalapril	114-123	kininogen 1	Homo sapiens	18-28
3028457-3	1987	Three hours later bradykinin was injected into the skin of the back in doses increasing from 10(-11) to 10(-9) M. Enalapril increased the bradykinin-induced wheal.	Enalapril	114-123	kininogen 1	Homo sapiens	138-148
3028458-1	1987	The effect of a potent inhibitor of angiotensin-converting enzyme, ramipril, was studied on both inhaled histamine and bradykinin-induced bronchoconstriction in six male, normotensive, mild asthmatic subjects.	Ramipril	67-75	kininogen 1	Homo sapiens	119-129
3038403-2	1987	Angiotensin I (AI) or bradykinin (BK) increased PGI2 generation and ACE activity, while the ACE inhibitor, captopril decreased both of them, and angiotensin II (AII) did not show any effect.	Epoprostenol	48-52	kininogen 1	Homo sapiens	22-32
3038403-2	1987	Angiotensin I (AI) or bradykinin (BK) increased PGI2 generation and ACE activity, while the ACE inhibitor, captopril decreased both of them, and angiotensin II (AII) did not show any effect.	Epoprostenol	48-52	kininogen 1	Homo sapiens	34-36
3038403-3	1987	The increasing rate of PGI2 generation induced by AI or BK was not affected by the pretreatment with captopril.	Epoprostenol	23-27	kininogen 1	Homo sapiens	56-58
3038403-4	1987	These results suggest that the accumulation of AI or BK via the inhibition of ACE by captopril did not cause the enhancement of PGI2 generation.	Captopril	85-94	kininogen 1	Homo sapiens	53-55
3038403-5	1987	Rather, it was proposed that the enhanced PGI2 generation by AI or BK might be regulated by ACE activation derived from these substances, as an autoregulation mechanism.	Epoprostenol	42-46	kininogen 1	Homo sapiens	67-69
3301083-6	1987	Captopril increased circulating bradykinin (P less than 0.05), prostaglandin E2 (P less than 0.05) and 6-keto-prostaglandin F1 alpha (P less than 0.05).	Captopril	0-9	kininogen 1	Homo sapiens	32-42
3541715-4	1987	Bradykinin was approximately 10 times more potent than histamine and methacholine, and there was a significant correlation between the subjects" sensitivity to histamine and bradykinin.	Histamine	160-169	kininogen 1	Homo sapiens	174-184
3541715-8	1987	However, ipratropium bromide (0.25 mg by nebulizer) significantly inhibited the effect of bradykinin, the PD35 being 0.8 mumol (range, 0.16 to 3.4) and 0.15 mumol (range, 0.047 to 1.15) after active dose and placebo, respectively (p less than 0.05).	Ipratropium	9-28	kininogen 1	Homo sapiens	90-100
3541715-9	1987	Likewise, cromolyn sodium (40 mg dry powder) also significantly reduced response to bradykinin, with a PD35 of 0.04 mumol (range, 0.13 to 0.31) after placebo and 0.39 mumol (range, 0.05 to 4.45) after SCG (p less than 0.05).	Cromolyn Sodium	10-25	kininogen 1	Homo sapiens	84-94
3541715-11	1987	Bradykinin at 10(-4) caused only 21.5 +/- 5.5% of the maximal carbamylcholine contraction in 11 of 18 airways.	Carbachol	62-77	kininogen 1	Homo sapiens	0-10
3816966-4	1986	Indomethacin pretreatment abolished the BK effect.	Indomethacin	0-12	kininogen 1	Homo sapiens	40-42
2442780-4	1987	The inhibition of water flow by bradykinin was enhanced by captopril.	Water	18-23	kininogen 1	Homo sapiens	32-42
2442780-4	1987	The inhibition of water flow by bradykinin was enhanced by captopril.	Captopril	59-68	kininogen 1	Homo sapiens	32-42
2442780-5	1987	These data indicate that captopril increased the amount of bradykinin in toad bladder cells resulting in the production of PGE2 which inhibited the increase in water flow induced by vasopressin.	Captopril	25-34	kininogen 1	Homo sapiens	59-69
2442780-5	1987	These data indicate that captopril increased the amount of bradykinin in toad bladder cells resulting in the production of PGE2 which inhibited the increase in water flow induced by vasopressin.	Dinoprostone	123-127	kininogen 1	Homo sapiens	59-69
2442780-7	1987	Thus, it was concluded that captopril inhibits the vasopressin-stimulated water flow indirectly by inhibiting the degradation of bradykinin and thereby enhancing the production of PGE2, and directly at a site following the production of cyclic adenosine monophosphate by vasopressin.	Captopril	28-37	kininogen 1	Homo sapiens	129-139
3494310-8	1987	Quantitation of cleaved and single-chain HMWK is possible using dilutions of dextran sulfate-activated NHP on unreduced SDS-PAGE and dilutions of unactivated NHP with reduced SDS-PAGE as standards.	Dextran Sulfate	77-92	kininogen 1	Homo sapiens	41-45
3102270-5	1986	Prostaglandin E2 synthesis and release by these HTM cells from two different individuals could be stimulated by bradykinin, arachidonic acid and the calcium ionophore, A23187.	Dinoprostone	0-16	kininogen 1	Homo sapiens	112-122
3025093-2	1986	Carrageenan-induced inflammation has been attributed to a variety of autocoids including histamine, bradykinin, complement, superoxide, and prostaglandins.	Carrageenan	0-11	kininogen 1	Homo sapiens	100-110
3827839-9	1986	Bradykinin and 5-hydroxytryptamine also provoked inositol phosphate accumulation in WRK 1 cells.	Inositol Phosphates	49-67	kininogen 1	Homo sapiens	0-10
3771575-0	1986	Bradykinin stimulation of inositol polyphosphate production in porcine aortic endothelial cells.	Phytic Acid	26-48	kininogen 1	Homo sapiens	0-10
3771575-1	1986	Bradykinin stimulation of inositol polyphosphate production was followed using [3H]inositol-labeled porcine aortic endothelial cells grown in culture.	Phytic Acid	26-48	kininogen 1	Homo sapiens	0-10
3771575-1	1986	Bradykinin stimulation of inositol polyphosphate production was followed using [3H]inositol-labeled porcine aortic endothelial cells grown in culture.	Tritium	80-82	kininogen 1	Homo sapiens	0-10
3771575-1	1986	Bradykinin stimulation of inositol polyphosphate production was followed using [3H]inositol-labeled porcine aortic endothelial cells grown in culture.	Inositol	26-34	kininogen 1	Homo sapiens	0-10
3771575-6	1986	These data suggest that bradykinin stimulates phospholipase C metabolism of PIPP to IP3 by a mechanism which does not contain a pertussis toxin sensitive GTP-binding protein.	Inositol 1,4,5-Trisphosphate	84-87	kininogen 1	Homo sapiens	24-34
3827839-10	1986	The effects of sub-optimal concentrations of bradykinin and vasopressin upon inositol phosphate accumulation were additive, but those of optimal concentrations of the hormones were not.	Inositol Phosphates	77-95	kininogen 1	Homo sapiens	45-55
3093068-5	1986	With adherent cells in the absence of thioglycolate, radioimmunoassayable PGE2 was stimulated by epinephrine less than 12-O-tetradecanoylphorbol-13-acetate = thrombin less than bradykinin = A23187 much less than arachidonic acid.	Dinoprostone	74-78	kininogen 1	Homo sapiens	177-187
3024076-0	1986	Phosphatidylinositol turnover in neuroblastoma cells: regulation by bradykinin, acetylcholine, but not mu- and delta-opioid receptors.	Phosphatidylinositols	0-20	kininogen 1	Homo sapiens	68-78
3806937-0	1986	[Enflurane reduces the inhibition of dorsal horn lamina V type neuronal activity induced by bradykinin injection into the femoral artery contralateral to the recording site].	Enflurane	1-10	kininogen 1	Homo sapiens	92-102
3021818-1	1986	Stimuli of prostacyclin (PGI2) biosynthesis such as thrombin, bradykinin, histamine, and A23187 increase guanosine 3",5"-cyclic monophosphate (cyclic GMP) levels in primary monolayer cultures of human umbilical vein endothelium by about twofold.	Epoprostenol	11-23	kininogen 1	Homo sapiens	62-72
3021818-1	1986	Stimuli of prostacyclin (PGI2) biosynthesis such as thrombin, bradykinin, histamine, and A23187 increase guanosine 3",5"-cyclic monophosphate (cyclic GMP) levels in primary monolayer cultures of human umbilical vein endothelium by about twofold.	Epoprostenol	25-29	kininogen 1	Homo sapiens	62-72
3021818-1	1986	Stimuli of prostacyclin (PGI2) biosynthesis such as thrombin, bradykinin, histamine, and A23187 increase guanosine 3",5"-cyclic monophosphate (cyclic GMP) levels in primary monolayer cultures of human umbilical vein endothelium by about twofold.	Cyclic GMP	105-141	kininogen 1	Homo sapiens	62-72
3562319-0	1986	Interaction of bradykinin with sodium dodecyl sulfate and certain acidic lipids.	Sodium Dodecyl Sulfate	31-53	kininogen 1	Homo sapiens	15-25
3562319-1	1986	The striking change in the circular dichroism (CD) of bradykinin (BK) occasioned by its interaction with sodium dodecyl sulfate (SDS) is evidently due in large part to a change in the conformation of the C-terminal tetrapeptide moiety of the hormone.	Sodium Dodecyl Sulfate	105-127	kininogen 1	Homo sapiens	54-64
3562319-1	1986	The striking change in the circular dichroism (CD) of bradykinin (BK) occasioned by its interaction with sodium dodecyl sulfate (SDS) is evidently due in large part to a change in the conformation of the C-terminal tetrapeptide moiety of the hormone.	Sodium Dodecyl Sulfate	105-127	kininogen 1	Homo sapiens	66-68
3562319-1	1986	The striking change in the circular dichroism (CD) of bradykinin (BK) occasioned by its interaction with sodium dodecyl sulfate (SDS) is evidently due in large part to a change in the conformation of the C-terminal tetrapeptide moiety of the hormone.	Sodium Dodecyl Sulfate	129-132	kininogen 1	Homo sapiens	54-64
3562319-1	1986	The striking change in the circular dichroism (CD) of bradykinin (BK) occasioned by its interaction with sodium dodecyl sulfate (SDS) is evidently due in large part to a change in the conformation of the C-terminal tetrapeptide moiety of the hormone.	Sodium Dodecyl Sulfate	129-132	kininogen 1	Homo sapiens	66-68
3562319-4	1986	The cooperative nature of the interaction is attributed to the SDS-promoted aggregation of BK.	Sodium Dodecyl Sulfate	63-66	kininogen 1	Homo sapiens	91-93
3562319-6	1986	CD reveals that BK also interacts with acidic lipids which bear a net electrical charge (e.g., cerebroside sulfate and phosphatidyl inositol) but not with lipids bearing no net charge (e.g., cerebroside and phosphatidyl choline).	cerebroside sulfate	95-114	kininogen 1	Homo sapiens	16-18
3562319-6	1986	CD reveals that BK also interacts with acidic lipids which bear a net electrical charge (e.g., cerebroside sulfate and phosphatidyl inositol) but not with lipids bearing no net charge (e.g., cerebroside and phosphatidyl choline).	Phosphatidylinositols	119-140	kininogen 1	Homo sapiens	16-18
3562319-6	1986	CD reveals that BK also interacts with acidic lipids which bear a net electrical charge (e.g., cerebroside sulfate and phosphatidyl inositol) but not with lipids bearing no net charge (e.g., cerebroside and phosphatidyl choline).	Cerebrosides	95-106	kininogen 1	Homo sapiens	16-18
3562319-6	1986	CD reveals that BK also interacts with acidic lipids which bear a net electrical charge (e.g., cerebroside sulfate and phosphatidyl inositol) but not with lipids bearing no net charge (e.g., cerebroside and phosphatidyl choline).	Phosphatidylcholines	207-227	kininogen 1	Homo sapiens	16-18
3025938-1	1986	Monosodium urate (MSU)-induced synovitis in the dog"s stifle (knee joint) is similar to an acute gouty attack in man in which a loss of function of the joint correlates with massive influx of neutrophils and the release of an assortment of inflammatory mediators (e.g. histamine, bradykinin, lysosomal enzymes, complement and eicosanoids) into the synovial space.	Uric Acid	0-16	kininogen 1	Homo sapiens	280-290
3025938-1	1986	Monosodium urate (MSU)-induced synovitis in the dog"s stifle (knee joint) is similar to an acute gouty attack in man in which a loss of function of the joint correlates with massive influx of neutrophils and the release of an assortment of inflammatory mediators (e.g. histamine, bradykinin, lysosomal enzymes, complement and eicosanoids) into the synovial space.	Uric Acid	18-21	kininogen 1	Homo sapiens	280-290
3018483-0	1986	Effects of nitroprusside on the bradykinin responsiveness of human fibroblasts.	Nitroprusside	11-24	kininogen 1	Homo sapiens	32-42
3018483-1	1986	The effects of agents that cause vasodilatation and hypotension, such as endogenously produced bradykinin (BK) or the drug nitroprusside (NP), appear to result from effects on cyclic nucleotides (cGMP, cAMP) and arachidonate metabolism.	Nucleotides, Cyclic	176-194	kininogen 1	Homo sapiens	95-105
3018483-1	1986	The effects of agents that cause vasodilatation and hypotension, such as endogenously produced bradykinin (BK) or the drug nitroprusside (NP), appear to result from effects on cyclic nucleotides (cGMP, cAMP) and arachidonate metabolism.	Nucleotides, Cyclic	176-194	kininogen 1	Homo sapiens	107-109
3018483-1	1986	The effects of agents that cause vasodilatation and hypotension, such as endogenously produced bradykinin (BK) or the drug nitroprusside (NP), appear to result from effects on cyclic nucleotides (cGMP, cAMP) and arachidonate metabolism.	Cyclic GMP	196-200	kininogen 1	Homo sapiens	95-105
3018483-1	1986	The effects of agents that cause vasodilatation and hypotension, such as endogenously produced bradykinin (BK) or the drug nitroprusside (NP), appear to result from effects on cyclic nucleotides (cGMP, cAMP) and arachidonate metabolism.	Cyclic GMP	196-200	kininogen 1	Homo sapiens	107-109
3018483-1	1986	The effects of agents that cause vasodilatation and hypotension, such as endogenously produced bradykinin (BK) or the drug nitroprusside (NP), appear to result from effects on cyclic nucleotides (cGMP, cAMP) and arachidonate metabolism.	Cyclic AMP	202-206	kininogen 1	Homo sapiens	95-105
3018483-1	1986	The effects of agents that cause vasodilatation and hypotension, such as endogenously produced bradykinin (BK) or the drug nitroprusside (NP), appear to result from effects on cyclic nucleotides (cGMP, cAMP) and arachidonate metabolism.	Cyclic AMP	202-206	kininogen 1	Homo sapiens	107-109
3018483-1	1986	The effects of agents that cause vasodilatation and hypotension, such as endogenously produced bradykinin (BK) or the drug nitroprusside (NP), appear to result from effects on cyclic nucleotides (cGMP, cAMP) and arachidonate metabolism.	Arachidonic Acid	212-224	kininogen 1	Homo sapiens	95-105
3018483-1	1986	The effects of agents that cause vasodilatation and hypotension, such as endogenously produced bradykinin (BK) or the drug nitroprusside (NP), appear to result from effects on cyclic nucleotides (cGMP, cAMP) and arachidonate metabolism.	Arachidonic Acid	212-224	kininogen 1	Homo sapiens	107-109
3018483-3	1986	Addition of BK or NP to cultured human fibroblasts caused a rapid increase in cGMP.	Cyclic GMP	78-82	kininogen 1	Homo sapiens	12-14
3018483-5	1986	The increase in cGMP produced by BK reached a maximum at approximately 1 min and then fell; the rise with NP was more than 10 times that with BK.	Cyclic GMP	16-20	kininogen 1	Homo sapiens	33-35
3018483-5	1986	The increase in cGMP produced by BK reached a maximum at approximately 1 min and then fell; the rise with NP was more than 10 times that with BK.	Cyclic GMP	16-20	kininogen 1	Homo sapiens	142-144
3018483-6	1986	At 30 sec, cGMP content with NP plus BK was less than with NP alone.	Cyclic GMP	11-15	kininogen 1	Homo sapiens	37-39
3018483-7	1986	At later times, however, effects of BK and NP were slightly more than additive and maximal cGMP levels were reached at 90 sec.	Cyclic GMP	91-95	kininogen 1	Homo sapiens	36-38
3018483-8	1986	BK increased prostaglandin production by the fibroblasts; it is believed that the kinin-induced elevation in cAMP content is secondary to increased prostaglandin formation.	Prostaglandins	13-26	kininogen 1	Homo sapiens	0-2
3018483-8	1986	BK increased prostaglandin production by the fibroblasts; it is believed that the kinin-induced elevation in cAMP content is secondary to increased prostaglandin formation.	Cyclic AMP	109-113	kininogen 1	Homo sapiens	0-2
3018483-8	1986	BK increased prostaglandin production by the fibroblasts; it is believed that the kinin-induced elevation in cAMP content is secondary to increased prostaglandin formation.	Prostaglandins	148-161	kininogen 1	Homo sapiens	0-2
3018483-9	1986	NP caused a small, early increase in cAMP without significant effect on prostaglandin I2 (PGI2); after 2.5 min, effects on PGI2 and cAMP were greater with BK and NP than with BK alone.	Epoprostenol	123-127	kininogen 1	Homo sapiens	155-157
3018483-9	1986	NP caused a small, early increase in cAMP without significant effect on prostaglandin I2 (PGI2); after 2.5 min, effects on PGI2 and cAMP were greater with BK and NP than with BK alone.	Epoprostenol	123-127	kininogen 1	Homo sapiens	175-177
3018483-9	1986	NP caused a small, early increase in cAMP without significant effect on prostaglandin I2 (PGI2); after 2.5 min, effects on PGI2 and cAMP were greater with BK and NP than with BK alone.	Cyclic AMP	132-136	kininogen 1	Homo sapiens	155-157
3018483-11	1986	Increases in cAMP or PGI2 with BK or BK plus NP were blocked by indomethacin or ETYA.	Cyclic AMP	13-17	kininogen 1	Homo sapiens	31-33
3018483-11	1986	Increases in cAMP or PGI2 with BK or BK plus NP were blocked by indomethacin or ETYA.	Cyclic AMP	13-17	kininogen 1	Homo sapiens	37-39
3018483-11	1986	Increases in cAMP or PGI2 with BK or BK plus NP were blocked by indomethacin or ETYA.	Epoprostenol	21-25	kininogen 1	Homo sapiens	31-33
3018483-11	1986	Increases in cAMP or PGI2 with BK or BK plus NP were blocked by indomethacin or ETYA.	Epoprostenol	21-25	kininogen 1	Homo sapiens	37-39
3018483-11	1986	Increases in cAMP or PGI2 with BK or BK plus NP were blocked by indomethacin or ETYA.	Indomethacin	64-76	kininogen 1	Homo sapiens	31-33
3018483-11	1986	Increases in cAMP or PGI2 with BK or BK plus NP were blocked by indomethacin or ETYA.	Indomethacin	64-76	kininogen 1	Homo sapiens	37-39
3018483-11	1986	Increases in cAMP or PGI2 with BK or BK plus NP were blocked by indomethacin or ETYA.	5,8,11,14-Eicosatetraynoic Acid	80-84	kininogen 1	Homo sapiens	31-33
3018483-11	1986	Increases in cAMP or PGI2 with BK or BK plus NP were blocked by indomethacin or ETYA.	5,8,11,14-Eicosatetraynoic Acid	80-84	kininogen 1	Homo sapiens	37-39
3018483-12	1986	These effects of BK or BK plus NP on cAMP thus appear to be mediated through cyclooxygenase products of arachidonate metabolism.	Cyclic AMP	37-41	kininogen 1	Homo sapiens	17-19
3018483-12	1986	These effects of BK or BK plus NP on cAMP thus appear to be mediated through cyclooxygenase products of arachidonate metabolism.	Cyclic AMP	37-41	kininogen 1	Homo sapiens	23-25
3018483-12	1986	These effects of BK or BK plus NP on cAMP thus appear to be mediated through cyclooxygenase products of arachidonate metabolism.	Arachidonic Acid	104-116	kininogen 1	Homo sapiens	17-19
3018483-12	1986	These effects of BK or BK plus NP on cAMP thus appear to be mediated through cyclooxygenase products of arachidonate metabolism.	Arachidonic Acid	104-116	kininogen 1	Homo sapiens	23-25
3529950-11	1986	In these segments, synthesis of PGE2 is stimulated by bradykinin and to a somewhat more variable degree by vasopressin.	Dinoprostone	32-36	kininogen 1	Homo sapiens	54-64
3541940-9	1987	The IC50 values for bradykinin, diisopropylfluorophosphate (DFP), and N-benzyloxycarbonyl-Pro-Prolinal (Z-Pro-Prolinal) to inhibit Z-Gly-Pro-MCA hydrolysis by PPCE were 5.9 +/- 1.4 X 10(-7) M, 8.8 +/- 3.1 X 10(-7) and 7.9 +/- 0.3 X 10(-9) M respectively.	N-benzyloxycarbonylglycine	131-136	kininogen 1	Homo sapiens	20-30
3551924-1	1987	A high-Mr neutral endopeptidase-24.5 (NE) that cleaved bradykinin at the Phe5-Ser6 bond was purified to apparent homogeneity from human lung by (NH4)2SO4 fractionation, ion-exchange chromatography and gel filtration.	Ammonium Sulfate	144-153	kininogen 1	Homo sapiens	55-65
3730610-1	1986	Purified human high-mol-wt kininogen (HMWK), the cofactor of the contact phase of blood coagulation, migrated as a single band (approximately 110,000 mol wt) in a continuous buffer sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), but appeared as two separated bands (approximately 120,000 and 105,000 mol wt) when analyzed in a discontinuous buffer SDS-PAGE system.	Sodium Dodecyl Sulfate	181-203	kininogen 1	Homo sapiens	15-36
3730610-1	1986	Purified human high-mol-wt kininogen (HMWK), the cofactor of the contact phase of blood coagulation, migrated as a single band (approximately 110,000 mol wt) in a continuous buffer sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), but appeared as two separated bands (approximately 120,000 and 105,000 mol wt) when analyzed in a discontinuous buffer SDS-PAGE system.	Sodium Dodecyl Sulfate	181-203	kininogen 1	Homo sapiens	38-42
3730610-1	1986	Purified human high-mol-wt kininogen (HMWK), the cofactor of the contact phase of blood coagulation, migrated as a single band (approximately 110,000 mol wt) in a continuous buffer sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), but appeared as two separated bands (approximately 120,000 and 105,000 mol wt) when analyzed in a discontinuous buffer SDS-PAGE system.	polyacrylamide	204-218	kininogen 1	Homo sapiens	15-36
3730610-1	1986	Purified human high-mol-wt kininogen (HMWK), the cofactor of the contact phase of blood coagulation, migrated as a single band (approximately 110,000 mol wt) in a continuous buffer sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), but appeared as two separated bands (approximately 120,000 and 105,000 mol wt) when analyzed in a discontinuous buffer SDS-PAGE system.	polyacrylamide	204-218	kininogen 1	Homo sapiens	38-42
3730610-1	1986	Purified human high-mol-wt kininogen (HMWK), the cofactor of the contact phase of blood coagulation, migrated as a single band (approximately 110,000 mol wt) in a continuous buffer sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), but appeared as two separated bands (approximately 120,000 and 105,000 mol wt) when analyzed in a discontinuous buffer SDS-PAGE system.	Sodium Dodecyl Sulfate	240-243	kininogen 1	Homo sapiens	15-36
3730610-1	1986	Purified human high-mol-wt kininogen (HMWK), the cofactor of the contact phase of blood coagulation, migrated as a single band (approximately 110,000 mol wt) in a continuous buffer sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), but appeared as two separated bands (approximately 120,000 and 105,000 mol wt) when analyzed in a discontinuous buffer SDS-PAGE system.	Sodium Dodecyl Sulfate	240-243	kininogen 1	Homo sapiens	38-42
3730610-1	1986	Purified human high-mol-wt kininogen (HMWK), the cofactor of the contact phase of blood coagulation, migrated as a single band (approximately 110,000 mol wt) in a continuous buffer sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), but appeared as two separated bands (approximately 120,000 and 105,000 mol wt) when analyzed in a discontinuous buffer SDS-PAGE system.	Sodium Dodecyl Sulfate	370-373	kininogen 1	Homo sapiens	15-36
3730610-1	1986	Purified human high-mol-wt kininogen (HMWK), the cofactor of the contact phase of blood coagulation, migrated as a single band (approximately 110,000 mol wt) in a continuous buffer sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), but appeared as two separated bands (approximately 120,000 and 105,000 mol wt) when analyzed in a discontinuous buffer SDS-PAGE system.	Sodium Dodecyl Sulfate	370-373	kininogen 1	Homo sapiens	38-42
3741422-3	1986	The more widely recognized biosynthetic pathway is by the extracellular dipeptide cleavage of angiotensin I by an enzyme which also degrades bradykinin, i.e., angiotensin converting enzyme.	Dipeptides	72-81	kininogen 1	Homo sapiens	141-151
3087737-5	1986	Histamine, bradykinin, and the ionophore, A23187, stimulated release of PGI2 and PGE2 to as much as 25 times basal release.	Epoprostenol	72-76	kininogen 1	Homo sapiens	11-21
3087737-5	1986	Histamine, bradykinin, and the ionophore, A23187, stimulated release of PGI2 and PGE2 to as much as 25 times basal release.	Dinoprostone	81-85	kininogen 1	Homo sapiens	11-21
3087737-6	1986	Dexamethasone (10(-11) to 10(-7) M) reduced PG formation in cells that were stimulated by histamine, bradykinin, calcium ionophore, or mechanical agitation.	Dexamethasone	0-13	kininogen 1	Homo sapiens	101-111
3087737-6	1986	Dexamethasone (10(-11) to 10(-7) M) reduced PG formation in cells that were stimulated by histamine, bradykinin, calcium ionophore, or mechanical agitation.	Prostaglandins	44-46	kininogen 1	Homo sapiens	101-111
3722381-3	1986	Zn++ was required for 125I-HMWK binding to unstimulated platelets and binding was maximal at 50 microM Zn++.	Zinc	0-4	kininogen 1	Homo sapiens	27-31
3722381-3	1986	Zn++ was required for 125I-HMWK binding to unstimulated platelets and binding was maximal at 50 microM Zn++.	Zinc	103-107	kininogen 1	Homo sapiens	27-31
3013204-2	1986	Bradykinin was cleaved at two sites to produce the pentapeptide Arg-Pro-Pro-Gly-Phe plus dipeptides Ser-Pro and Phe-Arg.	Dipeptides	89-99	kininogen 1	Homo sapiens	0-10
3013204-2	1986	Bradykinin was cleaved at two sites to produce the pentapeptide Arg-Pro-Pro-Gly-Phe plus dipeptides Ser-Pro and Phe-Arg.	seryl-proline	100-107	kininogen 1	Homo sapiens	0-10
3013204-2	1986	Bradykinin was cleaved at two sites to produce the pentapeptide Arg-Pro-Pro-Gly-Phe plus dipeptides Ser-Pro and Phe-Arg.	phenylalanylarginine	112-119	kininogen 1	Homo sapiens	0-10
3013204-3	1986	Lysyl bradykinin was cleaved similarly to release the same dipeptides plus the hexapeptide Lys-Arg-Pro-Pro-Gly-Phe.	Dipeptides	59-69	kininogen 1	Homo sapiens	6-16
3013204-3	1986	Lysyl bradykinin was cleaved similarly to release the same dipeptides plus the hexapeptide Lys-Arg-Pro-Pro-Gly-Phe.	Lys-Arg	91-98	kininogen 1	Homo sapiens	6-16
3013204-3	1986	Lysyl bradykinin was cleaved similarly to release the same dipeptides plus the hexapeptide Lys-Arg-Pro-Pro-Gly-Phe.	Glycine	107-110	kininogen 1	Homo sapiens	6-16
3013204-3	1986	Lysyl bradykinin was cleaved similarly to release the same dipeptides plus the hexapeptide Lys-Arg-Pro-Pro-Gly-Phe.	Phenylalanine	111-114	kininogen 1	Homo sapiens	6-16
3013204-11	1986	On the other hand, increasing NaCl concentration was inhibitory for bradykinin digestion.	Sodium Chloride	30-34	kininogen 1	Homo sapiens	68-78
3013204-12	1986	The rate of Lys-bradykinin digestion was increased from 0 to 1 mM NaCl and decreased thereafter up to physiologic concentration.	Sodium Chloride	66-70	kininogen 1	Homo sapiens	16-26
3635531-5	1986	Amino acid sequencing revealed a structure similar to Lys-bradykinin except that proline in position 4 was replaced by alanine ([Ala3]Lys-bradykinin).	Lysine	54-57	kininogen 1	Homo sapiens	58-68
2872993-9	1986	Several neurohumoral agents have been found to stimulate chloride secretion, such as PGs, beta-adrenergic agonists, VIP, substance P, and bradykinin.	Chlorides	57-65	kininogen 1	Homo sapiens	138-148
3718539-1	1986	Carboxypeptidase N removed the C-terminal arginine from bradykinin or lysyl bradykinin to leave the des-Arg derivative of each, and no further degradation occurred regardless of enzyme concentration or time of incubation.	Arginine	42-50	kininogen 1	Homo sapiens	56-66
3718546-0	1986	[Study of bradykinin conformation in a dimethylsulfoxide solution by two-dimensional 1H-NMR spectroscopy].	Dimethyl Sulfoxide	39-56	kininogen 1	Homo sapiens	10-20
3718539-1	1986	Carboxypeptidase N removed the C-terminal arginine from bradykinin or lysyl bradykinin to leave the des-Arg derivative of each, and no further degradation occurred regardless of enzyme concentration or time of incubation.	Arginine	42-50	kininogen 1	Homo sapiens	76-86
3718539-1	1986	Carboxypeptidase N removed the C-terminal arginine from bradykinin or lysyl bradykinin to leave the des-Arg derivative of each, and no further degradation occurred regardless of enzyme concentration or time of incubation.	des-arg	100-107	kininogen 1	Homo sapiens	76-86
3718539-4	1986	However, angiotensin converting enzyme degraded des-Arg9-bradykinin in plasma or serum prior to such Phe removal to yield the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	Arginine	52-55	kininogen 1	Homo sapiens	57-67
3718539-4	1986	However, angiotensin converting enzyme degraded des-Arg9-bradykinin in plasma or serum prior to such Phe removal to yield the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	Glycine	151-154	kininogen 1	Homo sapiens	57-67
3718539-4	1986	However, angiotensin converting enzyme degraded des-Arg9-bradykinin in plasma or serum prior to such Phe removal to yield the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	Phenylalanine	155-158	kininogen 1	Homo sapiens	57-67
3718539-4	1986	However, angiotensin converting enzyme degraded des-Arg9-bradykinin in plasma or serum prior to such Phe removal to yield the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	tripeptide K-26	167-177	kininogen 1	Homo sapiens	57-67
3718539-4	1986	However, angiotensin converting enzyme degraded des-Arg9-bradykinin in plasma or serum prior to such Phe removal to yield the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	Serine	178-181	kininogen 1	Homo sapiens	57-67
3718539-4	1986	However, angiotensin converting enzyme degraded des-Arg9-bradykinin in plasma or serum prior to such Phe removal to yield the pentapeptide Arg-Pro-Pro-Gly-Phe and the tripeptide Ser-Pro-Phe.	Phenylalanine	155-158	kininogen 1	Homo sapiens	57-67
3718546-0	1986	[Study of bradykinin conformation in a dimethylsulfoxide solution by two-dimensional 1H-NMR spectroscopy].	Hydrogen	85-87	kininogen 1	Homo sapiens	10-20
3718546-1	1986	The role of charged groups of the nonapeptide bradykinin in stabilization of its spatial structure in dimethyl sulfoxide solution was investigated.	Dimethyl Sulfoxide	102-120	kininogen 1	Homo sapiens	46-56
3518739-1	1986	The effect of bradykinin on insulin-stimulated glucose metabolism was studied in 5 operated patients using the euglycemic insulin clamp technique and the forearm catheter technique.	Glucose	47-54	kininogen 1	Homo sapiens	14-24
3633200-4	1986	We hypothesized that modification of arginine residues may prevent cleavage of HMW kininogen, since the initial kallikrein-induced cleavage sites on the HMW kininogen molecule are at the NH2 terminal and the COOH terminal of the bradykinin-containing portion of the molecule, each of which contains arginine.	Arginine	37-45	kininogen 1	Homo sapiens	229-239
3633200-5	1986	We found that modification with butanedione of four arginine residues in the HMW kininogen molecule prevented bradykinin release, which results from cleavage of HMW kininogen.	Diacetyl	32-43	kininogen 1	Homo sapiens	110-120
3633200-5	1986	We found that modification with butanedione of four arginine residues in the HMW kininogen molecule prevented bradykinin release, which results from cleavage of HMW kininogen.	Arginine	52-60	kininogen 1	Homo sapiens	110-120
3016357-5	1986	Captopril solely inhibited PGI2 generation and the reported hypothesis that captopril enhances PGI2 generation by the accumulation of AI or BK via inhibition of ACE was not confirmed in this experimental system.	Captopril	76-85	kininogen 1	Homo sapiens	140-142
3964260-2	1986	Carbachol, bradykinin, and histamine produced significantly greater accumulation of [3H] inositol-1-phosphate over basal levels, with histamine producing the greatest effect.	[3h] inositol-1-phosphate	84-109	kininogen 1	Homo sapiens	11-21
3964260-2	1986	Carbachol, bradykinin, and histamine produced significantly greater accumulation of [3H] inositol-1-phosphate over basal levels, with histamine producing the greatest effect.	Histamine	134-143	kininogen 1	Homo sapiens	11-21
3016357-2	1986	Addition of angiotensin I (AI) or bradykinin (BK) enhanced PGI2 generation and increased the level of ACE activity in the culture medium, while the addition of ACE inhibitor (captopril) caused a dose dependent suppression of PGI2 generation and ACE activity.	Epoprostenol	59-63	kininogen 1	Homo sapiens	34-44
3016357-2	1986	Addition of angiotensin I (AI) or bradykinin (BK) enhanced PGI2 generation and increased the level of ACE activity in the culture medium, while the addition of ACE inhibitor (captopril) caused a dose dependent suppression of PGI2 generation and ACE activity.	Epoprostenol	59-63	kininogen 1	Homo sapiens	46-48
3016357-2	1986	Addition of angiotensin I (AI) or bradykinin (BK) enhanced PGI2 generation and increased the level of ACE activity in the culture medium, while the addition of ACE inhibitor (captopril) caused a dose dependent suppression of PGI2 generation and ACE activity.	Epoprostenol	225-229	kininogen 1	Homo sapiens	34-44
3016357-2	1986	Addition of angiotensin I (AI) or bradykinin (BK) enhanced PGI2 generation and increased the level of ACE activity in the culture medium, while the addition of ACE inhibitor (captopril) caused a dose dependent suppression of PGI2 generation and ACE activity.	Epoprostenol	225-229	kininogen 1	Homo sapiens	46-48
3016357-3	1986	The enhancement of PGI2 generation induced by AI or BK was not affected by pretreatment with captopril, and angiotensin II (AII) did not show any effect on either PGI2 generation or ACE activity.	Epoprostenol	19-23	kininogen 1	Homo sapiens	52-54
3490738-9	1986	In previous work benzamidine was found to protect the cofactor function of purified HMrK in the assay system used, and EDTA was found to inhibit purified human plasma kallikrein assayed as plasminogen activator.	benzamidine	17-28	kininogen 1	Homo sapiens	84-88
3490738-10	1986	The present results support the previous observations, and indicate that acetone treatment of fresh human plasma (benzamidine present) results in the activation of plasma kallikrein in a functional state that requires kinin-free, but otherwise native HMrK as a cofactor for the activation of XII.	Acetone	73-80	kininogen 1	Homo sapiens	251-255
3490738-10	1986	The present results support the previous observations, and indicate that acetone treatment of fresh human plasma (benzamidine present) results in the activation of plasma kallikrein in a functional state that requires kinin-free, but otherwise native HMrK as a cofactor for the activation of XII.	benzamidine	114-125	kininogen 1	Homo sapiens	251-255
3748890-5	1986	The sensitivity of guinea pig ileum to bradykinin in Tyrode medium is highest near the pH 7, while the response to unspecific bioactive material produced by trypsin rises when pH increases from 7 to 8.	tyrode	53-59	kininogen 1	Homo sapiens	39-49
3004657-3	1986	Bradykinin, alpha-melanocyte-stimulating (alpha-MSH), luteinizing hormone-releasing hormone (LH-RH), oxytocin and carbamylcholine stimulated cAMP accumulation selectively in one or two of the above structures.	Cyclic AMP	141-145	kininogen 1	Homo sapiens	0-10
2421602-3	1986	The picrate-Coomassie blue method fixed and stained a small peptide (bradykinin, nine amino acids) that was not observed in gels stained with fast green, silver, or Coomassie blue following fixation in 50% trichloroacetic acid.	picric acid	4-11	kininogen 1	Homo sapiens	69-79
2421602-3	1986	The picrate-Coomassie blue method fixed and stained a small peptide (bradykinin, nine amino acids) that was not observed in gels stained with fast green, silver, or Coomassie blue following fixation in 50% trichloroacetic acid.	Coomassie blue	12-26	kininogen 1	Homo sapiens	69-79
2421602-3	1986	The picrate-Coomassie blue method fixed and stained a small peptide (bradykinin, nine amino acids) that was not observed in gels stained with fast green, silver, or Coomassie blue following fixation in 50% trichloroacetic acid.	Trichloroacetic Acid	206-226	kininogen 1	Homo sapiens	69-79
3513809-0	1986	Effect of captopril on bradykinin inactivation by human foetal placental circulation.	Captopril	10-19	kininogen 1	Homo sapiens	23-33
3513809-4	1986	Bradykinin (100 ng ml-1) was infused through the foetal placental vessels before and during captopril 4 X 10(-7) M. Bradykinin produced a transient increase in placental vascular resistance that was not potentiated by captopril.	Captopril	92-101	kininogen 1	Homo sapiens	0-10
3513809-4	1986	Bradykinin (100 ng ml-1) was infused through the foetal placental vessels before and during captopril 4 X 10(-7) M. Bradykinin produced a transient increase in placental vascular resistance that was not potentiated by captopril.	Captopril	92-101	kininogen 1	Homo sapiens	116-126
3513809-5	1986	Bradykinin activity was completely abolished after passage through the foetal placental circulation, and the inactivation was blocked by captopril.	Captopril	137-146	kininogen 1	Homo sapiens	0-10
2423824-4	1986	Comparing the structure-activity relationships of the peptides, the amino acid sequence Arg-Pro at the N-terminal region of bradykinin and substance P or Pro-Arg at the C-terminal part of tuftsin and rigin appear to be responsible for the lymphokine secretion.	Proline	92-95	kininogen 1	Homo sapiens	124-134
3080005-2	1986	The Ca2+-entry blockers nifedipine and verapamil suppressed the basal, as well as the thrombin-, bradykinin-, and ionophore A23187-stimulated biosynthesis by about 50-60%, but high concentrations were required and the inhibition was never complete.	Nifedipine	24-34	kininogen 1	Homo sapiens	97-107
3080005-2	1986	The Ca2+-entry blockers nifedipine and verapamil suppressed the basal, as well as the thrombin-, bradykinin-, and ionophore A23187-stimulated biosynthesis by about 50-60%, but high concentrations were required and the inhibition was never complete.	Verapamil	39-48	kininogen 1	Homo sapiens	97-107
3080005-4	1986	Although the thrombin-stimulated prostacyclin formation was not significantly influenced by a Ca2+-poor or a Ca2+-free buffer, prostacyclin release stimulated by A23187 and bradykinin was diminished in the presence of these modified incubation media; the reduction of bradykinin stimulated biosynthesis was rather small (30%).	Epoprostenol	127-139	kininogen 1	Homo sapiens	173-183
3080005-4	1986	Although the thrombin-stimulated prostacyclin formation was not significantly influenced by a Ca2+-poor or a Ca2+-free buffer, prostacyclin release stimulated by A23187 and bradykinin was diminished in the presence of these modified incubation media; the reduction of bradykinin stimulated biosynthesis was rather small (30%).	Calcimycin	162-168	kininogen 1	Homo sapiens	268-278
3812088-5	1986	At 60 microM concentration, both the 280K and 48K enzymes cleaved (Lys6)-Met5)-enkephalin fastest followed by (Arg6)-(Met5)-enkephalin, anaphylatoxin C3a, (arg6)-(Leu5)-enkephalin, C3a octapeptide and bradykinin.	lys6)-met5)-enkephalin	67-89	kininogen 1	Homo sapiens	201-211
2433913-2	1986	Following challenge of allergic individuals, HMWK, TK, kinin and albumin all increased dramatically, correlating (p less than 0.001) with the onset of clinical symptoms and with increases in histamine and TAME-esterase activity.	Histamine	191-200	kininogen 1	Homo sapiens	45-49
2880482-1	1986	The arachidonate cascade of human or rat platelets were found to be modified by peptides (bradykinin, angiotensin I, angiotensin II, Asp1-Val5-angiotensin II-amide, somatostatin) and proteases (trypsin, kallikrein).	Arachidonic Acid	4-16	kininogen 1	Homo sapiens	90-100
3544729-8	1986	Captopril (25 mg) potentiated the blood pressure lowering effect of bradykinin about 20-fold.	Captopril	0-9	kininogen 1	Homo sapiens	68-78
3544729-10	1986	The results of our studies show that bradykinin lowers blood pressure by a direct mechanism, which acts independently of salt intake, beta-receptors and prostaglandins.	Salts	121-125	kininogen 1	Homo sapiens	37-47
3544729-10	1986	The results of our studies show that bradykinin lowers blood pressure by a direct mechanism, which acts independently of salt intake, beta-receptors and prostaglandins.	Prostaglandins	153-167	kininogen 1	Homo sapiens	37-47
3544729-11	1986	Inhibition of inactivation of bradykinin by captopril enhances its activity markedly.	Captopril	44-53	kininogen 1	Homo sapiens	30-40
3000474-9	1986	The cleavage of HMWK was specifically prevented by inhibitors of calcium-activated cysteine proteases (leupeptin, N-ethylmaleimide, iodoacetamide, and EDTA) but not by inhibitors of serine proteases (DFP, benzamidine, soybean trypsin inhibitor, or aprotinin).	leupeptin	103-112	kininogen 1	Homo sapiens	16-20
3000474-9	1986	The cleavage of HMWK was specifically prevented by inhibitors of calcium-activated cysteine proteases (leupeptin, N-ethylmaleimide, iodoacetamide, and EDTA) but not by inhibitors of serine proteases (DFP, benzamidine, soybean trypsin inhibitor, or aprotinin).	Ethylmaleimide	114-130	kininogen 1	Homo sapiens	16-20
3000474-9	1986	The cleavage of HMWK was specifically prevented by inhibitors of calcium-activated cysteine proteases (leupeptin, N-ethylmaleimide, iodoacetamide, and EDTA) but not by inhibitors of serine proteases (DFP, benzamidine, soybean trypsin inhibitor, or aprotinin).	Iodoacetamide	132-145	kininogen 1	Homo sapiens	16-20
3000474-9	1986	The cleavage of HMWK was specifically prevented by inhibitors of calcium-activated cysteine proteases (leupeptin, N-ethylmaleimide, iodoacetamide, and EDTA) but not by inhibitors of serine proteases (DFP, benzamidine, soybean trypsin inhibitor, or aprotinin).	Edetic Acid	151-155	kininogen 1	Homo sapiens	16-20
3000474-9	1986	The cleavage of HMWK was specifically prevented by inhibitors of calcium-activated cysteine proteases (leupeptin, N-ethylmaleimide, iodoacetamide, and EDTA) but not by inhibitors of serine proteases (DFP, benzamidine, soybean trypsin inhibitor, or aprotinin).	benzamidine	205-216	kininogen 1	Homo sapiens	16-20
3000474-11	1986	Treatment of platelet cytosol with leupeptin prevented the increase in the coagulant activity of exogenous HMWK.	leupeptin	35-44	kininogen 1	Homo sapiens	107-111
3004512-1	1986	To investigate conformations of peptide inhibitors of the angiotensin-converting enzyme in the enzyme-inhibitor complex, the synthesis, studies of inhibitory activity, and conformational calculations of analogues of bradykinin-potentiating peptides with N-methylalanine or D-alanine in place of L-proline or L-alanine residues have been carried out.	N-methylalanine	254-269	kininogen 1	Homo sapiens	216-226
3513880-3	1986	Dose-related increases in plasma concentrations of 6-oxo-PGF1 alpha occurred during administration of bradykinin (100-3200 ng kg-1 min-1).	6-Ketoprostaglandin F1 alpha	51-67	kininogen 1	Homo sapiens	102-112
3006897-1	1986	Bradykinin and 22 of its analogs were evaluated for their abilities to inhibit the hydrolysis of [3H]hippurylglycylglycine by purified porcine kidney angiotensin I converting enzyme.	[3h]hippurylglycylglycine	97-122	kininogen 1	Homo sapiens	0-10
3006897-2	1986	The mean inhibitory concentration (IC50) for bradykinin was 1.2 +/- 0.2 X 10(-6) M. Except for Ile-Ser-bradykinin and [Sar4]-bradykinin, none of the kinin analogs were more potent in this regard than bradykinin.	Ile-Ser	95-102	kininogen 1	Homo sapiens	103-113
3006897-2	1986	The mean inhibitory concentration (IC50) for bradykinin was 1.2 +/- 0.2 X 10(-6) M. Except for Ile-Ser-bradykinin and [Sar4]-bradykinin, none of the kinin analogs were more potent in this regard than bradykinin.	Ile-Ser	95-102	kininogen 1	Homo sapiens	103-113
3006897-2	1986	The mean inhibitory concentration (IC50) for bradykinin was 1.2 +/- 0.2 X 10(-6) M. Except for Ile-Ser-bradykinin and [Sar4]-bradykinin, none of the kinin analogs were more potent in this regard than bradykinin.	Ile-Ser	95-102	kininogen 1	Homo sapiens	103-113
3791384-1	1986	Voltage-clamped colonic epithelia were fixed for morphological observation minutes after bradykinin was added to produce its well-characterized increase in short circuit current representing net chloride secretion.	Chlorides	195-203	kininogen 1	Homo sapiens	89-99
3016357-5	1986	Captopril solely inhibited PGI2 generation and the reported hypothesis that captopril enhances PGI2 generation by the accumulation of AI or BK via inhibition of ACE was not confirmed in this experimental system.	Epoprostenol	95-99	kininogen 1	Homo sapiens	140-142
3016357-6	1986	Rather, it is proposed that AI or BK induced PGI2 generation may be regulated by the increased breakdown of AI or BK, as an autoregulation mechanism, that is derived from increased ACE activity by AI or BK.	Epoprostenol	45-49	kininogen 1	Homo sapiens	34-36
3016357-6	1986	Rather, it is proposed that AI or BK induced PGI2 generation may be regulated by the increased breakdown of AI or BK, as an autoregulation mechanism, that is derived from increased ACE activity by AI or BK.	Epoprostenol	45-49	kininogen 1	Homo sapiens	114-116
3016357-6	1986	Rather, it is proposed that AI or BK induced PGI2 generation may be regulated by the increased breakdown of AI or BK, as an autoregulation mechanism, that is derived from increased ACE activity by AI or BK.	Epoprostenol	45-49	kininogen 1	Homo sapiens	114-116
3123940-1	1986	Endo-oligopeptidase A known to hydrolyse the Phe5-Ser6 bond of bradykinin and the Arg8-Arg9 bond of neurotensin has been shown to produce, by a single cleavage, leucine5-enkephalin from small prodynorphin derived enkephalin-containing peptides.	leucine5-enkephalin	161-180	kininogen 1	Homo sapiens	63-73
3022274-5	1986	In NIDD as well as in POP subjects, impaired peripheral insulin responsiveness, as evaluated by whole body glucose consumption, was improved up to 50% by application of BK (80 micrograms/h i.v.)	Glucose	107-114	kininogen 1	Homo sapiens	169-171
3006092-1	1986	Influence of inhibitors of prostaglandin synthesis and its possible role in the inotropic effects of bradykinin.	Prostaglandins	27-40	kininogen 1	Homo sapiens	101-111
2868930-6	1985	Addition of 10(-3) M verapamil, 10(-6) M dexamethasone or 10(-7) M somatostatin to the incubation medium inhibited BK-induced beta-END-LI release from the cells.	Verapamil	21-30	kininogen 1	Homo sapiens	115-117
3014236-5	1986	Also, the classical mediators of inflammation, histamine and bradykinin, may be connected with the release of oxygen radicals.	Reactive Oxygen Species	110-125	kininogen 1	Homo sapiens	61-71
2868930-6	1985	Addition of 10(-3) M verapamil, 10(-6) M dexamethasone or 10(-7) M somatostatin to the incubation medium inhibited BK-induced beta-END-LI release from the cells.	Dexamethasone	41-54	kininogen 1	Homo sapiens	115-117
2868930-8	1985	These results indicate that BK stimulates beta-END-LI release and that calcium ion is involved in the mechanism of this effect.	Calcium	71-78	kininogen 1	Homo sapiens	28-30
3936495-2	1985	We investigated the binding of HMWK to factor XIa utilizing two active site directed fluorescent probes: nitrobenzoxadiazole aminopentyl methylphosphonofluoridate for serine and dansyl-glu-gly-arg-chloromethyl ketone for histidine.	Serine	167-173	kininogen 1	Homo sapiens	31-35
3936495-2	1985	We investigated the binding of HMWK to factor XIa utilizing two active site directed fluorescent probes: nitrobenzoxadiazole aminopentyl methylphosphonofluoridate for serine and dansyl-glu-gly-arg-chloromethyl ketone for histidine.	dansylglutamyl-glycyl-arginine chloromethyl ketone	178-216	kininogen 1	Homo sapiens	31-35
3936495-2	1985	We investigated the binding of HMWK to factor XIa utilizing two active site directed fluorescent probes: nitrobenzoxadiazole aminopentyl methylphosphonofluoridate for serine and dansyl-glu-gly-arg-chloromethyl ketone for histidine.	Histidine	221-230	kininogen 1	Homo sapiens	31-35
3000601-3	1985	Desensitization of the kinase C pathway by prolonged exposure to phorbol abolished the induction of c-myc by subsequent phorbol challenge and attenuated c-myc induction by PDGF and bradykinin, but did not affect PDGF-stimulated mitogenesis.	phorbol	65-72	kininogen 1	Homo sapiens	181-191
3809718-2	1986	In humans, the excretion rate of both BK and LBK decreased markedly 90 min after the water load.	Water	85-90	kininogen 1	Homo sapiens	38-40
3903519-0	1985	Aspirin causes short-lived inhibition of bradykinin-stimulated prostacyclin production in man.	Aspirin	0-7	kininogen 1	Homo sapiens	41-51
3903519-0	1985	Aspirin causes short-lived inhibition of bradykinin-stimulated prostacyclin production in man.	Epoprostenol	63-75	kininogen 1	Homo sapiens	41-51
3903519-6	1985	Bradykinin stimulates PGI2 synthesis by cultured human vascular endothelial cells and we have shown that it stimulates PGI2 production by man in vivo.	Epoprostenol	22-26	kininogen 1	Homo sapiens	0-10
3903519-6	1985	Bradykinin stimulates PGI2 synthesis by cultured human vascular endothelial cells and we have shown that it stimulates PGI2 production by man in vivo.	Epoprostenol	119-123	kininogen 1	Homo sapiens	0-10
3903519-7	1985	We report here that an oral dose of aspirin (600 mg) causes rapid and substantial inhibition of bradykinin-stimulated PGI2 production, but recovery occurs within 6 hours; this implies that endothelial PGI2 synthesis would be spared most of the time during dosing once daily with even this relatively large dose of aspirin.	Aspirin	36-43	kininogen 1	Homo sapiens	96-106
3903519-7	1985	We report here that an oral dose of aspirin (600 mg) causes rapid and substantial inhibition of bradykinin-stimulated PGI2 production, but recovery occurs within 6 hours; this implies that endothelial PGI2 synthesis would be spared most of the time during dosing once daily with even this relatively large dose of aspirin.	Epoprostenol	118-122	kininogen 1	Homo sapiens	96-106
2862164-0	1985	Cultured endothelial cells synthesize both platelet-activating factor and prostacyclin in response to histamine, bradykinin, and adenosine triphosphate.	Epoprostenol	74-86	kininogen 1	Homo sapiens	113-123
3929859-4	1985	Bradykinin is 1,000-fold more potent than the other agonists tested, which include histamine, norepinephrine, epinephrine, eledoisin-related peptide, arginine-vasopressin, lysine-vasopressin, desmopressin acetate, carbachol, and acetylcholine.	Histamine	83-92	kininogen 1	Homo sapiens	0-10
3929859-4	1985	Bradykinin is 1,000-fold more potent than the other agonists tested, which include histamine, norepinephrine, epinephrine, eledoisin-related peptide, arginine-vasopressin, lysine-vasopressin, desmopressin acetate, carbachol, and acetylcholine.	Norepinephrine	94-108	kininogen 1	Homo sapiens	0-10
3929859-4	1985	Bradykinin is 1,000-fold more potent than the other agonists tested, which include histamine, norepinephrine, epinephrine, eledoisin-related peptide, arginine-vasopressin, lysine-vasopressin, desmopressin acetate, carbachol, and acetylcholine.	Carbachol	214-223	kininogen 1	Homo sapiens	0-10
3929859-4	1985	Bradykinin is 1,000-fold more potent than the other agonists tested, which include histamine, norepinephrine, epinephrine, eledoisin-related peptide, arginine-vasopressin, lysine-vasopressin, desmopressin acetate, carbachol, and acetylcholine.	Acetylcholine	229-242	kininogen 1	Homo sapiens	0-10
3003038-3	1985	[Des-Pro3]-bradykinin was found to have a potent inhibitory action against angiotensin-converting enzyme with a K1 of 4.5 X 10(-12) M, which is approximately 7 times more potent than Captopril.	Captopril	183-192	kininogen 1	Homo sapiens	11-21
4062989-1	1985	H NMR resonances of [cyclo (9----18) Lys1, Gly6]bradykinin (CBK) in (CD3)2SO and H2O solution have been assigned by combined analysis of two-dimensional COSY and NOESY spectra.	(cd3)2so	68-76	kininogen 1	Homo sapiens	48-58
4062989-1	1985	H NMR resonances of [cyclo (9----18) Lys1, Gly6]bradykinin (CBK) in (CD3)2SO and H2O solution have been assigned by combined analysis of two-dimensional COSY and NOESY spectra.	Water	81-84	kininogen 1	Homo sapiens	48-58
2931612-6	1985	Addition of 10(-3) M verapamil or 10(-6) M dexamethasone to the incubation medium inhibited BK-induced beta-EpLI release from the cells.	Verapamil	21-30	kininogen 1	Homo sapiens	92-94
2931612-6	1985	Addition of 10(-3) M verapamil or 10(-6) M dexamethasone to the incubation medium inhibited BK-induced beta-EpLI release from the cells.	Dexamethasone	43-56	kininogen 1	Homo sapiens	92-94
4043214-0	1985	Role of prostaglandins and the areas postrema in the central pressor action of bradykinin.	Prostaglandins	8-22	kininogen 1	Homo sapiens	79-89
4043214-5	1985	It is concluded that intact areas postrema and normal prostaglandin synthesis are essential for the full expression of the central pressor action of bradykinin.	Prostaglandins	54-67	kininogen 1	Homo sapiens	149-159
3891415-8	1985	Bradykinin not thus degraded can act on endothelial receptors and stimulate the release of prostacyclin (PGI2).	Epoprostenol	91-103	kininogen 1	Homo sapiens	0-10
3891415-8	1985	Bradykinin not thus degraded can act on endothelial receptors and stimulate the release of prostacyclin (PGI2).	Epoprostenol	105-109	kininogen 1	Homo sapiens	0-10
3891415-9	1985	Thus bradykinin can amplify the release of another vasodilator, PGI2, and can stimulate the release of a powerful antiaggregatory agent (PGI2).	Epoprostenol	64-68	kininogen 1	Homo sapiens	5-15
3891415-9	1985	Thus bradykinin can amplify the release of another vasodilator, PGI2, and can stimulate the release of a powerful antiaggregatory agent (PGI2).	Epoprostenol	137-141	kininogen 1	Homo sapiens	5-15
2862164-1	1985	Cultured human endothelial cells synthesize prostacyclin (PGI2), a potent inhibitor of platelet function, when stimulated with histamine, bradykinin, or ATP.	Epoprostenol	44-56	kininogen 1	Homo sapiens	138-148
2862164-1	1985	Cultured human endothelial cells synthesize prostacyclin (PGI2), a potent inhibitor of platelet function, when stimulated with histamine, bradykinin, or ATP.	Epoprostenol	58-62	kininogen 1	Homo sapiens	138-148
2862164-3	1985	In fact, the synthesis of this potent activator of platelets and neutrophils was induced by stimulation of the same receptor subtype that induced PGI2 synthesis: stimulation of a histamine H1 or a bradykinin B2 receptor induced both PAF and PGI2 synthesis.	Epoprostenol	146-150	kininogen 1	Homo sapiens	197-207
2862164-3	1985	In fact, the synthesis of this potent activator of platelets and neutrophils was induced by stimulation of the same receptor subtype that induced PGI2 synthesis: stimulation of a histamine H1 or a bradykinin B2 receptor induced both PAF and PGI2 synthesis.	Epoprostenol	241-245	kininogen 1	Homo sapiens	197-207
3872909-10	1985	32PO4-labeled lipomodulin was detected in the extract of 23A4 cells 3 to 5 min after the addition of GEF, bradykinin, or TPA.	32po4	0-5	kininogen 1	Homo sapiens	106-116
3872909-4	1985	In the presence of glycosylation-enhancing factor (GEF) or bradykinin, however, the same cells produce IgE-binding factors with N-linked oligosaccharides (glycosylated form).	n-linked oligosaccharides	128-153	kininogen 1	Homo sapiens	59-69
3872909-6	1985	Analysis of the biochemical processes for the release of GIF from 23A4 cells showed that affinity-purified GEF or bradykinin induced transient phospholipid methylation and diacylglycerol (DAG) formation, and enhanced 45Ca uptake into the cells.	Phospholipids	143-155	kininogen 1	Homo sapiens	114-124
3872909-6	1985	Analysis of the biochemical processes for the release of GIF from 23A4 cells showed that affinity-purified GEF or bradykinin induced transient phospholipid methylation and diacylglycerol (DAG) formation, and enhanced 45Ca uptake into the cells.	Diglycerides	172-186	kininogen 1	Homo sapiens	114-124
3872909-6	1985	Analysis of the biochemical processes for the release of GIF from 23A4 cells showed that affinity-purified GEF or bradykinin induced transient phospholipid methylation and diacylglycerol (DAG) formation, and enhanced 45Ca uptake into the cells.	Diglycerides	188-191	kininogen 1	Homo sapiens	114-124
2857603-4	1985	Bradykinin (10 micrograms/ml) increases the rate threefold and this is substantially prevented by indomethacin (1.5 X 10(-5) mol/l), as also is a fivefold stimulation by cyclic GMP (10(-5) mol/l).	Indomethacin	98-110	kininogen 1	Homo sapiens	0-10
2857603-4	1985	Bradykinin (10 micrograms/ml) increases the rate threefold and this is substantially prevented by indomethacin (1.5 X 10(-5) mol/l), as also is a fivefold stimulation by cyclic GMP (10(-5) mol/l).	Cyclic GMP	170-180	kininogen 1	Homo sapiens	0-10
3897676-0	1985	[Responses of plasma bradykinin and the renin-angiotensin axis to furosemide in essential hypertension].	Furosemide	66-76	kininogen 1	Homo sapiens	21-31
3081913-1	1986	In studies on human skin fibroblasts originating from three patients with Bartter"s syndrome and in corresponding age and sex matched controls, the bradykinin stimulated release of PGE2, PGI2, PGF2 alpha and of arachidonic acid was examined.	Dinoprostone	181-185	kininogen 1	Homo sapiens	148-158
3081913-1	1986	In studies on human skin fibroblasts originating from three patients with Bartter"s syndrome and in corresponding age and sex matched controls, the bradykinin stimulated release of PGE2, PGI2, PGF2 alpha and of arachidonic acid was examined.	Epoprostenol	187-191	kininogen 1	Homo sapiens	148-158
3081913-1	1986	In studies on human skin fibroblasts originating from three patients with Bartter"s syndrome and in corresponding age and sex matched controls, the bradykinin stimulated release of PGE2, PGI2, PGF2 alpha and of arachidonic acid was examined.	Dinoprost	193-203	kininogen 1	Homo sapiens	148-158
3081913-1	1986	In studies on human skin fibroblasts originating from three patients with Bartter"s syndrome and in corresponding age and sex matched controls, the bradykinin stimulated release of PGE2, PGI2, PGF2 alpha and of arachidonic acid was examined.	Arachidonic Acid	211-227	kininogen 1	Homo sapiens	148-158
3081913-3	1986	Earlier studies were confirmed and extended by one more pair of fibroblast cultures, showing a decreased bradykinin stimulated PGE2 production in fibroblasts from patients with Bartter"s syndrome as compared to control.	Dinoprostone	127-131	kininogen 1	Homo sapiens	105-115
3081913-4	1986	The difference in bradykinin stimulated PGE2 production was significant, irrespective of the extracellular potassium concentrations, to which the cultures were exposed.	Dinoprostone	40-44	kininogen 1	Homo sapiens	18-28
3081913-5	1986	The bradykinin stimulated PGE2 and PGF2 alpha-production by control fibroblasts was directly proportional to extracellular potassium concentrations, whereas the PG-production of Bartter"s syndrome fibroblasts remained uninfluenced by extracellular potassium.	Dinoprostone	26-30	kininogen 1	Homo sapiens	4-14
3081913-5	1986	The bradykinin stimulated PGE2 and PGF2 alpha-production by control fibroblasts was directly proportional to extracellular potassium concentrations, whereas the PG-production of Bartter"s syndrome fibroblasts remained uninfluenced by extracellular potassium.	Dinoprost	35-39	kininogen 1	Homo sapiens	4-14
3081913-5	1986	The bradykinin stimulated PGE2 and PGF2 alpha-production by control fibroblasts was directly proportional to extracellular potassium concentrations, whereas the PG-production of Bartter"s syndrome fibroblasts remained uninfluenced by extracellular potassium.	Potassium	123-132	kininogen 1	Homo sapiens	4-14
3081913-5	1986	The bradykinin stimulated PGE2 and PGF2 alpha-production by control fibroblasts was directly proportional to extracellular potassium concentrations, whereas the PG-production of Bartter"s syndrome fibroblasts remained uninfluenced by extracellular potassium.	Prostaglandins	26-28	kininogen 1	Homo sapiens	4-14
3081913-7	1986	The direct proportionality between bradykinin stimulated PGE2 production and potassium concentrations in control fibroblasts is, despite the apparent contradiction, in accordance with findings in the literature.	Dinoprostone	57-61	kininogen 1	Homo sapiens	35-45
2991035-9	1985	The plasma bradykinin concentration (PBC) increased within 1 h, the highest values occurring at 3 h after drug administration, and returned to baseline levels within 24 h in low-renin hypertensives, while the PBC was significantly increased at 4 h and had not returned to baseline levels within 24 h in normal- and high-renin hypertensives.	potassium bicarbonate	37-40	kininogen 1	Homo sapiens	11-21
3923866-4	1985	Bradykinin improved sperm velocity at 22 degrees C. Angiotensin I and II, acetylcarnitine and LH stimulated sperm velocity at 37 degrees C. The latter two substances increased also sperm motility at 37 degrees C. Angiotensin III, spermine, spermidine and FSH showed no effect on sperm motility neither at 22 degrees C nor at 37 degrees C. These observations indicate that distinct physiological compounds found in seminal plasma stimulate directly sperm motility and/or velocity in vitro and support the assumption that the sperm motility stimulating principle of human semen is complex and of multifactorial origin.	Spermine	230-238	kininogen 1	Homo sapiens	0-10
3986521-8	1985	With only 3 exceptions the 40 units excited by KCl were also activated by bradykinin which was applied in doses from 0.026 to 26 micrograms.	Potassium Chloride	47-50	kininogen 1	Homo sapiens	74-84
2861197-1	1985	The activation of Factor XII and prekallikrein by polysaccharide sulfates and sulfatides in the presence of high-molecular-weight (HMW) kininogen was studied, and compared with the kaolin-mediated activation reaction.	polysaccharide sulfates	50-73	kininogen 1	Homo sapiens	108-145
2861197-5	1985	However, this accelerating effect of HMW kininogen on the amylose sulfate- and sulfatide-mediated activations (reaction 1) was diminished after treatment with fluorescein iso-thiocyanate, whereas the effect on the kaolin-mediated activation was not influenced by fluorescein-labeling.	amylose sulfate	58-73	kininogen 1	Homo sapiens	37-50
2861197-5	1985	However, this accelerating effect of HMW kininogen on the amylose sulfate- and sulfatide-mediated activations (reaction 1) was diminished after treatment with fluorescein iso-thiocyanate, whereas the effect on the kaolin-mediated activation was not influenced by fluorescein-labeling.	Sulfoglycosphingolipids	79-88	kininogen 1	Homo sapiens	37-50
2861197-5	1985	However, this accelerating effect of HMW kininogen on the amylose sulfate- and sulfatide-mediated activations (reaction 1) was diminished after treatment with fluorescein iso-thiocyanate, whereas the effect on the kaolin-mediated activation was not influenced by fluorescein-labeling.	Fluorescein-5-isothiocyanate	159-186	kininogen 1	Homo sapiens	37-50
2861197-5	1985	However, this accelerating effect of HMW kininogen on the amylose sulfate- and sulfatide-mediated activations (reaction 1) was diminished after treatment with fluorescein iso-thiocyanate, whereas the effect on the kaolin-mediated activation was not influenced by fluorescein-labeling.	Fluorescein	159-170	kininogen 1	Homo sapiens	37-50
2861197-6	1985	In addition, reaction 2 mediated by amylose sulfate and sulfatide was extremely slow even in the presence of HMW kininogen, and the results also differed from those with kaolin.	amylose sulfate	36-51	kininogen 1	Homo sapiens	109-122
2861197-6	1985	In addition, reaction 2 mediated by amylose sulfate and sulfatide was extremely slow even in the presence of HMW kininogen, and the results also differed from those with kaolin.	Sulfoglycosphingolipids	56-65	kininogen 1	Homo sapiens	109-122
2861197-7	1985	The sulfatide-mediated activation of reaction 1 was not inhibited by fragment 1.2 (His-rich fragment), which is released from HMW kininogen by the action of kallikrein, and is known to be a potent inhibitor of the kaolin-dependent activation.	Sulfoglycosphingolipids	4-13	kininogen 1	Homo sapiens	126-139
3004113-2	1985	Acute effects on blood pressure, the renin-angiotensin system and blood bradykinin after a single dose of captopril.	Captopril	106-115	kininogen 1	Homo sapiens	72-82
2408830-9	1985	Ca2+-dependent secretory agents initiate phospholipid hydrolysis and stimulate secretion via the resulting hydrolytic products: arachidonic acid metabolites when bradykinin is the stimulus or diacylglycerol and/or inositol trisphosphate when acetylcholine is the stimulus.	Arachidonic Acid	128-144	kininogen 1	Homo sapiens	162-172
3872909-11	1985	These results indicate that GEF and bradykinin induced the activation of methyltransferases and phospholipase C for the formation of DAG, which in turn activated Ca2+-activated, phospholipid-dependent protein kinase (protein kinase C) for the phosphorylation of lipomodulin.	Diglycerides	133-136	kininogen 1	Homo sapiens	36-46
6470707-2	1984	Addition of [3H]bradykinin to extracts permitted calculation of recoveries and monitoring of chromatographic fractions.	Tritium	13-15	kininogen 1	Homo sapiens	16-26
2409028-11	1985	Using high performance liquid chromatography we have separated bradykinin from kallidin, des-Arg9-bradykinin (the degradation product of carboxypeptidase N) as well as the fragments Arg-Pro-Pro-Gly-Phe, Ser-Pro, and Phe-Arg, the degradation products formed by angiotensin-converting enzyme.	Arginine	93-96	kininogen 1	Homo sapiens	63-73
2985930-0	1985	Effect of bradykinin on prostaglandin production by human skin fibroblasts in culture.	Prostaglandins	24-37	kininogen 1	Homo sapiens	10-20
3918285-6	1985	A significant increase in PGE2 formed with bradykinin was found in the tonsillar hypertrophy group.	Dinoprostone	26-30	kininogen 1	Homo sapiens	43-53
6099145-2	1984	High molecular weight kininogen was bound to stimulated platelets in the presence of ZnCl2 in a specific and saturable manner.	zinc chloride	85-90	kininogen 1	Homo sapiens	0-31
6099145-4	1984	Optimal binding of high molecular weight kininogen occurred near the plasma concentrations of both zinc and calcium ions.	Calcium	108-115	kininogen 1	Homo sapiens	19-50
2416638-5	1985	Subsequent flooding of the preparation with more normal plasma causes lift-off of the oxide where underlying fibrinogen is being displaced by the HMK of the newly applied plasma.	Oxides	86-91	kininogen 1	Homo sapiens	146-149
2417254-5	1985	Modification of arginine residues in ACE with cylcohexanedione or butanedione inhibited hydrolysis of SP, bradykinin and Bz-Gly-Phe-Arg (80-93%) indicating an active site arginine is required for hydrolysis of SP.	Arginine	16-24	kininogen 1	Homo sapiens	106-116
2417254-5	1985	Modification of arginine residues in ACE with cylcohexanedione or butanedione inhibited hydrolysis of SP, bradykinin and Bz-Gly-Phe-Arg (80-93%) indicating an active site arginine is required for hydrolysis of SP.	cylcohexanedione	46-62	kininogen 1	Homo sapiens	106-116
2417254-5	1985	Modification of arginine residues in ACE with cylcohexanedione or butanedione inhibited hydrolysis of SP, bradykinin and Bz-Gly-Phe-Arg (80-93%) indicating an active site arginine is required for hydrolysis of SP.	Diacetyl	66-77	kininogen 1	Homo sapiens	106-116
3909277-2	1985	The present study was carried out to test the hypothesis of a possible effectiveness of captopril--an enzymatic inhibitor of both angiotensin II formation and bradykinin degradation--on hypoxic pulmonary hypertension.	Captopril	88-97	kininogen 1	Homo sapiens	159-169
3909277-4	1985	In our patients, captopril significantly lowered pulmonary arterial pressure and vascular resistance only when combined with oxygen, suggesting that an increase in bradykinin availability and/or a decrease in angiotensin II synthesis might be important factors in reversing pulmonary arterial hypertension only after blunting of the hypoxic stimulus on pulmonary circulation.	Captopril	17-26	kininogen 1	Homo sapiens	164-174
6099336-2	1984	The solid phase synthesis of a partially modified retro-inverso analogue of the bradykinin potentiating peptide BPP9a, [gLys6, (R,S)-mPhe7, Ala8] BPP9a is described.	glys6	120-125	kininogen 1	Homo sapiens	80-90
6099336-2	1984	The solid phase synthesis of a partially modified retro-inverso analogue of the bradykinin potentiating peptide BPP9a, [gLys6, (R,S)-mPhe7, Ala8] BPP9a is described.	(r,s)-mphe7	127-138	kininogen 1	Homo sapiens	80-90
6439745-4	1984	Fibroblasts pretreated with control medium released PGE2 only modestly in response to 1 nM bradykinin for 1 h (basal, 50 +/- 7 pg PGE2/micrograms protein; stimulated, 104 +/- 12 pg PGE2/micrograms protein), whereas cells that had been pretreated with MNCF showed a greatly facilitated bradykinin-induced release of PGE2.	Dinoprostone	52-56	kininogen 1	Homo sapiens	91-101
6501443-6	1984	Bradykinin led to selective opening of the blood-brain barrier for Na+-fluorescein at superfusate concentrations of greater than or equal to 4 x 10(-7) M, but not for FITC-dextran or FITC-albumin.	na+-fluorescein	67-82	kininogen 1	Homo sapiens	0-10
6501443-7	1984	Topical administration of l-isoproterenol (10(-4) M) was found to prevent extravasation of Na+-fluorescein in the presence of bradykinin concentrations of 4 x 10(-6) M. Protection of the blood-brain barrier by isoproterenol was not observed when higher concentrations of bradykinin were employed.	LEVISOPRENALINE	26-41	kininogen 1	Homo sapiens	126-136
6501443-7	1984	Topical administration of l-isoproterenol (10(-4) M) was found to prevent extravasation of Na+-fluorescein in the presence of bradykinin concentrations of 4 x 10(-6) M. Protection of the blood-brain barrier by isoproterenol was not observed when higher concentrations of bradykinin were employed.	LEVISOPRENALINE	26-41	kininogen 1	Homo sapiens	271-281
6501443-7	1984	Topical administration of l-isoproterenol (10(-4) M) was found to prevent extravasation of Na+-fluorescein in the presence of bradykinin concentrations of 4 x 10(-6) M. Protection of the blood-brain barrier by isoproterenol was not observed when higher concentrations of bradykinin were employed.	na+-fluorescein	91-106	kininogen 1	Homo sapiens	271-281
6501443-7	1984	Topical administration of l-isoproterenol (10(-4) M) was found to prevent extravasation of Na+-fluorescein in the presence of bradykinin concentrations of 4 x 10(-6) M. Protection of the blood-brain barrier by isoproterenol was not observed when higher concentrations of bradykinin were employed.	Isoproterenol	28-41	kininogen 1	Homo sapiens	126-136
6501443-7	1984	Topical administration of l-isoproterenol (10(-4) M) was found to prevent extravasation of Na+-fluorescein in the presence of bradykinin concentrations of 4 x 10(-6) M. Protection of the blood-brain barrier by isoproterenol was not observed when higher concentrations of bradykinin were employed.	Isoproterenol	28-41	kininogen 1	Homo sapiens	271-281
6501443-9	1984	Intracarotid infusion of bradykinin led also to a selective opening of the blood-brain barrier for Na+-fluorescein, but not for FITC-dextran or FITC-albumin.	na+-fluorescein	99-114	kininogen 1	Homo sapiens	25-35
6501443-9	1984	Intracarotid infusion of bradykinin led also to a selective opening of the blood-brain barrier for Na+-fluorescein, but not for FITC-dextran or FITC-albumin.	fluorescein isothiocyanate dextran	128-140	kininogen 1	Homo sapiens	25-35
6501443-9	1984	Intracarotid infusion of bradykinin led also to a selective opening of the blood-brain barrier for Na+-fluorescein, but not for FITC-dextran or FITC-albumin.	Fluorescein-5-isothiocyanate	128-132	kininogen 1	Homo sapiens	25-35
6530804-0	1984	[Studies on the mechanism of endotoxin shock--using bradykinin depletor cellulose sulphate].	depletor cellulose sulphate	63-90	kininogen 1	Homo sapiens	52-62
6098010-2	1984	Factor XIIf-mediated hypotension was dose-dependent and augmented by pretreatment with captopril, an inhibitor of the angiotensin I- and bradykinin-processing enzyme.	Captopril	87-96	kininogen 1	Homo sapiens	137-147
6497904-2	1984	Comparison of the kinetics of hydrolysis of the enkephalin hexapeptides and bradykinin by carboxypeptidase N revealed the following values for the Km and kcat: Arg6-Met5-enkephalin, 49 microM, 1024 min-1; Arg6-Leu5-enkephalin, 57 microM, 375 min-1; Lys6-Met5-enkephalin, 216 microM, 6204 min-1; bradykinin, 19 microM, 58 min-1.	arg6-met5-enkephalin	160-180	kininogen 1	Homo sapiens	76-86
6497904-2	1984	Comparison of the kinetics of hydrolysis of the enkephalin hexapeptides and bradykinin by carboxypeptidase N revealed the following values for the Km and kcat: Arg6-Met5-enkephalin, 49 microM, 1024 min-1; Arg6-Leu5-enkephalin, 57 microM, 375 min-1; Lys6-Met5-enkephalin, 216 microM, 6204 min-1; bradykinin, 19 microM, 58 min-1.	lys6-met5-enkephalin	249-269	kininogen 1	Homo sapiens	76-86
6497904-4	1984	Preincubation of the enzyme with 0.1 mM CoCl2 increased both the kcat and Km of bradykinin and Arg6-Met5-enkephalin.	cobaltous chloride	40-45	kininogen 1	Homo sapiens	80-90
6149790-1	1984	Activity produced by direct microelectrophoretic application of glutamate onto 19 convergent neurones in trigeminal nucleus caudalis, was strongly depressed during and after the application of heterotopic noxious conditioning stimuli: noxious heat (52 degrees C) applied to the tail, noxious pinches applied to the tail or hindpaws and intraperitoneal injections of bradykinin produced mean reductions in activity of 80-90%.	Glutamic Acid	64-73	kininogen 1	Homo sapiens	366-376
6470707-1	1984	Bradykinin-like activity was purified from acetic acid extracts of saline-perfused rat brains by gel filtration chromatography and two reverse-phase HPLC systems capable of resolving bradykinin from lysyl-bradykinin and other bradykinin analogs and fragments.	Acetic Acid	43-54	kininogen 1	Homo sapiens	0-10
6400378-2	1984	Factor XIIf-mediated hypotension was dose-dependent and augmented by pretreatment with captopril, an inhibitor of the bradykinin-processing enzyme kininase II.	Captopril	87-96	kininogen 1	Homo sapiens	118-128
6435618-0	1984	Serum, bradykinin and vasopressin stimulate release of inositol phosphates from human fibroblasts.	Inositol Phosphates	55-74	kininogen 1	Homo sapiens	7-17
6435618-1	1984	The mitogens serum, vasopressin and bradykinin stimulate a significant rise in the inositol phosphate content of cultured human fibroblasts within 10 seconds, while serum- and bradykinin-stimulated arachidonic acid release does not occur until after 30 seconds.	Inositol Phosphates	83-101	kininogen 1	Homo sapiens	36-46
6435618-1	1984	The mitogens serum, vasopressin and bradykinin stimulate a significant rise in the inositol phosphate content of cultured human fibroblasts within 10 seconds, while serum- and bradykinin-stimulated arachidonic acid release does not occur until after 30 seconds.	Arachidonic Acid	198-214	kininogen 1	Homo sapiens	176-186
6432879-1	1984	Intestine (both small and large) secretes chloride in response to prostaglandins and agents, such as bradykinin, that increase prostaglandin synthesis.	Chlorides	42-50	kininogen 1	Homo sapiens	101-111
6146639-1	1984	The interaction of bradykinin (BK) with its specific receptors on intact cultured human fibroblasts results in production of prostaglandins, including prostacyclin (PGI2), and accumulation of cyclic AMP.	Prostaglandins	125-139	kininogen 1	Homo sapiens	19-29
6148020-2	1984	After application to the serosa, bradykinin (10 micrograms/ml) evoked increases in mean arterial pressure of 12 +/- 2 mmHg, heart rate of 5 +/- 1 beats/min, left ventricular dP/dt (at 40 mmHg developed pressure) of 305 +/- 54 mmHg/s and systemic vascular resistance of 0.04 +/- 0.01 PRU.	dp	174-176	kininogen 1	Homo sapiens	33-43
6148020-2	1984	After application to the serosa, bradykinin (10 micrograms/ml) evoked increases in mean arterial pressure of 12 +/- 2 mmHg, heart rate of 5 +/- 1 beats/min, left ventricular dP/dt (at 40 mmHg developed pressure) of 305 +/- 54 mmHg/s and systemic vascular resistance of 0.04 +/- 0.01 PRU.	Thymidine	177-179	kininogen 1	Homo sapiens	33-43
6146639-0	1984	Autoregulation of bradykinin receptors and bradykinin-induced prostacyclin formation in human fibroblasts.	Epoprostenol	62-74	kininogen 1	Homo sapiens	43-53
6146639-1	1984	The interaction of bradykinin (BK) with its specific receptors on intact cultured human fibroblasts results in production of prostaglandins, including prostacyclin (PGI2), and accumulation of cyclic AMP.	Prostaglandins	125-139	kininogen 1	Homo sapiens	31-33
6146639-1	1984	The interaction of bradykinin (BK) with its specific receptors on intact cultured human fibroblasts results in production of prostaglandins, including prostacyclin (PGI2), and accumulation of cyclic AMP.	Epoprostenol	151-163	kininogen 1	Homo sapiens	19-29
6146639-1	1984	The interaction of bradykinin (BK) with its specific receptors on intact cultured human fibroblasts results in production of prostaglandins, including prostacyclin (PGI2), and accumulation of cyclic AMP.	Epoprostenol	151-163	kininogen 1	Homo sapiens	31-33
6146639-1	1984	The interaction of bradykinin (BK) with its specific receptors on intact cultured human fibroblasts results in production of prostaglandins, including prostacyclin (PGI2), and accumulation of cyclic AMP.	Epoprostenol	165-169	kininogen 1	Homo sapiens	19-29
6146639-1	1984	The interaction of bradykinin (BK) with its specific receptors on intact cultured human fibroblasts results in production of prostaglandins, including prostacyclin (PGI2), and accumulation of cyclic AMP.	Epoprostenol	165-169	kininogen 1	Homo sapiens	31-33
6146639-1	1984	The interaction of bradykinin (BK) with its specific receptors on intact cultured human fibroblasts results in production of prostaglandins, including prostacyclin (PGI2), and accumulation of cyclic AMP.	Cyclic AMP	192-202	kininogen 1	Homo sapiens	19-29
6146639-1	1984	The interaction of bradykinin (BK) with its specific receptors on intact cultured human fibroblasts results in production of prostaglandins, including prostacyclin (PGI2), and accumulation of cyclic AMP.	Cyclic AMP	192-202	kininogen 1	Homo sapiens	31-33
6146639-2	1984	Incubation of cells with 1 microM BK for 5 min at 37 degrees C led to a marked reduction (75-90%) in BK-induced PGI2 release and in total number of [3H]BK-binding sites with no change in dissociation constant (6.1 and 7.6 nM for control and BK-treated cells, respectively).	Epoprostenol	112-116	kininogen 1	Homo sapiens	34-36
6146639-2	1984	Incubation of cells with 1 microM BK for 5 min at 37 degrees C led to a marked reduction (75-90%) in BK-induced PGI2 release and in total number of [3H]BK-binding sites with no change in dissociation constant (6.1 and 7.6 nM for control and BK-treated cells, respectively).	Epoprostenol	112-116	kininogen 1	Homo sapiens	101-103
6146639-2	1984	Incubation of cells with 1 microM BK for 5 min at 37 degrees C led to a marked reduction (75-90%) in BK-induced PGI2 release and in total number of [3H]BK-binding sites with no change in dissociation constant (6.1 and 7.6 nM for control and BK-treated cells, respectively).	Epoprostenol	112-116	kininogen 1	Homo sapiens	101-103
6146639-2	1984	Incubation of cells with 1 microM BK for 5 min at 37 degrees C led to a marked reduction (75-90%) in BK-induced PGI2 release and in total number of [3H]BK-binding sites with no change in dissociation constant (6.1 and 7.6 nM for control and BK-treated cells, respectively).	Tritium	149-151	kininogen 1	Homo sapiens	34-36
6146639-5	1984	After incubation with BK for approximately equal to 15 min, further incubation in the absence of BK for 30 min at 37 degrees C almost completely restored both receptor number and BK-induced PGI2 release.	Epoprostenol	190-194	kininogen 1	Homo sapiens	22-24
6146639-5	1984	After incubation with BK for approximately equal to 15 min, further incubation in the absence of BK for 30 min at 37 degrees C almost completely restored both receptor number and BK-induced PGI2 release.	Epoprostenol	190-194	kininogen 1	Homo sapiens	97-99
6146639-5	1984	After incubation with BK for approximately equal to 15 min, further incubation in the absence of BK for 30 min at 37 degrees C almost completely restored both receptor number and BK-induced PGI2 release.	Epoprostenol	190-194	kininogen 1	Homo sapiens	97-99
6146639-8	1984	During prolonged incubation without removal of BK, cells began to recover receptors by 5 h; greater than 99% of the bradykinin initially present disappeared by 3 h. Bacitracin greatly retarded BK disappearance and totally prevented recovery.	Bacitracin	165-175	kininogen 1	Homo sapiens	116-126
6146639-8	1984	During prolonged incubation without removal of BK, cells began to recover receptors by 5 h; greater than 99% of the bradykinin initially present disappeared by 3 h. Bacitracin greatly retarded BK disappearance and totally prevented recovery.	Bacitracin	165-175	kininogen 1	Homo sapiens	193-195
6208535-8	1984	Modification of arginine residues in ACE with cyclohexanedione or butanedione similarly inhibited hydrolysis of SP, bradykinin and Bz-Gly-Phe-Arg (80-93%) indicating an active site arginine is required for hydrolysis of SP.	Arginine	16-24	kininogen 1	Homo sapiens	116-126
6431752-5	1984	The rate of HMrK destruction in our experiments varied with the kallikrein preparation used, but assays of their hydrolytic activities against benzoyl arginine ethylester (BAEe) or the plasma kallikrein selective tripeptide substrate H-D-Pro-Phe-Arg-pNA (S-2302) did not discriminate between enzyme preparations with different HMrK-destroying capacities.	benzoylarginine ethyl ester	143-170	kininogen 1	Homo sapiens	12-16
6431752-5	1984	The rate of HMrK destruction in our experiments varied with the kallikrein preparation used, but assays of their hydrolytic activities against benzoyl arginine ethylester (BAEe) or the plasma kallikrein selective tripeptide substrate H-D-Pro-Phe-Arg-pNA (S-2302) did not discriminate between enzyme preparations with different HMrK-destroying capacities.	h-d-pro-phe-arg-pna	234-253	kininogen 1	Homo sapiens	12-16
6208535-8	1984	Modification of arginine residues in ACE with cyclohexanedione or butanedione similarly inhibited hydrolysis of SP, bradykinin and Bz-Gly-Phe-Arg (80-93%) indicating an active site arginine is required for hydrolysis of SP.	1,2-cyclohexanedione	46-62	kininogen 1	Homo sapiens	116-126
6430899-1	1984	We employed des-Arg9-bradykinin to investigate the relation between bradykinin-induced prostaglandin (PG) synthesis and bradykinin-induced protein accumulation.	Prostaglandins	87-100	kininogen 1	Homo sapiens	68-78
6373049-9	1984	Phospholipase activators were synergistic (bradykinin) or additive (angiotensin II) with high density lipoprotein in stimulation of prostaglandin synthesis.	Prostaglandins	132-145	kininogen 1	Homo sapiens	43-53
6430899-1	1984	We employed des-Arg9-bradykinin to investigate the relation between bradykinin-induced prostaglandin (PG) synthesis and bradykinin-induced protein accumulation.	Prostaglandins	87-100	kininogen 1	Homo sapiens	68-78
6430899-1	1984	We employed des-Arg9-bradykinin to investigate the relation between bradykinin-induced prostaglandin (PG) synthesis and bradykinin-induced protein accumulation.	Prostaglandins	102-104	kininogen 1	Homo sapiens	68-78
6430899-1	1984	We employed des-Arg9-bradykinin to investigate the relation between bradykinin-induced prostaglandin (PG) synthesis and bradykinin-induced protein accumulation.	Prostaglandins	102-104	kininogen 1	Homo sapiens	68-78
6430899-2	1984	In this feedback control system, bradykinin-induced PG synthesis limits bradykinin-induced protein production.	Prostaglandins	52-54	kininogen 1	Homo sapiens	33-43
6430899-2	1984	In this feedback control system, bradykinin-induced PG synthesis limits bradykinin-induced protein production.	Prostaglandins	52-54	kininogen 1	Homo sapiens	72-82
6430899-3	1984	At low concentration (5 X 10(-8) M), des-Arg9-bradykinin was significantly less active than bradykinin in stimulating the formation of prostaglandins by human fetal lung fibroblasts in culture.	Prostaglandins	135-149	kininogen 1	Homo sapiens	46-56
6430899-5	1984	In the presence of indomethacin, bradykinin-induced protein formation was increased further, whereas des-Arg9-bradykinin-induced protein formation was unchanged.	Indomethacin	19-31	kininogen 1	Homo sapiens	33-43
6430899-7	1984	The incorporation of [3H]thymidine into DNA in lung fibroblast cultures was increased 3-fold by des-Arg9-bradykinin alone or by bradykinin in combination with indomethacin.	[3h]thymidine	21-34	kininogen 1	Homo sapiens	105-115
6430899-7	1984	The incorporation of [3H]thymidine into DNA in lung fibroblast cultures was increased 3-fold by des-Arg9-bradykinin alone or by bradykinin in combination with indomethacin.	[3h]thymidine	21-34	kininogen 1	Homo sapiens	128-138
6430899-8	1984	Des-Arg9-[Leu8]bradykinin inhibited the des-Arg9-bradykinin-induced protein formation and cell division.	des-arg9	40-48	kininogen 1	Homo sapiens	15-25
6430899-8	1984	Des-Arg9-[Leu8]bradykinin inhibited the des-Arg9-bradykinin-induced protein formation and cell division.	des-arg9	40-48	kininogen 1	Homo sapiens	49-59
6146940-0	1984	Neurotransmitter-blocking agents influence antinociceptive effects of carbamazepine, baclofen, pentazocine and morphine on bradykinin-induced trigeminal pain.	Carbamazepine	70-83	kininogen 1	Homo sapiens	123-133
6146940-0	1984	Neurotransmitter-blocking agents influence antinociceptive effects of carbamazepine, baclofen, pentazocine and morphine on bradykinin-induced trigeminal pain.	Baclofen	85-93	kininogen 1	Homo sapiens	123-133
6146940-0	1984	Neurotransmitter-blocking agents influence antinociceptive effects of carbamazepine, baclofen, pentazocine and morphine on bradykinin-induced trigeminal pain.	Pentazocine	95-106	kininogen 1	Homo sapiens	123-133
6146940-0	1984	Neurotransmitter-blocking agents influence antinociceptive effects of carbamazepine, baclofen, pentazocine and morphine on bradykinin-induced trigeminal pain.	Morphine	111-119	kininogen 1	Homo sapiens	123-133
6208535-8	1984	Modification of arginine residues in ACE with cyclohexanedione or butanedione similarly inhibited hydrolysis of SP, bradykinin and Bz-Gly-Phe-Arg (80-93%) indicating an active site arginine is required for hydrolysis of SP.	Diacetyl	66-77	kininogen 1	Homo sapiens	116-126
6564947-5	1984	Procedural losses are monitored by measuring the recovery of [3H]bradykinin and [3H]lysylbradykinin.	Tritium	62-64	kininogen 1	Homo sapiens	65-75
6564947-6	1984	Simple methods for labeling of bradykinin and lysylbradykinin with tritium are also presented.	Tritium	67-74	kininogen 1	Homo sapiens	31-41
6564947-7	1984	Recoveries of [3H]bradykinin and [3H]lysylbradykinin from biological material ranged between 77 and 91%.	Tritium	15-17	kininogen 1	Homo sapiens	18-28
6435182-6	1984	We conclude that these observations using dispersed endometrial cells are consistent with previous work showing that histamine, bradykinin and PMA act by stimulating acylhydrolase activity, thereby liberating precursors such as arachidonic acid which are converted to prostaglandins by the cyclo-oxygenase complex.	Arachidonic Acid	228-244	kininogen 1	Homo sapiens	128-138
6435182-6	1984	We conclude that these observations using dispersed endometrial cells are consistent with previous work showing that histamine, bradykinin and PMA act by stimulating acylhydrolase activity, thereby liberating precursors such as arachidonic acid which are converted to prostaglandins by the cyclo-oxygenase complex.	Prostaglandins	268-282	kininogen 1	Homo sapiens	128-138
6329831-2	1984	Bradykinin inhibited secretion of hydrochloric acid in the frog gastric mucosa.	Hydrochloric Acid	34-51	kininogen 1	Homo sapiens	0-10
6143761-0	1984	Detection and quantitation of fluorescamine-labeled bradykinin, its analogues and metabolites using high-performance liquid chromatography.	Fluorescamine	30-43	kininogen 1	Homo sapiens	52-62
6709646-0	1984	Cleavage of the Arg1-Pro2 bond of bradykinin by a human lung peptidase: isolation, characterization, and inhibition by several beta-lactam antibiotics.	beta-Lactams	127-138	kininogen 1	Homo sapiens	34-44
6709646-2	1984	The enzyme also catalyzes the cleavage of arginine from des-[Arg9]-bradykinin and the hydrolysis of several X-proline dipeptides including L-arginyl-L-proline, L-leucyl-L-proline, and L-alanyl-L-proline.	Arginine	42-50	kininogen 1	Homo sapiens	67-77
6709646-2	1984	The enzyme also catalyzes the cleavage of arginine from des-[Arg9]-bradykinin and the hydrolysis of several X-proline dipeptides including L-arginyl-L-proline, L-leucyl-L-proline, and L-alanyl-L-proline.	x-proline	108-117	kininogen 1	Homo sapiens	67-77
6709646-2	1984	The enzyme also catalyzes the cleavage of arginine from des-[Arg9]-bradykinin and the hydrolysis of several X-proline dipeptides including L-arginyl-L-proline, L-leucyl-L-proline, and L-alanyl-L-proline.	Dipeptides	118-128	kininogen 1	Homo sapiens	67-77
6709646-2	1984	The enzyme also catalyzes the cleavage of arginine from des-[Arg9]-bradykinin and the hydrolysis of several X-proline dipeptides including L-arginyl-L-proline, L-leucyl-L-proline, and L-alanyl-L-proline.	arginylproline	139-158	kininogen 1	Homo sapiens	67-77
6709646-2	1984	The enzyme also catalyzes the cleavage of arginine from des-[Arg9]-bradykinin and the hydrolysis of several X-proline dipeptides including L-arginyl-L-proline, L-leucyl-L-proline, and L-alanyl-L-proline.	leucylproline	160-178	kininogen 1	Homo sapiens	67-77
6709646-2	1984	The enzyme also catalyzes the cleavage of arginine from des-[Arg9]-bradykinin and the hydrolysis of several X-proline dipeptides including L-arginyl-L-proline, L-leucyl-L-proline, and L-alanyl-L-proline.	alanylproline	184-202	kininogen 1	Homo sapiens	67-77
6381834-0	1984	[Effect of angiotensin I converting enzyme inhibitor (captopril) on blood pressure and bradykinin in patients with excessive aldosterone secretion].	Captopril	54-63	kininogen 1	Homo sapiens	87-97
6141950-1	1984	Bradykinin stimulates [3H]thymidine incorporation and DNA synthesis in resting, serum-deprived NIL8 hamster cells.	Tritium	23-25	kininogen 1	Homo sapiens	0-10
6141950-3	1984	Other kinin peptides including lys-bradykinin (kallidin) and met-lys-bradykinin also stimulate [3H]thymidine incorporation in the NIL8 cells, whereas desarg9-bradykinin is without effect, suggesting action of the kinin peptides through type B2 receptors.	Tritium	96-98	kininogen 1	Homo sapiens	35-45
6141950-3	1984	Other kinin peptides including lys-bradykinin (kallidin) and met-lys-bradykinin also stimulate [3H]thymidine incorporation in the NIL8 cells, whereas desarg9-bradykinin is without effect, suggesting action of the kinin peptides through type B2 receptors.	Tritium	96-98	kininogen 1	Homo sapiens	69-79
6141950-3	1984	Other kinin peptides including lys-bradykinin (kallidin) and met-lys-bradykinin also stimulate [3H]thymidine incorporation in the NIL8 cells, whereas desarg9-bradykinin is without effect, suggesting action of the kinin peptides through type B2 receptors.	Tritium	96-98	kininogen 1	Homo sapiens	69-79
6141950-4	1984	Bradykinin also stimulates DNA synthesis in IMR-90 human fibroblasts; however, this effect is observed only in the presence of indomethacin, which blocks prostaglandin synthesis.	Indomethacin	127-139	kininogen 1	Homo sapiens	0-10
6141950-4	1984	Bradykinin also stimulates DNA synthesis in IMR-90 human fibroblasts; however, this effect is observed only in the presence of indomethacin, which blocks prostaglandin synthesis.	Prostaglandins	154-167	kininogen 1	Homo sapiens	0-10
6141950-5	1984	These results suggest that prostaglandins act as negative modulators of the growth-stimulatory effects of bradykinin in the fibroblasts.	Prostaglandins	27-41	kininogen 1	Homo sapiens	106-116
6141950-7	1984	The direct effect of bradykinin observed in the NIL8 cells may be attributable to the relative resistance of these cells to growth inhibition by prostaglandins.	Prostaglandins	145-159	kininogen 1	Homo sapiens	21-31
6143761-5	1984	Labeled kinins were eluted in the following order: bradykinin, Lys-bradykinin, and Met-Lys-bradykinin.	Lysine	63-66	kininogen 1	Homo sapiens	67-77
6143761-5	1984	Labeled kinins were eluted in the following order: bradykinin, Lys-bradykinin, and Met-Lys-bradykinin.	Lysine	63-66	kininogen 1	Homo sapiens	67-77
6437213-2	1984	The purified enzyme cleaved arginine from des-(Arg9)-bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe) had a molecular weight in nondenaturing buffers of 155,000 +/- 6,900 daltons, was not inactivated by chelating agents, had a pH optimum of 7.2, and was stimulated by manganous ions.	Arginine	28-36	kininogen 1	Homo sapiens	53-63
6141801-4	1984	Venoconstriction caused by U46619, bradykinin and 5-hydroxytryptamine was reduced during inhibition of phospholipase A2 with mepacrine.	Quinacrine	125-134	kininogen 1	Homo sapiens	35-45
6437213-2	1984	The purified enzyme cleaved arginine from des-(Arg9)-bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe) had a molecular weight in nondenaturing buffers of 155,000 +/- 6,900 daltons, was not inactivated by chelating agents, had a pH optimum of 7.2, and was stimulated by manganous ions.	arg-pro-pro-gly	65-80	kininogen 1	Homo sapiens	53-63
6437213-2	1984	The purified enzyme cleaved arginine from des-(Arg9)-bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe) had a molecular weight in nondenaturing buffers of 155,000 +/- 6,900 daltons, was not inactivated by chelating agents, had a pH optimum of 7.2, and was stimulated by manganous ions.	Phenylalanine	81-84	kininogen 1	Homo sapiens	53-63
6437213-2	1984	The purified enzyme cleaved arginine from des-(Arg9)-bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe) had a molecular weight in nondenaturing buffers of 155,000 +/- 6,900 daltons, was not inactivated by chelating agents, had a pH optimum of 7.2, and was stimulated by manganous ions.	Serine	85-88	kininogen 1	Homo sapiens	53-63
6437213-2	1984	The purified enzyme cleaved arginine from des-(Arg9)-bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe) had a molecular weight in nondenaturing buffers of 155,000 +/- 6,900 daltons, was not inactivated by chelating agents, had a pH optimum of 7.2, and was stimulated by manganous ions.	H-Pro-Phe-OH	89-96	kininogen 1	Homo sapiens	53-63
6437213-4	1984	Extensively washed and intact human erythrocytes cleaved arginine from exogenously supplied des-(Arg9)-bradykinin; arginine was the earliest-appearing reaction product.	Arginine	57-65	kininogen 1	Homo sapiens	103-113
6437213-4	1984	Extensively washed and intact human erythrocytes cleaved arginine from exogenously supplied des-(Arg9)-bradykinin; arginine was the earliest-appearing reaction product.	Arginine	115-123	kininogen 1	Homo sapiens	103-113
6437780-1	1984	By inhibiting ACE, captopril blocks the conversion of AI or AII and augments the effects of bradykinin both in vitro and in vivo.	Captopril	19-28	kininogen 1	Homo sapiens	92-102
6142832-4	1984	The data obtained also attest to a possible involvement of the imidazole group of histidine in the realization of the myotropic effect of bradykinin.	imidazole	63-72	kininogen 1	Homo sapiens	138-148
6142832-4	1984	The data obtained also attest to a possible involvement of the imidazole group of histidine in the realization of the myotropic effect of bradykinin.	Histidine	82-91	kininogen 1	Homo sapiens	138-148
6085073-1	1984	In a previous study of plasma specimens from reactors to clinical dextran, it was concluded that a factor activated by acetone converted the high-molecular-weight kininogen (HMrK) into a non-functional state.	Dextrans	66-73	kininogen 1	Homo sapiens	141-172
6525060-4	1984	Bradykinin (PG biosynthesis stimulator) results in the increased PG production with a simultaneous decrease of the lipid granules number.	Prostaglandins	12-14	kininogen 1	Homo sapiens	0-10
6525060-4	1984	Bradykinin (PG biosynthesis stimulator) results in the increased PG production with a simultaneous decrease of the lipid granules number.	Prostaglandins	65-67	kininogen 1	Homo sapiens	0-10
6607067-1	1984	Activation of bovine factor IX by surface bound factor XIa which was generated either by activation of human citrated factor IX deficient plasma or a mixture of purified human factors XII, high molecular weight kininogen (HMWK) and XI in glass tubes, is accelerated by cephalin.	Phosphatidylethanolamines	269-277	kininogen 1	Homo sapiens	189-220
6085073-1	1984	In a previous study of plasma specimens from reactors to clinical dextran, it was concluded that a factor activated by acetone converted the high-molecular-weight kininogen (HMrK) into a non-functional state.	Dextrans	66-73	kininogen 1	Homo sapiens	174-178
6085073-1	1984	In a previous study of plasma specimens from reactors to clinical dextran, it was concluded that a factor activated by acetone converted the high-molecular-weight kininogen (HMrK) into a non-functional state.	Acetone	119-126	kininogen 1	Homo sapiens	141-172
6206350-3	1984	Activation of vasodilator mechanisms by endogenously produced vasodilator prostaglandins in isolated arteries or in vivo can attenuate the vasoconstrictor activity of angiotensin II and in some cases mediate the vasodilator effects of bradykinin.	Prostaglandins	74-88	kininogen 1	Homo sapiens	235-245
6085073-1	1984	In a previous study of plasma specimens from reactors to clinical dextran, it was concluded that a factor activated by acetone converted the high-molecular-weight kininogen (HMrK) into a non-functional state.	Acetone	119-126	kininogen 1	Homo sapiens	174-178
6715551-3	1984	Two distinct chemical species were obtained which were characterized on a chromatographic, chemical as well as charge basis as a mono-iodinated form of [Tyr8]-bradykinin using the lactoperoxidase procedure and a di-iodinated entity using chloramine-T technique.	chloramine-T	238-250	kininogen 1	Homo sapiens	159-169
6423923-7	1984	The mechanism of these effects was studied using doses of bradykinin or A23187 which resulted in increases in Ca2+ influx and prostacyclin synthesis of similar magnitude for each agonist.	Epoprostenol	126-138	kininogen 1	Homo sapiens	58-68
6423923-1	1984	Both bradykinin (EC50 = 8 ng/ml) and the ionophore A23187 (EC50 = 3 X 10(-7) M) potently stimulated arachidonate release and prostaglandin synthesis in porcine aortic endothelial cells.	Arachidonic Acid	100-112	kininogen 1	Homo sapiens	5-15
6423923-10	1984	Pimozide inhibited bradykinin-stimulated prostacyclin synthesis at low doses (ID50 = 3 X 10(-6) M).	Pimozide	0-8	kininogen 1	Homo sapiens	19-29
6423923-1	1984	Both bradykinin (EC50 = 8 ng/ml) and the ionophore A23187 (EC50 = 3 X 10(-7) M) potently stimulated arachidonate release and prostaglandin synthesis in porcine aortic endothelial cells.	Prostaglandins	125-138	kininogen 1	Homo sapiens	5-15
6423923-4	1984	Whereas the arachidonate released in response to bradykinin was transient, that released in response to A23187 was more prolonged, and paralleled a continued influx of Ca2+.	Arachidonic Acid	12-24	kininogen 1	Homo sapiens	49-59
6423923-10	1984	Pimozide inhibited bradykinin-stimulated prostacyclin synthesis at low doses (ID50 = 3 X 10(-6) M).	Epoprostenol	41-53	kininogen 1	Homo sapiens	19-29
6140924-2	1983	125I-Labeled derivatives of [Tyr1]-kallidin and [Tyr-8]-bradykinin bound to the EDTA-inhibited enzyme, and binding was inhibited by nonradioactive BK.	Tyrosine	29-32	kininogen 1	Homo sapiens	147-149
6140924-2	1983	125I-Labeled derivatives of [Tyr1]-kallidin and [Tyr-8]-bradykinin bound to the EDTA-inhibited enzyme, and binding was inhibited by nonradioactive BK.	Edetic Acid	80-84	kininogen 1	Homo sapiens	56-66
6140924-2	1983	125I-Labeled derivatives of [Tyr1]-kallidin and [Tyr-8]-bradykinin bound to the EDTA-inhibited enzyme, and binding was inhibited by nonradioactive BK.	Edetic Acid	80-84	kininogen 1	Homo sapiens	147-149
6140924-7	1983	BK at 1.2 +/- 0.2 X 10(-6) M decreased the rate of [3H]-HGG hydrolysis by 50%.	Tritium	52-54	kininogen 1	Homo sapiens	0-2
6670737-4	1983	The resulting molecular weight (30,500 +/- 800 g/mol) and partial specific volume (0.660 +/- 0.008 ml/g) are consistent with the idea that a sizeable fraction of the carbohydrate of high-molecular-weight kininogen is associated with the light chain.	Carbohydrates	166-178	kininogen 1	Homo sapiens	182-213
6358755-3	1983	This enzyme, highly active in brain and other tissues, catabolizes proline-containing peptides such as substance P, neurotensin, luteinizing hormone-releasing hormone, thyrotropin releasing hormone, bradykinin and angiotensin II.	Proline	67-74	kininogen 1	Homo sapiens	199-209
6556144-2	1983	Bradykinin is destroyed by two enzymes: a plasma carboxypeptidase (anaphylatoxin inactivator) removes the COOH-terminal arginine to yield an inactive octapeptide, and a dipeptidase (identical to the angiotensin-converting enzyme) removes the COOH-terminal Phe-Arg to yield a fragment of seven amino acids that is further fragmented to an end product of five amino acids.	Carbonic Acid	106-110	kininogen 1	Homo sapiens	0-10
6556144-2	1983	Bradykinin is destroyed by two enzymes: a plasma carboxypeptidase (anaphylatoxin inactivator) removes the COOH-terminal arginine to yield an inactive octapeptide, and a dipeptidase (identical to the angiotensin-converting enzyme) removes the COOH-terminal Phe-Arg to yield a fragment of seven amino acids that is further fragmented to an end product of five amino acids.	Arginine	120-128	kininogen 1	Homo sapiens	0-10
6556144-2	1983	Bradykinin is destroyed by two enzymes: a plasma carboxypeptidase (anaphylatoxin inactivator) removes the COOH-terminal arginine to yield an inactive octapeptide, and a dipeptidase (identical to the angiotensin-converting enzyme) removes the COOH-terminal Phe-Arg to yield a fragment of seven amino acids that is further fragmented to an end product of five amino acids.	Carbonic Acid	242-246	kininogen 1	Homo sapiens	0-10
6556144-2	1983	Bradykinin is destroyed by two enzymes: a plasma carboxypeptidase (anaphylatoxin inactivator) removes the COOH-terminal arginine to yield an inactive octapeptide, and a dipeptidase (identical to the angiotensin-converting enzyme) removes the COOH-terminal Phe-Arg to yield a fragment of seven amino acids that is further fragmented to an end product of five amino acids.	phenylalanylarginine	256-263	kininogen 1	Homo sapiens	0-10
6553501-1	1983	Human high molecular weight kininogen (HMWK), a single-chain protein with mol wt 120,000, is cleaved by human urinary kallikrein (HUK) to release kinin from within a disulfide loop and form a two-chain protein that retains all the procoagulant activity of the native molecule.	Disulfides	166-175	kininogen 1	Homo sapiens	6-37
6685967-0	1983	Activation of factor XII in human plasma: protection by benzamidine of the cofactor function of high molecular weight kininogen.	benzamidine	56-67	kininogen 1	Homo sapiens	96-127
6685967-2	1983	When the incubation was carried out in the presence of benzamidine 7 mM, the cofactor capacity of high molecular weight kininogen (HMrK) was protected against destruction by a serine protease which was not plasma kallikrein.	benzamidine	55-66	kininogen 1	Homo sapiens	98-136
6626744-1	1983	Coagulation factor XI was purified from human plasma using ion-exchange chromatography and affinity chromatography on high molecular weight kininogen-Sepharose.	Sepharose	150-159	kininogen 1	Homo sapiens	118-149
6363144-5	1983	Captopril elevated plasma bradykinin concentration (PBK) from a control value of 12.5 +/- 4.1 (mean +/- s.d.)	Captopril	0-9	kininogen 1	Homo sapiens	26-36
6604770-5	1983	Indeed, small amounts of HMWK inhibited activation of HF by ellagic acid.	Ellagic Acid	60-72	kininogen 1	Homo sapiens	25-29
6604770-6	1983	Physiological concentration of HMWK had little or no influence on the activation of HF by sulfatides, kaolin, or glass, but higher concentrations (3 to 6 times more) showed the same inhibitory effect as after activation by ellagic acid.	Ellagic Acid	223-235	kininogen 1	Homo sapiens	31-35
6553501-1	1983	Human high molecular weight kininogen (HMWK), a single-chain protein with mol wt 120,000, is cleaved by human urinary kallikrein (HUK) to release kinin from within a disulfide loop and form a two-chain protein that retains all the procoagulant activity of the native molecule.	Disulfides	166-175	kininogen 1	Homo sapiens	39-43
6553501-2	1983	Cleavage of HMWK by HUK is associated with a reduction in size to mol wt 115,000, as assessed by SDS-PAGE of unreduced protein, whereas the two chains of the reduced protein present together as a single broad band with mol wt 64,000.	Sodium Dodecyl Sulfate	97-100	kininogen 1	Homo sapiens	12-16
6418250-2	1983	They produce the same prostaglandins after stimulation with bradykinin.	Prostaglandins	22-36	kininogen 1	Homo sapiens	60-70
6135711-3	1983	During incubation with intact fibroblasts, intact [3H]bradykinin was lost much more rapidly at 37 degrees than at 4 degrees C as determined by bioassay, high-performance liquid chromatography, and ion-exchange chromatography, and is likely to be degraded.	Tritium	51-53	kininogen 1	Homo sapiens	54-64
6418250-5	1983	During the first 5 min after removal of the drugs from the incubation medium, bradykinin-stimulated release remains dose-dependently inhibited (P less than 0.001) in ASA-, but not in dipyrone-treated cultures.	Aspirin	166-169	kininogen 1	Homo sapiens	78-88
6135711-4	1983	At 4 degrees, but not at 37 degrees C, bradykinin remained intact in the presence of 2 mM bacitracin, but not in the presence of soybean trypsin inhibitor or SQ-20881, an inhibitor of kininase II.	Bacitracin	90-100	kininogen 1	Homo sapiens	39-49
6135711-8	1983	The relative potencies of bradykinin analogues and unrelated peptides in competing for [3H]bradykinin binding indicated a specificity of the binding sites consistent with that of a B2 type receptor.	Tritium	88-90	kininogen 1	Homo sapiens	26-36
6135711-8	1983	The relative potencies of bradykinin analogues and unrelated peptides in competing for [3H]bradykinin binding indicated a specificity of the binding sites consistent with that of a B2 type receptor.	Tritium	88-90	kininogen 1	Homo sapiens	91-101
6135711-9	1983	Potencies of the peptides in displacing [3H]bradykinin correlated with their abilities to release prostacyclin, determined as its metabolite 6-keto-PGF1 alpha.	Tritium	41-43	kininogen 1	Homo sapiens	44-54
6135711-9	1983	Potencies of the peptides in displacing [3H]bradykinin correlated with their abilities to release prostacyclin, determined as its metabolite 6-keto-PGF1 alpha.	Epoprostenol	98-110	kininogen 1	Homo sapiens	44-54
6135711-9	1983	Potencies of the peptides in displacing [3H]bradykinin correlated with their abilities to release prostacyclin, determined as its metabolite 6-keto-PGF1 alpha.	6-Ketoprostaglandin F1 alpha	141-158	kininogen 1	Homo sapiens	44-54
6343536-2	1983	Sulfatides or EA rapidly and efficiently initiated intrinsic coagulation in normal plasma but, under the conditions tested, only trivially corrected the prolonged partial thromboplastin clotting times of plasma deficient in prekallikrein or HMWK.	Sulfoglycosphingolipids	0-10	kininogen 1	Homo sapiens	241-245
6867714-3	1983	Absence of magnesium in the medium significantly potentiated the contractile response of the vessels to bradykinin, angiotensin II, serotonin, and prostaglandin F2 alpha.	Magnesium	11-20	kininogen 1	Homo sapiens	104-114
6618444-0	1983	Dose-dependent effect of bradykinin on muscular blood flow and glucose uptake in man.	Glucose	63-70	kininogen 1	Homo sapiens	25-35
6618444-3	1983	At lower bradykinin concentrations (2.5-25 ng/min), muscular glucose uptake was raised parallel to the increased blood flow from basal 0.71 +/- 0.30 to 2.93 +/- 0.50 mumol/(100 g X min).	Glucose	61-68	kininogen 1	Homo sapiens	9-19
6311635-1	1983	In order to investigate the possible role of bradykinin in the hypotensive mechanism of angiotensin I converting enzyme inhibitor (Captopril) in renin-independent essential hypertension (EHT), we studied the effects of the single administration of 100 mg captopril on plasma bradykinin levels by sensitive radioimmunoassay in 21 EHT, who showed agonistic responses to 1Sar, 8Ile-angiotensin II (A IIA).	Captopril	131-140	kininogen 1	Homo sapiens	45-55
6575386-4	1983	With human urinary kallikrein, apparent second-order rate constants (kcat/Km) of 1.46 X 105, 8.6 X 104, and 5.08 X 104 M-1.S-1 were obtained with LMWK, HMWK, and alpha-N-p-tosyl-L-arginine methyl ester (TAMe), respectively; with human pancreatic kallikrein, values of 8.7 X 103 and 7.3 X 104 M-1.S-1 were obtained with HMWK and TAMe.	alpha-n-p	162-171	kininogen 1	Homo sapiens	152-156
6575386-4	1983	With human urinary kallikrein, apparent second-order rate constants (kcat/Km) of 1.46 X 105, 8.6 X 104, and 5.08 X 104 M-1.S-1 were obtained with LMWK, HMWK, and alpha-N-p-tosyl-L-arginine methyl ester (TAMe), respectively; with human pancreatic kallikrein, values of 8.7 X 103 and 7.3 X 104 M-1.S-1 were obtained with HMWK and TAMe.	Tosylarginine Methyl Ester	172-201	kininogen 1	Homo sapiens	152-156
6575386-4	1983	With human urinary kallikrein, apparent second-order rate constants (kcat/Km) of 1.46 X 105, 8.6 X 104, and 5.08 X 104 M-1.S-1 were obtained with LMWK, HMWK, and alpha-N-p-tosyl-L-arginine methyl ester (TAMe), respectively; with human pancreatic kallikrein, values of 8.7 X 103 and 7.3 X 104 M-1.S-1 were obtained with HMWK and TAMe.	Tosylarginine Methyl Ester	203-207	kininogen 1	Homo sapiens	152-156
6349683-8	1983	Both enzymes inactivated bradykinin by release of the C-terminal dipeptide but were inhibited differentially by specific inhibitors.	Dipeptides	65-74	kininogen 1	Homo sapiens	25-35
6311635-10	1983	The present results suggest that bradykinin may be involved in the hypotensive action of captopril in the EHT subgroup, where the renin-angiotensin system appears to play an inert role for the elevation of blood pressure.	Captopril	89-98	kininogen 1	Homo sapiens	33-43
6688484-5	1983	The 6-keto-PGF1 alpha/TxB2 ratio was increased by a thromboxane synthetase inhibitor and various peptides, e.g. DDAVP and bradykinin, and was decreased by arachidonic acid.	6-keto-pgf1	4-15	kininogen 1	Homo sapiens	122-132
6341768-1	1983	It has recently been observed that administration of bradykinin to diabetic patients improves peripheral glucose utilization.	Glucose	105-112	kininogen 1	Homo sapiens	53-63
6841471-3	1983	This dilatatory effect of bradykinin in vitro was found only in arteries preconstricted with prostaglandin F2 alpha or 5-hydroxytryptamine.	Dinoprost	93-115	kininogen 1	Homo sapiens	26-36
6841471-3	1983	This dilatatory effect of bradykinin in vitro was found only in arteries preconstricted with prostaglandin F2 alpha or 5-hydroxytryptamine.	Serotonin	119-138	kininogen 1	Homo sapiens	26-36
6136000-3	1983	On the cat middle cerebral artery in vitro (but not the basilar artery), under resting tension and when contracted with 5-hydroxytryptamine (5-HT) or KCl, concentration related relaxations were produced by BK, M-L-BK, and des-Arg9-BK, this being the order of relative potency of the three kinins.	Serotonin	120-139	kininogen 1	Homo sapiens	206-208
6136000-3	1983	On the cat middle cerebral artery in vitro (but not the basilar artery), under resting tension and when contracted with 5-hydroxytryptamine (5-HT) or KCl, concentration related relaxations were produced by BK, M-L-BK, and des-Arg9-BK, this being the order of relative potency of the three kinins.	Serotonin	120-139	kininogen 1	Homo sapiens	214-216
6136000-3	1983	On the cat middle cerebral artery in vitro (but not the basilar artery), under resting tension and when contracted with 5-hydroxytryptamine (5-HT) or KCl, concentration related relaxations were produced by BK, M-L-BK, and des-Arg9-BK, this being the order of relative potency of the three kinins.	Serotonin	141-145	kininogen 1	Homo sapiens	206-208
6136000-3	1983	On the cat middle cerebral artery in vitro (but not the basilar artery), under resting tension and when contracted with 5-hydroxytryptamine (5-HT) or KCl, concentration related relaxations were produced by BK, M-L-BK, and des-Arg9-BK, this being the order of relative potency of the three kinins.	Serotonin	141-145	kininogen 1	Homo sapiens	214-216
6136000-3	1983	On the cat middle cerebral artery in vitro (but not the basilar artery), under resting tension and when contracted with 5-hydroxytryptamine (5-HT) or KCl, concentration related relaxations were produced by BK, M-L-BK, and des-Arg9-BK, this being the order of relative potency of the three kinins.	Potassium Chloride	150-153	kininogen 1	Homo sapiens	206-208
6310481-6	1983	This response to bradykinin can still be seen during the veratridine-induced oscillations of the membrane potential.	Veratridine	57-68	kininogen 1	Homo sapiens	17-27
6688484-5	1983	The 6-keto-PGF1 alpha/TxB2 ratio was increased by a thromboxane synthetase inhibitor and various peptides, e.g. DDAVP and bradykinin, and was decreased by arachidonic acid.	Thromboxane B2	22-26	kininogen 1	Homo sapiens	122-132
6339626-6	1983	Complete cleavage of native single-chain HMWK by tryptase occurred in less than 10 min as analyzed by electrophoresis in sodium dodecyl sulfate polyacrylamide slab gels.	Sodium Dodecyl Sulfate	121-143	kininogen 1	Homo sapiens	41-45
6406551-9	1983	Platelet high-molecular weight kininogen was secreted from platelets after exposure to ionophore A23187 (3-15 microM), collagen (5-150 micrograms/ml), and thrombin (1.6 U/ml).	Calcimycin	97-103	kininogen 1	Homo sapiens	9-40
6339626-6	1983	Complete cleavage of native single-chain HMWK by tryptase occurred in less than 10 min as analyzed by electrophoresis in sodium dodecyl sulfate polyacrylamide slab gels.	polyacrylamide	144-158	kininogen 1	Homo sapiens	41-45
6302691-0	1983	Bradykinin stimulates phospholipid methylation, calcium influx, prostaglandin formation, and cAMP accumulation in human fibroblasts.	Phospholipids	22-34	kininogen 1	Homo sapiens	0-10
6302691-0	1983	Bradykinin stimulates phospholipid methylation, calcium influx, prostaglandin formation, and cAMP accumulation in human fibroblasts.	Calcium	48-55	kininogen 1	Homo sapiens	0-10
6302691-0	1983	Bradykinin stimulates phospholipid methylation, calcium influx, prostaglandin formation, and cAMP accumulation in human fibroblasts.	Prostaglandins	64-77	kininogen 1	Homo sapiens	0-10
6302691-0	1983	Bradykinin stimulates phospholipid methylation, calcium influx, prostaglandin formation, and cAMP accumulation in human fibroblasts.	Cyclic AMP	93-97	kininogen 1	Homo sapiens	0-10
6302691-1	1983	The biochemical events that lead to bradykinin stimulation of cAMP accumulation in human fibroblasts were examined.	Cyclic AMP	62-66	kininogen 1	Homo sapiens	36-46
6302691-2	1983	Treatment of human fibroblasts with bradykinin increases phospholipid methylation, Ca2+ influx, arachidonic acid release, prostaglandin formation, and cAMP content.	Phospholipids	57-69	kininogen 1	Homo sapiens	36-46
6302691-2	1983	Treatment of human fibroblasts with bradykinin increases phospholipid methylation, Ca2+ influx, arachidonic acid release, prostaglandin formation, and cAMP content.	Arachidonic Acid	96-112	kininogen 1	Homo sapiens	36-46
6302691-2	1983	Treatment of human fibroblasts with bradykinin increases phospholipid methylation, Ca2+ influx, arachidonic acid release, prostaglandin formation, and cAMP content.	Prostaglandins	122-135	kininogen 1	Homo sapiens	36-46
6302691-2	1983	Treatment of human fibroblasts with bradykinin increases phospholipid methylation, Ca2+ influx, arachidonic acid release, prostaglandin formation, and cAMP content.	Cyclic AMP	151-155	kininogen 1	Homo sapiens	36-46
6302691-5	1983	Bradykinin caused a release of arachidonic acid from methylated phospholipids (phosphatidylcholine) and phosphatidylinositol.	Arachidonic Acid	31-47	kininogen 1	Homo sapiens	0-10
6302691-5	1983	Bradykinin caused a release of arachidonic acid from methylated phospholipids (phosphatidylcholine) and phosphatidylinositol.	Phospholipids	64-77	kininogen 1	Homo sapiens	0-10
6302691-5	1983	Bradykinin caused a release of arachidonic acid from methylated phospholipids (phosphatidylcholine) and phosphatidylinositol.	Phosphatidylcholines	79-98	kininogen 1	Homo sapiens	0-10
6302691-5	1983	Bradykinin caused a release of arachidonic acid from methylated phospholipids (phosphatidylcholine) and phosphatidylinositol.	Phosphatidylinositols	104-124	kininogen 1	Homo sapiens	0-10
6302691-6	1983	3-Deazaadenosine, a methyltransferase inhibitor, almost completely inhibited bradykinin-stimulated phospholipid methylation and Ca2+ influx and partially reduced arachidonic acid release and prostaglandin formation but had no effect on cAMP formation.	3-deazaadenosine	0-16	kininogen 1	Homo sapiens	77-87
6302691-6	1983	3-Deazaadenosine, a methyltransferase inhibitor, almost completely inhibited bradykinin-stimulated phospholipid methylation and Ca2+ influx and partially reduced arachidonic acid release and prostaglandin formation but had no effect on cAMP formation.	Phospholipids	99-111	kininogen 1	Homo sapiens	77-87
6302691-6	1983	3-Deazaadenosine, a methyltransferase inhibitor, almost completely inhibited bradykinin-stimulated phospholipid methylation and Ca2+ influx and partially reduced arachidonic acid release and prostaglandin formation but had no effect on cAMP formation.	Arachidonic Acid	162-178	kininogen 1	Homo sapiens	77-87
6302691-6	1983	3-Deazaadenosine, a methyltransferase inhibitor, almost completely inhibited bradykinin-stimulated phospholipid methylation and Ca2+ influx and partially reduced arachidonic acid release and prostaglandin formation but had no effect on cAMP formation.	Prostaglandins	191-204	kininogen 1	Homo sapiens	77-87
6302691-6	1983	3-Deazaadenosine, a methyltransferase inhibitor, almost completely inhibited bradykinin-stimulated phospholipid methylation and Ca2+ influx and partially reduced arachidonic acid release and prostaglandin formation but had no effect on cAMP formation.	Cyclic AMP	236-240	kininogen 1	Homo sapiens	77-87
6302691-7	1983	Mepacrine, a phospholipase inhibitor, blocked bradykinin-induced arachidonic acid release, prostaglandin release, and cAMP accumulation.	Quinacrine	0-9	kininogen 1	Homo sapiens	46-56
6302691-7	1983	Mepacrine, a phospholipase inhibitor, blocked bradykinin-induced arachidonic acid release, prostaglandin release, and cAMP accumulation.	Arachidonic Acid	65-81	kininogen 1	Homo sapiens	46-56
6302691-7	1983	Mepacrine, a phospholipase inhibitor, blocked bradykinin-induced arachidonic acid release, prostaglandin release, and cAMP accumulation.	Prostaglandins	91-104	kininogen 1	Homo sapiens	46-56
6302691-7	1983	Mepacrine, a phospholipase inhibitor, blocked bradykinin-induced arachidonic acid release, prostaglandin release, and cAMP accumulation.	Cyclic AMP	118-122	kininogen 1	Homo sapiens	46-56
6302691-8	1983	Indomethacin, a cyclooxygenase inhibitor, blocked the effect of bradykinin on cAMP accumulation.	Indomethacin	0-12	kininogen 1	Homo sapiens	64-74
6302691-8	1983	Indomethacin, a cyclooxygenase inhibitor, blocked the effect of bradykinin on cAMP accumulation.	Cyclic AMP	78-82	kininogen 1	Homo sapiens	64-74
6302691-10	1983	These observations indicate that bradykinin generates cAMP via arachidonic acid release and subsequent formation of prostaglandins.	Cyclic AMP	54-58	kininogen 1	Homo sapiens	33-43
6302691-10	1983	These observations indicate that bradykinin generates cAMP via arachidonic acid release and subsequent formation of prostaglandins.	Arachidonic Acid	63-79	kininogen 1	Homo sapiens	33-43
6302691-10	1983	These observations indicate that bradykinin generates cAMP via arachidonic acid release and subsequent formation of prostaglandins.	Prostaglandins	116-130	kininogen 1	Homo sapiens	33-43
6339076-5	1983	In addition, it was observed that the Na+ influx stimulated by Lys-bradykinin or by the combination of four growth factors was completely inhibited by the amiloride analog benzamil.	Amiloride	155-164	kininogen 1	Homo sapiens	67-77
6339076-5	1983	In addition, it was observed that the Na+ influx stimulated by Lys-bradykinin or by the combination of four growth factors was completely inhibited by the amiloride analog benzamil.	benzamil	172-180	kininogen 1	Homo sapiens	67-77
6302363-4	1983	Cells from the hydronephrotic kidney increased prostaglandin (PG)E2 production in response to bradykinin.	Dinoprostone	47-67	kininogen 1	Homo sapiens	94-104
6302363-7	1983	The induction of increased PGE2 synthesis and bradykinin responsiveness in hydronephrotic cortex could be related to the exaggerated prostaglandin synthesis known to occur in hydronephrotic cortex.	Prostaglandins	133-146	kininogen 1	Homo sapiens	46-56
6839489-3	1983	Bradykinin immunoreactivity in the extract eluted as a single peak from an immunoaffinity column of anti-bradykinin IgG bound to Sepharose identically to both bradykinin and kininogen showing immunoidentity of these substances.	Sepharose	129-138	kininogen 1	Homo sapiens	0-10
6839489-3	1983	Bradykinin immunoreactivity in the extract eluted as a single peak from an immunoaffinity column of anti-bradykinin IgG bound to Sepharose identically to both bradykinin and kininogen showing immunoidentity of these substances.	Sepharose	129-138	kininogen 1	Homo sapiens	105-115
6839489-5	1983	The decrease in measured values of blood bradykinin after purification of the extract on CM-Sephadex C25 was a similar amount to that calculated as cross-reactivity with the amount of co-extracted kininogen.	sephadex	92-100	kininogen 1	Homo sapiens	41-51
6342203-0	1983	Prostacyclin release stimulated by thrombin or bradykinin in porcine endothelial cells cultured from aorta and umbilical vein.	Epoprostenol	0-12	kininogen 1	Homo sapiens	47-57
6342203-2	1983	Aortic cells studied in situ, in primary culture and in subculture responded to both agents with an increase in prostacyclin (PGI2) release; the increase was greater with bradykinin than with thrombin.	Epoprostenol	112-124	kininogen 1	Homo sapiens	171-181
6299331-8	1983	The chloride activation of the hydrolysis of furanacryloyl-Phe-Gly-Gly is compared with that of the physiological substrates angiotensin I and bradykinin.	furanacryloyl-phe-gly-gly	45-70	kininogen 1	Homo sapiens	143-153
6185600-6	1983	When plasmas deficient in prekallikrein, factor XII, or high-molecular-weight kininogen were treated with Flu-beta-Ala and dextran sulfate, the initial rate of fibrinolytic activity was less than normal.	flu-beta-ala	106-118	kininogen 1	Homo sapiens	56-87
6185600-6	1983	When plasmas deficient in prekallikrein, factor XII, or high-molecular-weight kininogen were treated with Flu-beta-Ala and dextran sulfate, the initial rate of fibrinolytic activity was less than normal.	Dextran Sulfate	123-138	kininogen 1	Homo sapiens	56-87
6185600-8	1983	Thus this dextran sulfate-dependent fibrinolytic activity is dependent on factor XII, prekallikrein, and high-molecular-weight kininogen, but the requirement is not absolute.	Dextran Sulfate	10-25	kininogen 1	Homo sapiens	105-136
6190379-0	1983	Analogs of bradykinin containing dehydrophenylalanine.	phenyldehydroalanine	33-53	kininogen 1	Homo sapiens	11-21
6574692-0	1983	Renal prostaglandins (PGs) and thromboxanes (TXs) release induced by bradykinin.	Prostaglandins	6-20	kininogen 1	Homo sapiens	69-79
6574692-0	1983	Renal prostaglandins (PGs) and thromboxanes (TXs) release induced by bradykinin.	Prostaglandins	22-25	kininogen 1	Homo sapiens	69-79
6574692-0	1983	Renal prostaglandins (PGs) and thromboxanes (TXs) release induced by bradykinin.	Thromboxanes	31-43	kininogen 1	Homo sapiens	69-79
6574692-0	1983	Renal prostaglandins (PGs) and thromboxanes (TXs) release induced by bradykinin.	Thromboxanes	45-48	kininogen 1	Homo sapiens	69-79
6129075-11	1983	In subsequent studies, stimulating the gallbladder with bradykinin, an endogenous polypeptide, evoked a reflex activation of the cardiovascular system similar to that seen with capsaicin (MAP = 14%; HR = 4%; dP/dt DP40 = 18%; SVR = 14%).	dp/dt	208-213	kininogen 1	Homo sapiens	56-66
6305163-0	1983	Release and metabolism of (1-14C)-arachidonic acid stimulated by bradykinin.	(1-14c)	26-33	kininogen 1	Homo sapiens	65-75
6305163-0	1983	Release and metabolism of (1-14C)-arachidonic acid stimulated by bradykinin.	Arachidonic Acid	34-50	kininogen 1	Homo sapiens	65-75
6344574-0	1983	Effects of bradykinin and its homologs on the metabolism of arachidonate by endothelial cells.	Arachidonic Acid	60-72	kininogen 1	Homo sapiens	11-21
6344581-0	1983	Effect of bradykinin upon impaired glucose assimilation in patients with chronic renal failure and in patients on regular haemodialysis.	Glucose	35-42	kininogen 1	Homo sapiens	10-20
6129075-11	1983	In subsequent studies, stimulating the gallbladder with bradykinin, an endogenous polypeptide, evoked a reflex activation of the cardiovascular system similar to that seen with capsaicin (MAP = 14%; HR = 4%; dP/dt DP40 = 18%; SVR = 14%).	dp40	214-218	kininogen 1	Homo sapiens	56-66
6361787-5	1983	Suprofen appears to exert its pharmacological effect by inhibiting synthesis of prostaglandins from precursor arachidonic acid, inhibiting the pain induced by bradykinin, and by raising the threshold to pain induced by prostaglandins.	Suprofen	0-8	kininogen 1	Homo sapiens	159-169
6149645-0	1983	Regulation by bradykinin of its receptor and of receptor-mediated prostacyclin formation in cultured human fibroblasts.	Epoprostenol	66-78	kininogen 1	Homo sapiens	14-24
7139956-3	1982	Iodination of [Tyr8]-bradykinin was carried out with a chloramine-T procedure resulting in a tracer with high specific activity.	chloramine-T	55-67	kininogen 1	Homo sapiens	21-31
7139956-4	1982	Bradykinin was isolated in the following way: blood was sampled directly into acetone, and lipids were removed by extraction with petroleum either (40-60 degrees C).	Acetone	78-85	kininogen 1	Homo sapiens	0-10
6214858-1	1982	Captopril (Capoten; Squibb) is a specific orally active antagonist of peptidyl-dipeptide carboxyhydrolase, the enzyme which converts angiotensin I to angiotensin II and which inactivates bradykinin.	Captopril	0-9	kininogen 1	Homo sapiens	187-197
6214858-1	1982	Captopril (Capoten; Squibb) is a specific orally active antagonist of peptidyl-dipeptide carboxyhydrolase, the enzyme which converts angiotensin I to angiotensin II and which inactivates bradykinin.	Captopril	11-18	kininogen 1	Homo sapiens	187-197
6924855-6	1982	Kinetic constants (kcat, Km) were determined for a series of seven extended N-aminoacyl-L-arginine methyl esters based on the C-terminal sequence of bradykinin (-Pro-Phe-Arg) or (Gly)n-Arg.	n-aminoacyl-l-arginine methyl esters	76-112	kininogen 1	Homo sapiens	149-159
6924855-6	1982	Kinetic constants (kcat, Km) were determined for a series of seven extended N-aminoacyl-L-arginine methyl esters based on the C-terminal sequence of bradykinin (-Pro-Phe-Arg) or (Gly)n-Arg.	phenylalanylarginine	166-173	kininogen 1	Homo sapiens	149-159
6755050-4	1982	The overproduction of prostaglandins mediates hyperreninemia, supranormal plasma bradykinin, supranormal plasma norepinephrine and vascular resistance to the pressor effects of angiotensin II and norepinephrine; treatment with a prostaglandin synthetase inhibitor corrects these abnormalities.	Prostaglandins	22-36	kininogen 1	Homo sapiens	81-91
6819604-3	1982	Addition of histamine or bradykinin enhanced release of prostaglandins in both arterial and venous endothelial cells.	Prostaglandins	56-70	kininogen 1	Homo sapiens	25-35
6819604-7	1982	Endothelial cells released 14C-arachidonic acid as well as 14C-prostaglandins in response to either histamine or bradykinin.	14c-arachidonic acid	27-47	kininogen 1	Homo sapiens	113-123
6819604-7	1982	Endothelial cells released 14C-arachidonic acid as well as 14C-prostaglandins in response to either histamine or bradykinin.	14c-prostaglandins	59-77	kininogen 1	Homo sapiens	113-123
6819604-9	1982	We conclude that the vasoactive compounds, histamine and bradykinin, stimulate formation of prostaglandins in endothelial cells by the release of arachidonic acid from phospholipids of the cell membrane.	Prostaglandins	92-106	kininogen 1	Homo sapiens	57-67
6819604-9	1982	We conclude that the vasoactive compounds, histamine and bradykinin, stimulate formation of prostaglandins in endothelial cells by the release of arachidonic acid from phospholipids of the cell membrane.	Arachidonic Acid	146-162	kininogen 1	Homo sapiens	57-67
6819604-9	1982	We conclude that the vasoactive compounds, histamine and bradykinin, stimulate formation of prostaglandins in endothelial cells by the release of arachidonic acid from phospholipids of the cell membrane.	Phospholipids	168-181	kininogen 1	Homo sapiens	57-67
6184749-4	1982	Bradykinin treatment of RPCT cells caused an accumulation of intracellular cAMP which was blocked by aspirin and was quantitatively similar to that observed with 10(-5) M PGE2.	Cyclic AMP	75-79	kininogen 1	Homo sapiens	0-10
6184749-4	1982	Bradykinin treatment of RPCT cells caused an accumulation of intracellular cAMP which was blocked by aspirin and was quantitatively similar to that observed with 10(-5) M PGE2.	Aspirin	101-108	kininogen 1	Homo sapiens	0-10
6184749-7	1982	However, at higher concentrations of PGs (e.g. 10(-5) M), the effects of AVP plus PGE1, PGE2, PGI2 or bradykinin on intracellular cAMP levels were not additive.	Cyclic AMP	130-134	kininogen 1	Homo sapiens	102-112
6293764-5	1982	In micromolar concentrations, both compounds inhibited prostacyclin (PGI2) release from bradykinin-, arachidonic acid-, and ionophore-stimulated, as well as unstimulated monolayers.	Epoprostenol	55-67	kininogen 1	Homo sapiens	88-98
6293764-5	1982	In micromolar concentrations, both compounds inhibited prostacyclin (PGI2) release from bradykinin-, arachidonic acid-, and ionophore-stimulated, as well as unstimulated monolayers.	Epoprostenol	69-73	kininogen 1	Homo sapiens	88-98
6810948-2	1982	Addition of arachidonic acid, bradykinin, the calcium ionophore A23187 or thrombin stimulated prostaglandin formation, whereas addition of angiotensin II did not.	Prostaglandins	94-107	kininogen 1	Homo sapiens	30-40
6810948-0	1982	Mechanism of bradykinin-stimulated prostacyclin synthesis in porcine aortic endothelial cells.	Epoprostenol	35-47	kininogen 1	Homo sapiens	13-23
7106672-2	1982	The antitoxic and antiphlogistic components of heparin could be proved by long-term pre-treatment with heparin ointment, based on clinical experimental trials of inhibition of the pyrexal reaction and reduction of erythema, weal and heat radiation produced by histamin and bradykinin i.c.	Heparin	47-54	kininogen 1	Homo sapiens	273-283
7106672-2	1982	The antitoxic and antiphlogistic components of heparin could be proved by long-term pre-treatment with heparin ointment, based on clinical experimental trials of inhibition of the pyrexal reaction and reduction of erythema, weal and heat radiation produced by histamin and bradykinin i.c.	Heparin	103-110	kininogen 1	Homo sapiens	273-283
6804154-5	1982	Dopamine may form an integral part of the renal natriuretic cascade by, in its turn, evoking both the kallikrein-bradykinin system and the production of renal prostaglandins.	Dopamine	0-8	kininogen 1	Homo sapiens	113-123
6921035-3	1982	Kinetic constants (kcat., Km) were determined for a series of seven extended N-aminoacyl-L-arginine methyl esters based on the C-terminal sequence of bradykinin (-Pro-Phe-Arg) or (Gly)n-Arg.	n-aminoacyl-l-arginine methyl esters	77-113	kininogen 1	Homo sapiens	150-160
6921035-3	1982	Kinetic constants (kcat., Km) were determined for a series of seven extended N-aminoacyl-L-arginine methyl esters based on the C-terminal sequence of bradykinin (-Pro-Phe-Arg) or (Gly)n-Arg.	phenylalanylarginine	167-174	kininogen 1	Homo sapiens	150-160
7067697-0	1982	Preferred solution conformation of des-Arg9-bradykinin and analysis of structure-conformation-activity relationships in the series [Alan]des-Arg9-bradykinin.	-arg9	38-43	kininogen 1	Homo sapiens	44-54
7067697-0	1982	Preferred solution conformation of des-Arg9-bradykinin and analysis of structure-conformation-activity relationships in the series [Alan]des-Arg9-bradykinin.	-arg9	38-43	kininogen 1	Homo sapiens	146-156
7067697-0	1982	Preferred solution conformation of des-Arg9-bradykinin and analysis of structure-conformation-activity relationships in the series [Alan]des-Arg9-bradykinin.	-arg9	140-145	kininogen 1	Homo sapiens	146-156
7067697-1	1982	This paper describes the solution conformation of the vasoactive peptide hormone des-Arg9-bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe).	arginyl-prolyl-proline	102-113	kininogen 1	Homo sapiens	90-100
7067697-1	1982	This paper describes the solution conformation of the vasoactive peptide hormone des-Arg9-bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe).	Glycine	114-117	kininogen 1	Homo sapiens	90-100
7067697-1	1982	This paper describes the solution conformation of the vasoactive peptide hormone des-Arg9-bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe).	Phenylalanine	118-121	kininogen 1	Homo sapiens	90-100
7067697-1	1982	This paper describes the solution conformation of the vasoactive peptide hormone des-Arg9-bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe).	Serine	122-125	kininogen 1	Homo sapiens	90-100
7067697-1	1982	This paper describes the solution conformation of the vasoactive peptide hormone des-Arg9-bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe).	Phenylalanine	130-133	kininogen 1	Homo sapiens	90-100
7067697-7	1982	A complete series of analogous ([Alan]des Arg9-bradykinin, with n = 1, 2...8) was then investigated by circular dichroism and 1H-NMR spectroscopy in order to study the conformational role played by each residue and to delineate the local and the long-range effects on conformation brought about by the Xaa leads to Ala substitutions.	Alanine	33-36	kininogen 1	Homo sapiens	47-57
7099984-1	1982	Laser Raman spectra of bradykinin in water, deuterium oxide, and the solid phase were recorded.	Water	37-42	kininogen 1	Homo sapiens	23-33
7099984-7	1982	The restrictive Cys-Cys disulfide in the cyclic bradykinin must serve to maintain a conformation acceptable to bradykinin receptors since the cyclic peptide exhibits biological activity.	cys-cys disulfide	16-33	kininogen 1	Homo sapiens	48-58
7099984-7	1982	The restrictive Cys-Cys disulfide in the cyclic bradykinin must serve to maintain a conformation acceptable to bradykinin receptors since the cyclic peptide exhibits biological activity.	cys-cys disulfide	16-33	kininogen 1	Homo sapiens	111-121
7066300-0	1982	Carbon-13 relaxation behavior in multiply enriched system: [90%-1,2-13C2-Gly6]bradykinin.	Carbon-13	0-9	kininogen 1	Homo sapiens	78-88
7036731-2	1982	Synthesis of these unsaturated fatty acids from arachidonate precursors is closely regulated by intrarenal factors, and circulating angiotensin II, catecholamines, arginine vasopressin and bradykinin.	Fatty Acids, Unsaturated	19-42	kininogen 1	Homo sapiens	189-199
7036731-2	1982	Synthesis of these unsaturated fatty acids from arachidonate precursors is closely regulated by intrarenal factors, and circulating angiotensin II, catecholamines, arginine vasopressin and bradykinin.	Arachidonic Acid	48-60	kininogen 1	Homo sapiens	189-199
6125894-0	1982	Bradykinin receptor-mediated chloride secretion in intestinal function.	Chlorides	29-37	kininogen 1	Homo sapiens	0-10
6954152-1	1982	Bradykinin stimulates protein production as well as prostaglandin production by lung fibroblasts in culture.	Prostaglandins	52-65	kininogen 1	Homo sapiens	0-10
6954152-2	1982	When prostaglandin (PG) synthesis by the fibroblasts is inhibited with indomethacin, then bradykinin also stimulates collagen production.	Prostaglandins	5-18	kininogen 1	Homo sapiens	90-100
6954152-2	1982	When prostaglandin (PG) synthesis by the fibroblasts is inhibited with indomethacin, then bradykinin also stimulates collagen production.	Prostaglandins	20-22	kininogen 1	Homo sapiens	90-100
6954152-3	1982	In the presence of indomethacin, the increase in protein production by bradykinin is much higher than in its absence.	Indomethacin	19-31	kininogen 1	Homo sapiens	71-81
6954152-4	1982	The addition of exogenous PGE2 to the fibroblasts which have been treated with indomethacin inhibited the stimulating effect of bradykinin on total protein production, especially collagen production.	Dinoprostone	26-30	kininogen 1	Homo sapiens	128-138
6954152-4	1982	The addition of exogenous PGE2 to the fibroblasts which have been treated with indomethacin inhibited the stimulating effect of bradykinin on total protein production, especially collagen production.	Indomethacin	79-91	kininogen 1	Homo sapiens	128-138
6954152-7	1982	These results point out an interaction between bradykinin and PGE2 in the regulation of protein production by fibroblasts with PGE2 acting as a feedback mechanism to dampen the effect of bradykinin.	Dinoprostone	127-131	kininogen 1	Homo sapiens	47-57
6954152-7	1982	These results point out an interaction between bradykinin and PGE2 in the regulation of protein production by fibroblasts with PGE2 acting as a feedback mechanism to dampen the effect of bradykinin.	Dinoprostone	127-131	kininogen 1	Homo sapiens	187-197
6980251-3	1982	In six patients receiving 250 ml of PPF, the mean arterial pressure decreased 22% to 54% within 1.5 min after infusion, whereas the plasma bradykinin concentration, measured by radioimmunoassay, increased significantly (p less than 0.0005) during the first minute.	2,5-diphenylfuran	36-39	kininogen 1	Homo sapiens	139-149
6980251-5	1982	In vitro, linear correlation (r = 0.94, p less than 0.0005) was observed between the level of PKA of 26 different lots of PPF and the concentrations of bradykinin that were generated in Hageman factor-deficient plasma after incubation with PPF.	2,5-diphenylfuran	122-125	kininogen 1	Homo sapiens	152-162
6980251-5	1982	In vitro, linear correlation (r = 0.94, p less than 0.0005) was observed between the level of PKA of 26 different lots of PPF and the concentrations of bradykinin that were generated in Hageman factor-deficient plasma after incubation with PPF.	2,5-diphenylfuran	240-243	kininogen 1	Homo sapiens	152-162
7042175-0	1982	Antihypertensive and renal effects of captopril in relation to renin activity and bradykinin-induced vasodilation.	Captopril	38-47	kininogen 1	Homo sapiens	82-92
6124421-2	1982	Human liver alanine aminopeptidase (EC 3.4.11.14; L-alpha-aminoacyl-peptide hydrolase) catalyzes the stepwise hydrolysis of methionyl-lysyl-bradykinin to yield methionine, lysine, and the limit nonapeptide, bradykinin which is resistant to further hydrolytic cleavage by this enzyme.	Methionine	160-170	kininogen 1	Homo sapiens	140-150
6124421-2	1982	Human liver alanine aminopeptidase (EC 3.4.11.14; L-alpha-aminoacyl-peptide hydrolase) catalyzes the stepwise hydrolysis of methionyl-lysyl-bradykinin to yield methionine, lysine, and the limit nonapeptide, bradykinin which is resistant to further hydrolytic cleavage by this enzyme.	Methionine	160-170	kininogen 1	Homo sapiens	207-217
6124421-2	1982	Human liver alanine aminopeptidase (EC 3.4.11.14; L-alpha-aminoacyl-peptide hydrolase) catalyzes the stepwise hydrolysis of methionyl-lysyl-bradykinin to yield methionine, lysine, and the limit nonapeptide, bradykinin which is resistant to further hydrolytic cleavage by this enzyme.	Lysine	172-178	kininogen 1	Homo sapiens	140-150
6124421-4	1982	This enzyme cleaves N-terminal arginyl residues unless the adjacent penultimate residue is proline as is the case for bradykinin.	Nitrogen	20-21	kininogen 1	Homo sapiens	118-128
6124421-4	1982	This enzyme cleaves N-terminal arginyl residues unless the adjacent penultimate residue is proline as is the case for bradykinin.	arginyl	31-38	kininogen 1	Homo sapiens	118-128
6124421-4	1982	This enzyme cleaves N-terminal arginyl residues unless the adjacent penultimate residue is proline as is the case for bradykinin.	Proline	91-98	kininogen 1	Homo sapiens	118-128
6176105-1	1982	Captopril is a remarkably effective new antihypertensive drug designed and developed as a potent and specific inhibitor of angiotensin-converting enzyme, a zinc metallopeptidase that participates in the synthesis of a hypertensive peptide, angiotensin II, and in the degradation of a hypotensive peptide, bradykinin.	Captopril	0-9	kininogen 1	Homo sapiens	305-315
6280473-2	1982	On the sodium-restricted diet, the hypotensive response to captopril was accompanied by significant increments in the metabolite of prostaglandin E2 (PGE2-M) and bradykinin and by significant decrements in angiotensin II.	Sodium	7-13	kininogen 1	Homo sapiens	162-172
6280473-2	1982	On the sodium-restricted diet, the hypotensive response to captopril was accompanied by significant increments in the metabolite of prostaglandin E2 (PGE2-M) and bradykinin and by significant decrements in angiotensin II.	Captopril	59-68	kininogen 1	Homo sapiens	162-172
7118404-5	1982	has been used to probe the DMSO solution conformation of all seven of the possible AIB/Pro isomers of bradykinin.	Dimethyl Sulfoxide	27-31	kininogen 1	Homo sapiens	102-112
7118404-9	1982	The data suggests that bradykinin can adopt several folded conformations, including beta-turns involving both Ser6-Pro7-Phe8-Arg9 and Phe5-Ser6-Pro7-Phe8.	ser6-pro7-phe8	110-124	kininogen 1	Homo sapiens	23-33
6810948-3	1982	Bradykinin was found to stimulate very potently arachidonic acid release from cells prelabelled with [3H]arachidonate, the response being dose-dependent and half-maximal at 8 ng/ml.	Arachidonic Acid	48-64	kininogen 1	Homo sapiens	0-10
6810948-3	1982	Bradykinin was found to stimulate very potently arachidonic acid release from cells prelabelled with [3H]arachidonate, the response being dose-dependent and half-maximal at 8 ng/ml.	[3h]arachidonate	101-117	kininogen 1	Homo sapiens	0-10
6810948-4	1982	The rate of release of label (primarily arachidonate) from cells was increased by bradykinin (100 ng/ml) approximately 8-fold, with a return to control levels by 10 min.	Arachidonic Acid	40-52	kininogen 1	Homo sapiens	82-92
6810948-6	1982	Both bradykinin and ionophore A23187 stimulated [3H]arachidonate release from endothelial cell phospholipids, an effect which was abolished in a dose-dependent manner by mepacrine.	[3h]arachidonate	48-64	kininogen 1	Homo sapiens	5-15
6810948-6	1982	Both bradykinin and ionophore A23187 stimulated [3H]arachidonate release from endothelial cell phospholipids, an effect which was abolished in a dose-dependent manner by mepacrine.	Phospholipids	95-108	kininogen 1	Homo sapiens	5-15
6810948-6	1982	Both bradykinin and ionophore A23187 stimulated [3H]arachidonate release from endothelial cell phospholipids, an effect which was abolished in a dose-dependent manner by mepacrine.	Quinacrine	170-179	kininogen 1	Homo sapiens	5-15
6810948-8	1982	Trifluoperazine, a compound which can inhibit calmodulin-mediated events, blocked the release of label stimulated by bradykinin.	Trifluoperazine	0-15	kininogen 1	Homo sapiens	117-127
6810948-9	1982	These data indicate that the likely mechanism of bradykinin-stimulated prostaglandin production in endothelial cells involves the activation of a phospholipase via a Ca2+-calmodulin-dependent pathway.	Prostaglandins	71-84	kininogen 1	Homo sapiens	49-59
6461333-2	1982	Ipratropium bromide has not only an anticholinergic effect but also has an attenuating one on the contractile responses induced by serotonin, prostaglandin F2 alpha, histamine and bradykinin, and has a potentiating one on the relaxation responses induced by prostaglandin E2, isoprenaline and adrenaline.	Ipratropium	0-19	kininogen 1	Homo sapiens	180-190
6274413-3	1981	Both enzymes released C-terminal tripeptides from des-Arg9-bradykinin, des-Arg9-(Leu8)-bradykinin, Pro-Pro-Gly-Phe-Ser-Pro-Phe, Pro-Gly-Phe-Ser-Pro-Phe, Gly-Phe-Ser-Pro-Phe, Bz-Gly-Ser-pro-Phe and Bz-Gly-Ala-Pro-Phe.	tripeptides	33-44	kininogen 1	Homo sapiens	59-69
6219630-4	1982	These findings support the hypothesis that epinephrine promotes a bradykinin release responsible for vasodilation.	Epinephrine	43-54	kininogen 1	Homo sapiens	66-76
6274413-3	1981	Both enzymes released C-terminal tripeptides from des-Arg9-bradykinin, des-Arg9-(Leu8)-bradykinin, Pro-Pro-Gly-Phe-Ser-Pro-Phe, Pro-Gly-Phe-Ser-Pro-Phe, Gly-Phe-Ser-Pro-Phe, Bz-Gly-Ser-pro-Phe and Bz-Gly-Ala-Pro-Phe.	tripeptides	33-44	kininogen 1	Homo sapiens	87-97
6274413-5	1981	These data indicate that kininase II can release C-terminal tripeptides of substrates having a proline residue in the penultimate position such as des-Arg9-bradykinin and its analogues, and that this enzyme is able not only to act as a dipeptidyl carboxypeptidase but also acts as a tripeptidyl carboxy-peptidase.	tripeptides	60-71	kininogen 1	Homo sapiens	156-166
6274413-5	1981	These data indicate that kininase II can release C-terminal tripeptides of substrates having a proline residue in the penultimate position such as des-Arg9-bradykinin and its analogues, and that this enzyme is able not only to act as a dipeptidyl carboxypeptidase but also acts as a tripeptidyl carboxy-peptidase.	Proline	95-102	kininogen 1	Homo sapiens	156-166
7340460-0	1981	Steady-state fluorescence polarization (FP) of 1,6-diphenyl-1,3,5-hexatriene (dph)-labelled platelets in the presence of bradykinin (bk).	Diphenylhexatriene	47-76	kininogen 1	Homo sapiens	121-131
6801733-7	1982	Bradykinin also induced uterine contractions, an effect blocked by pretreatment with suprofen.	Suprofen	85-93	kininogen 1	Homo sapiens	0-10
6801733-8	1982	Finally, histochemical studies demonstrated stimulation of uterine catecholamine levels (norepinephrine) by arachidonic acid, PGF2 alpha and bradykinin.	Catecholamines	67-80	kininogen 1	Homo sapiens	141-151
6801733-8	1982	Finally, histochemical studies demonstrated stimulation of uterine catecholamine levels (norepinephrine) by arachidonic acid, PGF2 alpha and bradykinin.	Norepinephrine	89-103	kininogen 1	Homo sapiens	141-151
6946924-0	1981	Solute concentration affects bradykinin-mediated increases in renal prostaglandin E2.	Dinoprostone	68-84	kininogen 1	Homo sapiens	29-39
6946924-1	1981	The effects of solute concentration on the bradykinin-mediated increase in inner medullary slice prostaglandin E2 (PGE2) synthesis were investigated.	Dinoprostone	97-113	kininogen 1	Homo sapiens	43-53
6946924-1	1981	The effects of solute concentration on the bradykinin-mediated increase in inner medullary slice prostaglandin E2 (PGE2) synthesis were investigated.	Dinoprostone	115-119	kininogen 1	Homo sapiens	43-53
6946924-3	1981	Bradykinin stimulation was prevented by the addition of the following solutes to Krebs buffer: 1.0 M urea, 0.5 or 1.0 M NaCl, 0.5 or 1.0 M mannitol, 1.0 M urea plus 0.5 M NaCl, or 1.0 M mannitol plus 0.5 M NaCl.	krebs	81-86	kininogen 1	Homo sapiens	0-10
6946924-3	1981	Bradykinin stimulation was prevented by the addition of the following solutes to Krebs buffer: 1.0 M urea, 0.5 or 1.0 M NaCl, 0.5 or 1.0 M mannitol, 1.0 M urea plus 0.5 M NaCl, or 1.0 M mannitol plus 0.5 M NaCl.	Urea	101-105	kininogen 1	Homo sapiens	0-10
6946924-3	1981	Bradykinin stimulation was prevented by the addition of the following solutes to Krebs buffer: 1.0 M urea, 0.5 or 1.0 M NaCl, 0.5 or 1.0 M mannitol, 1.0 M urea plus 0.5 M NaCl, or 1.0 M mannitol plus 0.5 M NaCl.	Sodium Chloride	120-124	kininogen 1	Homo sapiens	0-10
6946924-3	1981	Bradykinin stimulation was prevented by the addition of the following solutes to Krebs buffer: 1.0 M urea, 0.5 or 1.0 M NaCl, 0.5 or 1.0 M mannitol, 1.0 M urea plus 0.5 M NaCl, or 1.0 M mannitol plus 0.5 M NaCl.	Mannitol	139-147	kininogen 1	Homo sapiens	0-10
6946924-3	1981	Bradykinin stimulation was prevented by the addition of the following solutes to Krebs buffer: 1.0 M urea, 0.5 or 1.0 M NaCl, 0.5 or 1.0 M mannitol, 1.0 M urea plus 0.5 M NaCl, or 1.0 M mannitol plus 0.5 M NaCl.	Urea	155-159	kininogen 1	Homo sapiens	0-10
6946924-3	1981	Bradykinin stimulation was prevented by the addition of the following solutes to Krebs buffer: 1.0 M urea, 0.5 or 1.0 M NaCl, 0.5 or 1.0 M mannitol, 1.0 M urea plus 0.5 M NaCl, or 1.0 M mannitol plus 0.5 M NaCl.	Sodium Chloride	171-175	kininogen 1	Homo sapiens	0-10
6946924-3	1981	Bradykinin stimulation was prevented by the addition of the following solutes to Krebs buffer: 1.0 M urea, 0.5 or 1.0 M NaCl, 0.5 or 1.0 M mannitol, 1.0 M urea plus 0.5 M NaCl, or 1.0 M mannitol plus 0.5 M NaCl.	Mannitol	186-194	kininogen 1	Homo sapiens	0-10
6946924-3	1981	Bradykinin stimulation was prevented by the addition of the following solutes to Krebs buffer: 1.0 M urea, 0.5 or 1.0 M NaCl, 0.5 or 1.0 M mannitol, 1.0 M urea plus 0.5 M NaCl, or 1.0 M mannitol plus 0.5 M NaCl.	Sodium Chloride	171-175	kininogen 1	Homo sapiens	0-10
6946924-5	1981	Urea elicited a concentration-dependent, reversible inhibition of bradykinin stimulation, with 0.01 M urea being the lowest effective concentration.	Urea	0-4	kininogen 1	Homo sapiens	66-76
6946924-5	1981	Urea elicited a concentration-dependent, reversible inhibition of bradykinin stimulation, with 0.01 M urea being the lowest effective concentration.	Urea	102-106	kininogen 1	Homo sapiens	66-76
7340460-0	1981	Steady-state fluorescence polarization (FP) of 1,6-diphenyl-1,3,5-hexatriene (dph)-labelled platelets in the presence of bradykinin (bk).	Diphenylhexatriene	47-76	kininogen 1	Homo sapiens	133-135
7340460-0	1981	Steady-state fluorescence polarization (FP) of 1,6-diphenyl-1,3,5-hexatriene (dph)-labelled platelets in the presence of bradykinin (bk).	Diphenylhexatriene	78-81	kininogen 1	Homo sapiens	133-135
7340460-1	1981	Steady-state fluorescence polarization (FP) decreases, when 1,6-diphenyl-1,3,5-hextriene (dph) labelled platelets are exposed to bradykinin (bk).	6-phenylhexa-1,3,5-trienylbenzene	60-88	kininogen 1	Homo sapiens	129-139
7340460-1	1981	Steady-state fluorescence polarization (FP) decreases, when 1,6-diphenyl-1,3,5-hextriene (dph) labelled platelets are exposed to bradykinin (bk).	6-phenylhexa-1,3,5-trienylbenzene	60-88	kininogen 1	Homo sapiens	141-143
7340460-1	1981	Steady-state fluorescence polarization (FP) decreases, when 1,6-diphenyl-1,3,5-hextriene (dph) labelled platelets are exposed to bradykinin (bk).	Diphenylhexatriene	90-93	kininogen 1	Homo sapiens	129-139
7340460-1	1981	Steady-state fluorescence polarization (FP) decreases, when 1,6-diphenyl-1,3,5-hextriene (dph) labelled platelets are exposed to bradykinin (bk).	Diphenylhexatriene	90-93	kininogen 1	Homo sapiens	141-143
7340460-2	1981	At pH 8, the dose-response curve is bell-shaped with an optimum bk effect at 10(-7) M. In contrast to the ricinoleic-acid ester of glycerin-polyethyleneglycol, cremophor EL (CEL), bk is no more effective when platelets are pretreated with 10(-5) M p-bromophenacylbromide (B phi B).	cremophor EL	160-172	kininogen 1	Homo sapiens	64-66
6806831-0	1982	Antagonism by meseclazone and other nonsteroidal anti-inflammatory drugs of bradykinin-induced bronchospasm.	meseclazone	14-25	kininogen 1	Homo sapiens	76-86
7340460-2	1981	At pH 8, the dose-response curve is bell-shaped with an optimum bk effect at 10(-7) M. In contrast to the ricinoleic-acid ester of glycerin-polyethyleneglycol, cremophor EL (CEL), bk is no more effective when platelets are pretreated with 10(-5) M p-bromophenacylbromide (B phi B).	cremophor EL	174-177	kininogen 1	Homo sapiens	64-66
7340460-2	1981	At pH 8, the dose-response curve is bell-shaped with an optimum bk effect at 10(-7) M. In contrast to the ricinoleic-acid ester of glycerin-polyethyleneglycol, cremophor EL (CEL), bk is no more effective when platelets are pretreated with 10(-5) M p-bromophenacylbromide (B phi B).	4-bromophenacyl bromide	248-270	kininogen 1	Homo sapiens	64-66
6806831-1	1982	Bradykinin-induced bronchoconstriction is due, in part, to release of TXA2 and prostaglandins.	Prostaglandins	79-93	kininogen 1	Homo sapiens	0-10
7340460-3	1981	These results suggest that platelets are target cells for the peptide bk, which induces an FP decrease indirectly by stimulating the release of non-saturated fatty acids in the platelet membrane.	non-saturated fatty acids	144-169	kininogen 1	Homo sapiens	70-72
6796855-1	1981	Captopril is a specific inhibitor of kininase II which is responsible for the conversion of angiotensin I into the active angiotensin II and also for the inactivation of bradykinin.	Captopril	0-9	kininogen 1	Homo sapiens	170-180
7311167-5	1981	In the strips which reached a steady state 2 hr after administration of potassium, phospholipase A2 and bradykinin produced marked oscillations.	Potassium	72-81	kininogen 1	Homo sapiens	104-114
7330224-2	1981	Bradykinin and ascorbic acid were used to induce PG synthesis.	Prostaglandins	49-51	kininogen 1	Homo sapiens	0-10
7330224-4	1981	During active growth, PGE2 synthesis in response to stimulation by either bradykinin or ascorbic acid was low.	Dinoprostone	22-26	kininogen 1	Homo sapiens	74-84
7330224-6	1981	During quiescence bradykinin and ascorbic acid stimulated PG production markedly while the conversion of free arachidonic acid to PGE2 also increased markedly.	Prostaglandins	58-60	kininogen 1	Homo sapiens	18-28
6175175-4	1981	Rat high molecular weight kininogen (HMWK) added to acetone-treated citrated plasma likewise increased the activation, providing evidence of the protection by benzamidine of the cofactor function of HMWK.	Acetone	52-59	kininogen 1	Homo sapiens	37-41
6175175-4	1981	Rat high molecular weight kininogen (HMWK) added to acetone-treated citrated plasma likewise increased the activation, providing evidence of the protection by benzamidine of the cofactor function of HMWK.	Acetone	52-59	kininogen 1	Homo sapiens	199-203
6175175-4	1981	Rat high molecular weight kininogen (HMWK) added to acetone-treated citrated plasma likewise increased the activation, providing evidence of the protection by benzamidine of the cofactor function of HMWK.	benzamidine	159-170	kininogen 1	Homo sapiens	37-41
6175175-4	1981	Rat high molecular weight kininogen (HMWK) added to acetone-treated citrated plasma likewise increased the activation, providing evidence of the protection by benzamidine of the cofactor function of HMWK.	benzamidine	159-170	kininogen 1	Homo sapiens	199-203
6175175-7	1981	The stoichiometric factor XII concentration-effect curve obtained by diluting acetone-treated rat plasma with acetone-treated human factor XII deficient plasma showed that factor XII is present in functional excess, the concentration of HMWK deciding the extent of activation.	Acetone	78-85	kininogen 1	Homo sapiens	237-241
6175175-7	1981	The stoichiometric factor XII concentration-effect curve obtained by diluting acetone-treated rat plasma with acetone-treated human factor XII deficient plasma showed that factor XII is present in functional excess, the concentration of HMWK deciding the extent of activation.	Acetone	110-117	kininogen 1	Homo sapiens	237-241
6175175-8	1981	By diluting acetone-treated rat plasma with buffer, HMWK concentration-effect curves were obtained which were approximately linear over a range of 0.03-0.40 microgram (bradykinin equivalents) per ml kaolin incubate.	Acetone	12-19	kininogen 1	Homo sapiens	52-56
7250322-1	1981	In the isolated lapine kidney perfused with tyrode solution and prelabeled with [3H] norepinephrine, bradykinin (10 ng/ml) decreased the overflow of tritium elicited by sympathetic nerve stimulation both in the presence and absence of indomethacin.	tyrode	44-50	kininogen 1	Homo sapiens	101-111
6794012-0	1981	The influence of indomethacin on vasodilator responses to bradykinin and nitroglycerin in the cat.	Indomethacin	17-29	kininogen 1	Homo sapiens	58-68
6794012-1	1981	The effects of indomethacin, a cyclooxygenase inhibitor, on vasodilator responses to bradykinin and nitroglycerin were investigated in the peripheral vascular bed of the anesthetized cat.	Indomethacin	15-27	kininogen 1	Homo sapiens	85-95
6794012-6	1981	When the increase in (initial value) vascular resistance was taken into account by expressing vasodilator responses on a percent decrease basis, indomethacin only enhanced the vasodilator response to the highest does of bradykinin studies.	Indomethacin	145-157	kininogen 1	Homo sapiens	220-230
7250322-1	1981	In the isolated lapine kidney perfused with tyrode solution and prelabeled with [3H] norepinephrine, bradykinin (10 ng/ml) decreased the overflow of tritium elicited by sympathetic nerve stimulation both in the presence and absence of indomethacin.	[3h] norepinephrine	80-99	kininogen 1	Homo sapiens	101-111
7250322-1	1981	In the isolated lapine kidney perfused with tyrode solution and prelabeled with [3H] norepinephrine, bradykinin (10 ng/ml) decreased the overflow of tritium elicited by sympathetic nerve stimulation both in the presence and absence of indomethacin.	Tritium	149-156	kininogen 1	Homo sapiens	101-111
7250322-1	1981	In the isolated lapine kidney perfused with tyrode solution and prelabeled with [3H] norepinephrine, bradykinin (10 ng/ml) decreased the overflow of tritium elicited by sympathetic nerve stimulation both in the presence and absence of indomethacin.	Indomethacin	235-247	kininogen 1	Homo sapiens	101-111
7018190-7	1981	Captopril (SQ 14.225) is a competitive inhibitor of peptidyl dipeptide hydrolase, also known as angiotensin converting enzyme (ACE) or kininase II, which converts angiotensin I (A I) into angiotensin II (A II), hydrolyzes des-Asp-angiotensin I to angiotensin III (A III) and inactivates bradykinin (BK) (19).	Captopril	0-9	kininogen 1	Homo sapiens	287-297
6798592-2	1981	Infusions of PGE1, 1.0 and 0.1 micrograms/min, into the superior mesenteric artery dilated the mesenteric vascular bed and markedly inhibited vasoconstrictor responses to sympathetic nerve stimulation, norepinephrine and angiotensin and to vasodilator responses to bradykinin and nitroglycerin.	Alprostadil	13-17	kininogen 1	Homo sapiens	265-275
6798592-3	1981	The response to the highest dose of bradykinin was reversed to a pressor response during infusion of PGE1.	Alprostadil	101-105	kininogen 1	Homo sapiens	36-46
6798592-5	1981	When the decrease in (initial value) vascular resistance was taken into account by expressing vasodilator responses on a percent decrease basis, infusion of PGE1 reduced or reversed the vasodilator responses to bradykinin whereas the vasodilator responses to nitroglycerin were not altered.	Alprostadil	157-161	kininogen 1	Homo sapiens	211-221
6798592-6	1981	Results of these studies suggest that PGE1 may influence vasomotor tone and responses to pressor hormones and bradykinin in the mesenteric vascular bed of the cat.	Alprostadil	38-42	kininogen 1	Homo sapiens	110-120
6114491-7	1981	Stimulating human fibroblasts with bradykinin in the presence of monoclonal antilipomodulin antibody markedly enhanced arachidonic acid release due to the activation of phospholipase(s) in the intact cells, and this stimulatory effect was blocked by adding purified lipomodulin.	Arachidonic Acid	119-135	kininogen 1	Homo sapiens	35-45
6170971-3	1981	The immediate reduction in BP produced by teprotide was not solely attributable to the inhibition of conversion of angiotensin I to angiotensin II, because there was also a transient increase in serum bradykinin; however, the prolonged antihypertensive effect of teprotide appeared independent of bradykinin.	Teprotide	42-51	kininogen 1	Homo sapiens	201-211
6170971-3	1981	The immediate reduction in BP produced by teprotide was not solely attributable to the inhibition of conversion of angiotensin I to angiotensin II, because there was also a transient increase in serum bradykinin; however, the prolonged antihypertensive effect of teprotide appeared independent of bradykinin.	Teprotide	42-51	kininogen 1	Homo sapiens	297-307
6269554-3	1981	Inhibition of the conversion enzyme, notably with captopril, prevents the formation of angiotensin II from angiotensin I and also results in accumulation of a vasodilator and natriuretic peptide: bradykinin.	Captopril	50-59	kininogen 1	Homo sapiens	196-206
6113593-1	1981	[3H]Bradykinin binds to membranes from a variety of mammalian tissues in a saturable fashion with a dissociation constant of about 5 nM.	Tritium	1-3	kininogen 1	Homo sapiens	4-14
7018190-7	1981	Captopril (SQ 14.225) is a competitive inhibitor of peptidyl dipeptide hydrolase, also known as angiotensin converting enzyme (ACE) or kininase II, which converts angiotensin I (A I) into angiotensin II (A II), hydrolyzes des-Asp-angiotensin I to angiotensin III (A III) and inactivates bradykinin (BK) (19).	Captopril	0-9	kininogen 1	Homo sapiens	299-301
7238669-5	1981	The relaxing effect of bradykinin was investigated after maximal contraction with either prostaglandin F2 alpha, histamine or norepinephrine in 23 specimens.	Dinoprost	89-111	kininogen 1	Homo sapiens	23-33
6266379-4	1981	Captopril (SQ14225) blocks angiotensin I and potentiates bradykinin effects in vitro and in vivo.	Captopril	0-9	kininogen 1	Homo sapiens	57-67
6266379-4	1981	Captopril (SQ14225) blocks angiotensin I and potentiates bradykinin effects in vitro and in vivo.	Captopril	11-18	kininogen 1	Homo sapiens	57-67
6946268-1	1981	Prostaglandin (PG) production by human embryo lung fibroblasts (HELF) is stimulated by a number of effectors including angiotensin, thrombin, bradykinin and ascorbic acid.	Prostaglandins	0-13	kininogen 1	Homo sapiens	142-152
6946268-1	1981	Prostaglandin (PG) production by human embryo lung fibroblasts (HELF) is stimulated by a number of effectors including angiotensin, thrombin, bradykinin and ascorbic acid.	Prostaglandins	15-17	kininogen 1	Homo sapiens	142-152
6946268-3	1981	For example, angiotensin stimulates mainly PGE2 synthesis, thrombin stimulates production of both PGE2 and prostacyclin while bradykinin and ascorbic acid stimulate production of PGE2, PGF2 alpha, prostacyclin and thromboxane A2.	Dinoprost	185-195	kininogen 1	Homo sapiens	126-136
6946268-3	1981	For example, angiotensin stimulates mainly PGE2 synthesis, thrombin stimulates production of both PGE2 and prostacyclin while bradykinin and ascorbic acid stimulate production of PGE2, PGF2 alpha, prostacyclin and thromboxane A2.	Epoprostenol	197-209	kininogen 1	Homo sapiens	126-136
6946268-3	1981	For example, angiotensin stimulates mainly PGE2 synthesis, thrombin stimulates production of both PGE2 and prostacyclin while bradykinin and ascorbic acid stimulate production of PGE2, PGF2 alpha, prostacyclin and thromboxane A2.	Thromboxane A2	214-228	kininogen 1	Homo sapiens	126-136
6946268-5	1981	An overall drop in prostaglandin synthesis is observed with bradykinin stimulation.	Prostaglandins	19-32	kininogen 1	Homo sapiens	60-70
6946268-8	1981	Prostacyclin production in response to bradykinin drops in HSF as they are obtained from individuals of increasing chronologic age.	Epoprostenol	0-12	kininogen 1	Homo sapiens	39-49
6952269-0	1981	Prostaglandin synthesis by vascular smooth muscle cells is stimulated by bradykinin, prazosin and hydralazine.	Prostaglandins	0-13	kininogen 1	Homo sapiens	73-83
6111737-0	1980	[Acetylcholine-bradykinin: a new peptide-amine transmitter interaction].	Peptides	33-40	kininogen 1	Homo sapiens	15-25
6111737-0	1980	[Acetylcholine-bradykinin: a new peptide-amine transmitter interaction].	Amines	41-46	kininogen 1	Homo sapiens	15-25
7002184-3	1980	3 Prostaglandin E2 sensitizes the chemical receptors of afferent pain endings to other inflammatory mediators such as bradykinin and histamine.	Dinoprostone	2-18	kininogen 1	Homo sapiens	118-128
6998710-0	1980	Prostacyclin mediates the potentiated hypotensive effect of bradykinin following captopril treatment.	Epoprostenol	0-12	kininogen 1	Homo sapiens	60-70
6998710-0	1980	Prostacyclin mediates the potentiated hypotensive effect of bradykinin following captopril treatment.	Captopril	81-90	kininogen 1	Homo sapiens	60-70
6998710-1	1980	The effect of angiotensin-converting enzyme inhibition by captopril on the release of a prostacyclin-like substance by bradykinin, angiotensin I and angiotensin II was studied by means of the blood-bathed bioassay technique of Vane.	Captopril	58-67	kininogen 1	Homo sapiens	119-129
6998710-1	1980	The effect of angiotensin-converting enzyme inhibition by captopril on the release of a prostacyclin-like substance by bradykinin, angiotensin I and angiotensin II was studied by means of the blood-bathed bioassay technique of Vane.	Epoprostenol	88-100	kininogen 1	Homo sapiens	119-129
6998710-2	1980	Administration of captopril abolished the release of prostacyclin-like substance induced by angiotensin I, potentiated the release provoked by bradykinin and did not alter that due to angiotensin II.	Captopril	18-27	kininogen 1	Homo sapiens	143-153
6998710-3	1980	Potentiation of the bradykinin-induced renal vasodilatation with captopril could be completely reversed by indomethacin, which also abolished the kinin-induced release of prostacyclin-like substance.	Captopril	65-74	kininogen 1	Homo sapiens	20-30
6998710-3	1980	Potentiation of the bradykinin-induced renal vasodilatation with captopril could be completely reversed by indomethacin, which also abolished the kinin-induced release of prostacyclin-like substance.	Indomethacin	107-119	kininogen 1	Homo sapiens	20-30
6998710-3	1980	Potentiation of the bradykinin-induced renal vasodilatation with captopril could be completely reversed by indomethacin, which also abolished the kinin-induced release of prostacyclin-like substance.	Epoprostenol	171-183	kininogen 1	Homo sapiens	20-30
6159774-4	1980	Treatment of plasma from DR with acetone (25% v/v) induced a conversion of HMWK into a state which was non-functional as a cofactor in the surface-dependent activation of factor XII, and the passage of plasma from DR through a lysine-Sepharose column altered the HMWK present to a substance that released kinin only very slowly by incubation with HPK.	Acetone	33-40	kininogen 1	Homo sapiens	75-79
6159774-4	1980	Treatment of plasma from DR with acetone (25% v/v) induced a conversion of HMWK into a state which was non-functional as a cofactor in the surface-dependent activation of factor XII, and the passage of plasma from DR through a lysine-Sepharose column altered the HMWK present to a substance that released kinin only very slowly by incubation with HPK.	Acetone	33-40	kininogen 1	Homo sapiens	263-267
7436632-0	1980	Inhibitory effects of streptomycin on bronchoconstrictor, hypotensive and inflammatory responses to bradykinin and histamine.	Streptomycin	22-34	kininogen 1	Homo sapiens	100-110
7436632-1	1980	Streptomycin inhibits significantly the bronchoconstrictor effects of bradykinin and histamine.	Streptomycin	0-12	kininogen 1	Homo sapiens	70-80
7436632-3	1980	The hypotensive and inflammatory responses to bradykinin and histamine are also significantly suppressed with streptomycin.	Streptomycin	110-122	kininogen 1	Homo sapiens	46-56
6997175-1	1980	In order to investigate whether bradykinin which has been shown to improve carbohydrate metabolism of skeletal muscle exhibits also insulin-like activity on amino acid metabolism, balances of oxygen and 13 amino acids across the forearm and forearm blood flow were determined in normal subjects during the arterial infusion of insulin (n = 9, 250 mu-units x kg-1 x min-1), bradykinin (n = 7, 0.2 ng x kg-1 x min-1) and papverine (n = 5, 2 microgram x kg-1 x min-1).	Carbohydrates	75-87	kininogen 1	Homo sapiens	32-42
6997175-1	1980	In order to investigate whether bradykinin which has been shown to improve carbohydrate metabolism of skeletal muscle exhibits also insulin-like activity on amino acid metabolism, balances of oxygen and 13 amino acids across the forearm and forearm blood flow were determined in normal subjects during the arterial infusion of insulin (n = 9, 250 mu-units x kg-1 x min-1), bradykinin (n = 7, 0.2 ng x kg-1 x min-1) and papverine (n = 5, 2 microgram x kg-1 x min-1).	papverine	419-428	kininogen 1	Homo sapiens	32-42
6997175-3	1980	As insulin, bradykinin lessened the release of 9 amino acids: Glycine, serine, ornithin, valine, leucine, isoleucine and tyrosine.	Glycine	62-69	kininogen 1	Homo sapiens	12-22
6997175-3	1980	As insulin, bradykinin lessened the release of 9 amino acids: Glycine, serine, ornithin, valine, leucine, isoleucine and tyrosine.	Serine	71-77	kininogen 1	Homo sapiens	12-22
6997175-3	1980	As insulin, bradykinin lessened the release of 9 amino acids: Glycine, serine, ornithin, valine, leucine, isoleucine and tyrosine.	ornithin	79-87	kininogen 1	Homo sapiens	12-22
6997175-3	1980	As insulin, bradykinin lessened the release of 9 amino acids: Glycine, serine, ornithin, valine, leucine, isoleucine and tyrosine.	Valine	89-95	kininogen 1	Homo sapiens	12-22
6997175-3	1980	As insulin, bradykinin lessened the release of 9 amino acids: Glycine, serine, ornithin, valine, leucine, isoleucine and tyrosine.	Leucine	97-104	kininogen 1	Homo sapiens	12-22
6997175-3	1980	As insulin, bradykinin lessened the release of 9 amino acids: Glycine, serine, ornithin, valine, leucine, isoleucine and tyrosine.	Isoleucine	106-116	kininogen 1	Homo sapiens	12-22
6997175-3	1980	As insulin, bradykinin lessened the release of 9 amino acids: Glycine, serine, ornithin, valine, leucine, isoleucine and tyrosine.	Tyrosine	121-129	kininogen 1	Homo sapiens	12-22
6105087-0	1980	Selective reduction by some vasodilators and the prostaglandin antagonist SC-19220 of a response to the algesic effect of bradykinin.	Prostaglandins	49-62	kininogen 1	Homo sapiens	122-132
6105087-0	1980	Selective reduction by some vasodilators and the prostaglandin antagonist SC-19220 of a response to the algesic effect of bradykinin.	Dibenz(b,f)(1,4)oxazepine-10(11H)-carboxylic acid, 8-chloro-, 2-acetylhydrazide	74-82	kininogen 1	Homo sapiens	122-132
6251920-0	1980	[Effect of the calcium antagonist compound D600 on bradykinin-induced smooth muscle contraction and 14C-D600 binding by a fraction of myometrial cell plasma membranes].	Gallopamil	43-47	kininogen 1	Homo sapiens	51-61
6158390-2	1980	When six female seropositive rheumatoid patients were given placebo therapy for 48 h, their plasma kininogen level, 9.2 +/- 0.7 microgram bradykinin equivalents (bk eq) per ml, was found to be 59% greater than that of a group of eight healthy female volunteers (5.8 +/- 0.5 microgram/ml).	Ethoxyquin	149-151	kininogen 1	Homo sapiens	138-148
7435919-2	1980	The responses to the anaesthetic technique and drugs used demonstrated the interactions of serotonin and bradykinin.	Serotonin	91-100	kininogen 1	Homo sapiens	105-115
7443750-0	1980	Reversal of bradykinin action: possible involvement of prostaglandins or dual receptors.	Prostaglandins	55-69	kininogen 1	Homo sapiens	12-22
6250809-13	1980	II is the acylated C-terminal tripeptide of bradykinin, IV is an acylated tripeptide analog of BPP(5a) (&lt;Glu-Lys-Trp-Ala-Pro) and V is the acylated C-terminal tripeptide of angiotensin I.	tripeptide K-26	30-40	kininogen 1	Homo sapiens	44-54
7363463-3	1980	We present a method in which bradykinin is separated from components of higher relative molecular mass (including kininogens) in a single step, by use of a column of Sephadex G-25 medium (PD-10).	sephadex	166-179	kininogen 1	Homo sapiens	29-39
7363463-3	1980	We present a method in which bradykinin is separated from components of higher relative molecular mass (including kininogens) in a single step, by use of a column of Sephadex G-25 medium (PD-10).	pd-10	188-193	kininogen 1	Homo sapiens	29-39
7394060-3	1980	Bradykinin is a potent stimulator of prostaglandin E synthesis, a known vasodilator.	Prostaglandins E	37-52	kininogen 1	Homo sapiens	0-10
7351634-0	1980	Blockade by antiglucocorticoids, actinomycin D and cycloheximide of anti-inflammatory action of dexamethasone against bradykinin.	Dexamethasone	96-109	kininogen 1	Homo sapiens	118-128
6245567-0	1980	Prostacyclin release induced by bradykinin may contribute to the antihypertensive action of angiotensin-converting enzyme inhibitors.	Epoprostenol	0-12	kininogen 1	Homo sapiens	32-42
6111268-3	1980	The generation of PGI2 by lungs can be augmented by angiotensin ll, bradykinin and arachidonic acid provided that low concentrations of these substances are infused into pulmonary artery.	Epoprostenol	18-22	kininogen 1	Homo sapiens	68-78
6794096-7	1981	Meclofenamate (10(-7)M) pretreatment of strips subjected to dose-response studies using PGF2 alpha, PGE2, bradykinin (B K) and angiotensin II (AII) revealed a significant reduction in tension developed to both BK and AII.	Meclofenamic Acid	0-13	kininogen 1	Homo sapiens	106-116
6794096-7	1981	Meclofenamate (10(-7)M) pretreatment of strips subjected to dose-response studies using PGF2 alpha, PGE2, bradykinin (B K) and angiotensin II (AII) revealed a significant reduction in tension developed to both BK and AII.	Meclofenamic Acid	0-13	kininogen 1	Homo sapiens	118-121
6164149-2	1981	Pyridoxine, hemodesis and polyglucin were also found to be antagonists to the effects of bradykinin.	Pyridoxine	0-10	kininogen 1	Homo sapiens	89-99
6449838-2	1980	It is most likely that the utilization of glucose is enhanced directly within the energy metabolizing cell itself but not indirectly by way of an insulin release in the pancreatic islets, since the in vitro studies on isolated islets of Langerhans did not reveal any effect of bradykinin on insulin secretion or insulin release.	Glucose	42-49	kininogen 1	Homo sapiens	277-287
6159774-4	1980	Treatment of plasma from DR with acetone (25% v/v) induced a conversion of HMWK into a state which was non-functional as a cofactor in the surface-dependent activation of factor XII, and the passage of plasma from DR through a lysine-Sepharose column altered the HMWK present to a substance that released kinin only very slowly by incubation with HPK.	Lysine	227-233	kininogen 1	Homo sapiens	263-267
6159774-6	1980	Previous experiments with rat plasma demonstrated that plasmin and also a plasmin-like factor without affinity for lysine-Sepharose were able to destroy the capacity of HMWK to function as a cofactor in the surface-dependent activation of factor XII, without a corresponding release of kinin.	Lysine	115-121	kininogen 1	Homo sapiens	169-173
6159774-6	1980	Previous experiments with rat plasma demonstrated that plasmin and also a plasmin-like factor without affinity for lysine-Sepharose were able to destroy the capacity of HMWK to function as a cofactor in the surface-dependent activation of factor XII, without a corresponding release of kinin.	Sepharose	122-131	kininogen 1	Homo sapiens	169-173
7009095-3	1980	Generation of prostacyclin by lungs can be increased by angiotensin II, bradykinin and arachidonic acid provided that low concentrations of these substances are infused into the pulmonary artery.	Epoprostenol	14-26	kininogen 1	Homo sapiens	72-82
7238669-5	1981	The relaxing effect of bradykinin was investigated after maximal contraction with either prostaglandin F2 alpha, histamine or norepinephrine in 23 specimens.	Histamine	113-122	kininogen 1	Homo sapiens	23-33
7238669-5	1981	The relaxing effect of bradykinin was investigated after maximal contraction with either prostaglandin F2 alpha, histamine or norepinephrine in 23 specimens.	Norepinephrine	126-140	kininogen 1	Homo sapiens	23-33
7343317-1	1981	Among a vast number of chemical mediators of inflammation such as histamine, 5-hydroxytryptamine, bradykinin, SRS-A the metabolites of arachidonic acid (AA) attracted vivid attention in the last ten years.	Arachidonic Acid	135-151	kininogen 1	Homo sapiens	98-108
517656-4	1979	With continued bradykinin administration (120 min) RBF and prostaglandin secretory rates returned toward control values, although renin secretory rate remained elevated (P less than 0.02).	Prostaglandins	59-72	kininogen 1	Homo sapiens	15-25
517656-0	1979	Bradykinin-induced renal hemodynamic alterations: renin and prostaglandin relationships.	Prostaglandins	60-73	kininogen 1	Homo sapiens	0-10
230492-12	1979	IPA is readily deacylated from the renal phospholipid pool in response to bradykinin, a substance that also stimulates the release of arachidonic acid.	Phospholipids	41-53	kininogen 1	Homo sapiens	74-84
529011-0	1979	Intravital and electron microscopic study of bradykinin-induced vascular permeability changes using FITC-dextran as a tracer.	fluorescein isothiocyanate dextran	100-112	kininogen 1	Homo sapiens	45-55
529011-6	1979	FITC-dextran appeared as black precipitates in the vascular lumen and also outside the lumen in bradykinin-treated animals.	fluorescein isothiocyanate dextran	0-12	kininogen 1	Homo sapiens	96-106
40631-1	1979	On isolated ileum of the guinea pig the antihistamine drugs dimedrol, diprazin (pipolphen), tavegil and suprastin diminished spasmogenic effects of bradykinin and an enhancement of microvascular permeability induced by this polypeptid.	Diphenhydramine	60-68	kininogen 1	Homo sapiens	148-158
40631-1	1979	On isolated ileum of the guinea pig the antihistamine drugs dimedrol, diprazin (pipolphen), tavegil and suprastin diminished spasmogenic effects of bradykinin and an enhancement of microvascular permeability induced by this polypeptid.	Promethazine	70-78	kininogen 1	Homo sapiens	148-158
40631-1	1979	On isolated ileum of the guinea pig the antihistamine drugs dimedrol, diprazin (pipolphen), tavegil and suprastin diminished spasmogenic effects of bradykinin and an enhancement of microvascular permeability induced by this polypeptid.	Promethazine	80-89	kininogen 1	Homo sapiens	148-158
531222-0	1979	Bradykinin-stimulated release of [3H]arachidonic acid from phospholipids of HSDM1C1 cells: comparison of diacyl phospholipids and plasmalogens as sources of prostaglandin precursors.	[3h]arachidonic acid	33-53	kininogen 1	Homo sapiens	0-10
531222-0	1979	Bradykinin-stimulated release of [3H]arachidonic acid from phospholipids of HSDM1C1 cells: comparison of diacyl phospholipids and plasmalogens as sources of prostaglandin precursors.	Phospholipids	59-72	kininogen 1	Homo sapiens	0-10
531222-0	1979	Bradykinin-stimulated release of [3H]arachidonic acid from phospholipids of HSDM1C1 cells: comparison of diacyl phospholipids and plasmalogens as sources of prostaglandin precursors.	Prostaglandins	157-170	kininogen 1	Homo sapiens	0-10
531222-2	1979	In the present study, [3H]arachidonate-labeled phospholipids of HSDM1C1 cells, a cell line derived from a mouse fibrosarcoma, were examined to determine the donor of the arachidonic acid released upon bradykinin stimulation of the synthesis of PGE2.	Arachidonic Acid	170-186	kininogen 1	Homo sapiens	201-211
531222-4	1979	Bradykinin treatment stimulated a rapid hydrolysis of [3H]arachidonate from the cellular lipids and conversion of the released acid to PGE2, which was secreted into the medium.	[3h]arachidonate	54-70	kininogen 1	Homo sapiens	0-10
531222-4	1979	Bradykinin treatment stimulated a rapid hydrolysis of [3H]arachidonate from the cellular lipids and conversion of the released acid to PGE2, which was secreted into the medium.	Dinoprostone	135-139	kininogen 1	Homo sapiens	0-10
531222-7	1979	Indomethacin blocked the bradykinin-stimulated synthesis of PGE2 and to a lesser degree inhibited the release of [3H]arachidonate from the cellular lipids into the medium.	Indomethacin	0-12	kininogen 1	Homo sapiens	25-35
531222-7	1979	Indomethacin blocked the bradykinin-stimulated synthesis of PGE2 and to a lesser degree inhibited the release of [3H]arachidonate from the cellular lipids into the medium.	Dinoprostone	60-64	kininogen 1	Homo sapiens	25-35
531222-7	1979	Indomethacin blocked the bradykinin-stimulated synthesis of PGE2 and to a lesser degree inhibited the release of [3H]arachidonate from the cellular lipids into the medium.	[3h]arachidonate	113-129	kininogen 1	Homo sapiens	25-35
228783-7	1979	Clearance of bradykinin by lung converting enzyme decreased from 96% at PaO2 levels above 95 torr to 0% below 26 torr.	pao2	72-76	kininogen 1	Homo sapiens	13-23
38854-0	1979	Angiotensin and bradykinin interactions with phospholipids.	Phospholipids	45-58	kininogen 1	Homo sapiens	16-26
38854-1	1979	Reversible interactions were demonstrated between some phospholipids and some polypeptides related to angiotensin and bradykinin.	Phospholipids	55-68	kininogen 1	Homo sapiens	118-128
231702-0	1979	Potentiation of the algogenic action of bradykinin by an inhibitor of angiotensin I converting enzyme, captopril (SQ 14,225).	Captopril	103-112	kininogen 1	Homo sapiens	40-50
477733-4	1979	Prostaglandin E1 enhanced the effects of bradykinin and histamine on nociceptive cells.	Alprostadil	0-16	kininogen 1	Homo sapiens	41-51
225265-0	1979	Regulation of bradykinin-induced cyclic amp response by quinacrine and prostaglandin E2 and F2 alpha in human synovial fibroblasts.	Cyclic AMP	33-43	kininogen 1	Homo sapiens	14-24
225265-0	1979	Regulation of bradykinin-induced cyclic amp response by quinacrine and prostaglandin E2 and F2 alpha in human synovial fibroblasts.	Quinacrine	56-66	kininogen 1	Homo sapiens	14-24
225265-0	1979	Regulation of bradykinin-induced cyclic amp response by quinacrine and prostaglandin E2 and F2 alpha in human synovial fibroblasts.	Dinoprostone	71-87	kininogen 1	Homo sapiens	14-24
225265-1	1979	Bradykinin induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the release of [3H]arachidonic acid and [3H]-E prostaglandins from human synovial fibroblasts pre-labeled in their phospholipids.	Cyclic AMP	49-59	kininogen 1	Homo sapiens	0-10
225265-1	1979	Bradykinin induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the release of [3H]arachidonic acid and [3H]-E prostaglandins from human synovial fibroblasts pre-labeled in their phospholipids.	[3h]arachidonic acid	131-151	kininogen 1	Homo sapiens	0-10
225265-1	1979	Bradykinin induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the release of [3H]arachidonic acid and [3H]-E prostaglandins from human synovial fibroblasts pre-labeled in their phospholipids.	Tritium	132-134	kininogen 1	Homo sapiens	0-10
225265-1	1979	Bradykinin induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the release of [3H]arachidonic acid and [3H]-E prostaglandins from human synovial fibroblasts pre-labeled in their phospholipids.	Prostaglandins	163-177	kininogen 1	Homo sapiens	0-10
225265-1	1979	Bradykinin induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the release of [3H]arachidonic acid and [3H]-E prostaglandins from human synovial fibroblasts pre-labeled in their phospholipids.	Phospholipids	231-244	kininogen 1	Homo sapiens	0-10
225265-2	1979	Both these bradykinin-induced reactions are inhibited by quinacrine, an inhibitor of phospholipase A activity.	Quinacrine	57-67	kininogen 1	Homo sapiens	11-21
225265-3	1979	The cyclic AMP response of human synovial fibroblasts to bradykinin is potentiated by prostaglandin E2 and inhibited by prostaglandin F2 alpha.	Cyclic AMP	4-14	kininogen 1	Homo sapiens	57-67
225265-3	1979	The cyclic AMP response of human synovial fibroblasts to bradykinin is potentiated by prostaglandin E2 and inhibited by prostaglandin F2 alpha.	Dinoprostone	86-102	kininogen 1	Homo sapiens	57-67
225265-3	1979	The cyclic AMP response of human synovial fibroblasts to bradykinin is potentiated by prostaglandin E2 and inhibited by prostaglandin F2 alpha.	Dinoprost	120-142	kininogen 1	Homo sapiens	57-67
225265-4	1979	These data emphasize the critical role of the prostaglandin system in reactions induced by bradykinin and suggest mechansims by which inflammatory reactions due to bradykinin may be modulated.	Prostaglandins	46-59	kininogen 1	Homo sapiens	91-101
225265-4	1979	These data emphasize the critical role of the prostaglandin system in reactions induced by bradykinin and suggest mechansims by which inflammatory reactions due to bradykinin may be modulated.	Prostaglandins	46-59	kininogen 1	Homo sapiens	164-174
232084-1	1979	Captopril inhibits angiotensin II formation and bradykinin degradation in vivo.	Captopril	0-9	kininogen 1	Homo sapiens	48-58
230538-4	1979	These cells produce prostaglandins at measurable concentrations in response to treatment with ascorbic acid or bradykinin.	Prostaglandins	20-34	kininogen 1	Homo sapiens	111-121
447650-1	1979	The property of brain endopeptidases of attacking small biologically active polypeptides but not denatured proteins led us to compare them with pancreatic proteolytic enzymes with respect to hydrolysis of a synthetic peptide derived from bradykinin (Gly-Gly-Gly-Arg-bradykinin), free, bound to Affi-Gel 10, or bound to succinylated polylysine of 3,000 and 180,000 daltons, respectively.	gly-gly-gly-arg	250-265	kininogen 1	Homo sapiens	238-248
447650-1	1979	The property of brain endopeptidases of attacking small biologically active polypeptides but not denatured proteins led us to compare them with pancreatic proteolytic enzymes with respect to hydrolysis of a synthetic peptide derived from bradykinin (Gly-Gly-Gly-Arg-bradykinin), free, bound to Affi-Gel 10, or bound to succinylated polylysine of 3,000 and 180,000 daltons, respectively.	Polylysine	332-342	kininogen 1	Homo sapiens	238-248
384270-0	1979	Role of calcium in prostaglandin E release induced by bradykinin and the ionophore A 23187.	Calcium	8-15	kininogen 1	Homo sapiens	54-64
384270-0	1979	Role of calcium in prostaglandin E release induced by bradykinin and the ionophore A 23187.	Prostaglandins E	19-34	kininogen 1	Homo sapiens	54-64
485722-5	1979	When these procedures were after pretreatment with the analgesic agents, acetylsalicylic acid or dipyron a reduction in spike discharge was observed only with bradykinin after application of acetylsalicylic acid.	Aspirin	73-93	kininogen 1	Homo sapiens	159-169
485722-5	1979	When these procedures were after pretreatment with the analgesic agents, acetylsalicylic acid or dipyron a reduction in spike discharge was observed only with bradykinin after application of acetylsalicylic acid.	sodium;2-(1,5-dimethyl-3-oxo-2-phenylpyrazol-4-yl)propane-1-sulfonate	97-104	kininogen 1	Homo sapiens	159-169
485722-5	1979	When these procedures were after pretreatment with the analgesic agents, acetylsalicylic acid or dipyron a reduction in spike discharge was observed only with bradykinin after application of acetylsalicylic acid.	Aspirin	191-211	kininogen 1	Homo sapiens	159-169
378310-0	1979	Prostacyclin-release by bradykinin in vivo [proceedings].	Epoprostenol	0-12	kininogen 1	Homo sapiens	24-34
284420-2	1979	Sephadex-ellagic acid-exposed Hageman factor, whether purified or in plasma, activated plasma thromboplastin antecedent, but only when high molecular weight kininogen was presnet.	sephadex-ellagic acid	0-21	kininogen 1	Homo sapiens	135-166
495337-0	1979	Improvement of glucose assimilation and protein degradation by bradykinin in maturity onset diabetics and in surgical patients.	Glucose	15-22	kininogen 1	Homo sapiens	63-73
7363374-0	1980	Synthesis of bradykinin fragments and their analogs modified at a phenylalanine residue.	Phenylalanine	66-79	kininogen 1	Homo sapiens	13-23
517254-4	1979	(1) In a purified system, high molecular weight kininogen was absolutely required for activation of PTA by HF and ellagic acid (EA).	Ellagic Acid	114-126	kininogen 1	Homo sapiens	26-57
517254-4	1979	(1) In a purified system, high molecular weight kininogen was absolutely required for activation of PTA by HF and ellagic acid (EA).	Ellagic Acid	128-130	kininogen 1	Homo sapiens	26-57
230492-12	1979	IPA is readily deacylated from the renal phospholipid pool in response to bradykinin, a substance that also stimulates the release of arachidonic acid.	Arachidonic Acid	134-150	kininogen 1	Homo sapiens	74-84
35240-4	1979	It is shown that the two biologically essential arginine residues (Arg1 and Arg9) are important for the specific folded bradykinin conformation.	Arginine	48-56	kininogen 1	Homo sapiens	120-130
516007-0	1979	The anti-inflammatory action of heparin: heparin as an antagonist to histamine, bradykinin and prostaglandin E1.	Heparin	32-39	kininogen 1	Homo sapiens	80-90
119712-5	1979	Using this parameter, it is concluded that in bradykinin the gamma-turn probability is low in D2O and not strongly temperature dependent.	Deuterium Oxide	94-97	kininogen 1	Homo sapiens	46-56
156935-1	1979	Normal human placental eluate (0.15 M NaCl) has very high capacity for inactivating synthetic bradykinin (its specific activity is 20--50 times higher than that of normal human serum).	Sodium Chloride	38-42	kininogen 1	Homo sapiens	94-104
156935-2	1979	In chromatography on DEAE-Sephadex A 50, several fractions with bradykinin-inactivating capacity were recovered.	deae-sephadex a	21-36	kininogen 1	Homo sapiens	64-74
516007-0	1979	The anti-inflammatory action of heparin: heparin as an antagonist to histamine, bradykinin and prostaglandin E1.	Heparin	41-48	kininogen 1	Homo sapiens	80-90
728386-2	1978	Synthetic procedures have been developed for the preparation of peptides of arginine chloromethyl ketone and applied in the preparation of affinity labels which correspond to the -Pro-Phe-Arg- C terminus of bradykinin, a physiological cleavage site of kallikrein in kininogen.	arginine chloromethyl ketone	76-104	kininogen 1	Homo sapiens	207-217
32935-1	1978	The two equilibrium constants that define the extent of carbamino adduct formation with amines for all values of pH and PCO2 are determined for the alpha-amino groups of the peptide hormones angiotensin II(AII) and bradykinin (BK) by nuclear magnetic resonance techniques.	carbamino	56-65	kininogen 1	Homo sapiens	215-225
32935-1	1978	The two equilibrium constants that define the extent of carbamino adduct formation with amines for all values of pH and PCO2 are determined for the alpha-amino groups of the peptide hormones angiotensin II(AII) and bradykinin (BK) by nuclear magnetic resonance techniques.	carbamino	56-65	kininogen 1	Homo sapiens	227-229
32935-1	1978	The two equilibrium constants that define the extent of carbamino adduct formation with amines for all values of pH and PCO2 are determined for the alpha-amino groups of the peptide hormones angiotensin II(AII) and bradykinin (BK) by nuclear magnetic resonance techniques.	Amines	88-94	kininogen 1	Homo sapiens	215-225
32935-1	1978	The two equilibrium constants that define the extent of carbamino adduct formation with amines for all values of pH and PCO2 are determined for the alpha-amino groups of the peptide hormones angiotensin II(AII) and bradykinin (BK) by nuclear magnetic resonance techniques.	Amines	88-94	kininogen 1	Homo sapiens	227-229
32935-1	1978	The two equilibrium constants that define the extent of carbamino adduct formation with amines for all values of pH and PCO2 are determined for the alpha-amino groups of the peptide hormones angiotensin II(AII) and bradykinin (BK) by nuclear magnetic resonance techniques.	pco2	120-124	kininogen 1	Homo sapiens	215-225
32935-4	1978	The mole fraction, Z, of carbamino adduct form of AII or BK shows a maximum variation in going from metabolic alkalosis, Z congruent to 0.30, to metabolic acidosis, Z congruent to 0.02, with Z near 0.2 for normal acid-base conditions.	carbamino	25-34	kininogen 1	Homo sapiens	57-59
104988-4	1979	Human high molecular weight (HMW)-kininogen was highly purified from human plasma by chromatographies on QAE-Sephadex A-50 and CM-Sephadex C-50.	sephadex a	109-119	kininogen 1	Homo sapiens	6-43
104988-4	1979	Human high molecular weight (HMW)-kininogen was highly purified from human plasma by chromatographies on QAE-Sephadex A-50 and CM-Sephadex C-50.	sephadex c	130-140	kininogen 1	Homo sapiens	6-43
713429-0	1978	[Improvement of pathological glucose tolerance by bradykinin in diabetics and in surgical patients (author"s transl)].	Glucose	29-36	kininogen 1	Homo sapiens	50-60
713429-4	1978	In addition, the effect of BK on blood glucose concentration in the postabsorptive state was investigated in nine maturity onset diabetics and in five healthy volunteers.	Glucose	39-46	kininogen 1	Homo sapiens	27-29
713429-6	1978	In both groups of surgical patients BK improved glucose tolerance (k-values: group A without BK 1.03 +/- 0.12, with BK 1.31 +/- 0.07; group B without BK 0.85 +/- 0.18, with BK 1.25 +/- 0.21).	Glucose	48-55	kininogen 1	Homo sapiens	36-38
687639-3	1978	In contrast, the N-terminal Arg-Pro of bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) was not cleaved by the enzyme.	Arginine	28-31	kininogen 1	Homo sapiens	39-49
687639-3	1978	In contrast, the N-terminal Arg-Pro of bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) was not cleaved by the enzyme.	Arginine	51-54	kininogen 1	Homo sapiens	39-49
687639-3	1978	In contrast, the N-terminal Arg-Pro of bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) was not cleaved by the enzyme.	Proline	32-35	kininogen 1	Homo sapiens	39-49
687639-3	1978	In contrast, the N-terminal Arg-Pro of bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) was not cleaved by the enzyme.	prolylglycine	59-66	kininogen 1	Homo sapiens	39-49
687639-3	1978	In contrast, the N-terminal Arg-Pro of bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) was not cleaved by the enzyme.	Phenylalanine	67-70	kininogen 1	Homo sapiens	39-49
687639-3	1978	In contrast, the N-terminal Arg-Pro of bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) was not cleaved by the enzyme.	Serine	71-74	kininogen 1	Homo sapiens	39-49
687639-3	1978	In contrast, the N-terminal Arg-Pro of bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) was not cleaved by the enzyme.	Pro-Phe-Arg	75-86	kininogen 1	Homo sapiens	39-49
28141-0	1978	13C and 1H nuclear magnetic resonance studies of bradykinin and selected peptide fragments.	Hydrogen	8-10	kininogen 1	Homo sapiens	49-59
708052-0	1978	L-3,4-dehydroproline analogs of bradykinin.	3,4-dehydroproline	0-20	kininogen 1	Homo sapiens	32-42
207335-7	1978	A study of different substrates showed the activity to be highest with Z-Leu-Gly-Gly, followed by Z-Phe-His-Leu greater than bradykinin greater than Bz-Gly-Gly-Gly greater than Boc-Phe-Ala-Pro greater than Bz-Gly-His-Leu greater than angiotensin I.	z-leu-gly-gly	71-84	kininogen 1	Homo sapiens	125-135
96139-6	1978	Thus, with prostaglandin synthetase inhibition, values for urinary kallikrein and kinin and plasma bradykinin returned to normal pari passu with changes in PRA, in aldosterone, and in prostaglandin E.	Prostaglandins	11-24	kininogen 1	Homo sapiens	99-109
207335-7	1978	A study of different substrates showed the activity to be highest with Z-Leu-Gly-Gly, followed by Z-Phe-His-Leu greater than bradykinin greater than Bz-Gly-Gly-Gly greater than Boc-Phe-Ala-Pro greater than Bz-Gly-His-Leu greater than angiotensin I.	z-phe-his	98-107	kininogen 1	Homo sapiens	125-135
207335-7	1978	A study of different substrates showed the activity to be highest with Z-Leu-Gly-Gly, followed by Z-Phe-His-Leu greater than bradykinin greater than Bz-Gly-Gly-Gly greater than Boc-Phe-Ala-Pro greater than Bz-Gly-His-Leu greater than angiotensin I.	Leucine	73-76	kininogen 1	Homo sapiens	125-135
207335-7	1978	A study of different substrates showed the activity to be highest with Z-Leu-Gly-Gly, followed by Z-Phe-His-Leu greater than bradykinin greater than Bz-Gly-Gly-Gly greater than Boc-Phe-Ala-Pro greater than Bz-Gly-His-Leu greater than angiotensin I.	bz-gly-gly-gly	149-163	kininogen 1	Homo sapiens	125-135
207335-7	1978	A study of different substrates showed the activity to be highest with Z-Leu-Gly-Gly, followed by Z-Phe-His-Leu greater than bradykinin greater than Bz-Gly-Gly-Gly greater than Boc-Phe-Ala-Pro greater than Bz-Gly-His-Leu greater than angiotensin I.	boc-phe-ala-pro	177-192	kininogen 1	Homo sapiens	125-135
207335-7	1978	A study of different substrates showed the activity to be highest with Z-Leu-Gly-Gly, followed by Z-Phe-His-Leu greater than bradykinin greater than Bz-Gly-Gly-Gly greater than Boc-Phe-Ala-Pro greater than Bz-Gly-His-Leu greater than angiotensin I.	bz-gly-his	206-216	kininogen 1	Homo sapiens	125-135
76024-3	1978	Ventilation of the lungs with air or oxygen causes the release of bradykinin which is rapidly inactivated in the lungs.	Oxygen	37-43	kininogen 1	Homo sapiens	66-76
76024-6	1978	Formation of bradykinin by granulocytes is critically dependent on the local oxygen tension.	Oxygen	77-83	kininogen 1	Homo sapiens	13-23
640583-0	1978	Bradykinin and human forearm metabolism: inhibition of endogenous prostaglandin synthesis.	Prostaglandins	66-79	kininogen 1	Homo sapiens	0-10
580160-6	1978	The addition of purified human HMWK to the plasma before the acetone activation procedure was started, increased the yield of PKA activity in the final enzyme preparation.	Acetone	61-68	kininogen 1	Homo sapiens	31-35
580160-8	1978	It is suggested that the low PKA activity of the acetone activated enzyme preparation from plasma of rats treated with dextran was due to the loss of HMWK or a fraction of HMWK.	Acetone	49-56	kininogen 1	Homo sapiens	150-154
639619-2	1978	With bradykinin a normalization of the postoperative decreased assimilation of glucose was found.	Glucose	79-86	kininogen 1	Homo sapiens	5-15
722404-1	1978	Daily intralesional injections of bradykinin (250 microgram) into syngeneic SV40 virus-induced fibrosarcomas in inbred hamsters for 21 days produced marked inhibition of tumour growth, marked lymphoid cell infiltration of tumours, and significant elevations in plasma kallikrein and prekallikrein activity, compared with intralesional saline injections.	Sodium Chloride	335-341	kininogen 1	Homo sapiens	34-44
580160-8	1978	It is suggested that the low PKA activity of the acetone activated enzyme preparation from plasma of rats treated with dextran was due to the loss of HMWK or a fraction of HMWK.	Acetone	49-56	kininogen 1	Homo sapiens	172-176
580160-8	1978	It is suggested that the low PKA activity of the acetone activated enzyme preparation from plasma of rats treated with dextran was due to the loss of HMWK or a fraction of HMWK.	Dextrans	119-126	kininogen 1	Homo sapiens	150-154
580160-8	1978	It is suggested that the low PKA activity of the acetone activated enzyme preparation from plasma of rats treated with dextran was due to the loss of HMWK or a fraction of HMWK.	Dextrans	119-126	kininogen 1	Homo sapiens	172-176
418628-3	1978	The effect of steroids on phospholipase A2 activity in lungs was investigated and it was found that these drugs inhibited the enzyme activity in a time-dependent reversible fashion and that they will block the effect of stimuli such as RCS-RF (bradykinin being an exception).	Steroids	14-22	kininogen 1	Homo sapiens	244-254
636947-0	1978	Release of prostaglandins mediating the potentiation of bradykinin by BPF and chymotrypsin in rate isolated ileum [proceedings].	Prostaglandins	11-25	kininogen 1	Homo sapiens	56-66
636959-6	1978	Conversion of lysyl-bradykinin to bradykinin could be confirmed also by chromatography on CM-cellulose.	7,8-diacetoxy-3-(4-nitrophenyl)coumarin	90-102	kininogen 1	Homo sapiens	20-30
636959-6	1978	Conversion of lysyl-bradykinin to bradykinin could be confirmed also by chromatography on CM-cellulose.	7,8-diacetoxy-3-(4-nitrophenyl)coumarin	90-102	kininogen 1	Homo sapiens	34-44
619633-4	1978	Bradykinin increased UBF to 60 per cent of peak estradiol-induced levels, with concomitant increases in IUP tonus.	Estradiol	48-57	kininogen 1	Homo sapiens	0-10
619769-2	1978	In two patients with erythromelalgia a grossly abnormal bullous reaction to intradermally injected PGE1, PGE2, and PGF1alpha occurred, whereas a normal reaction appeared after injection of histamine, serotonin, and  bradykinin.	Alprostadil	99-103	kininogen 1	Homo sapiens	216-226
710977-1	1978	The effect of estriol on the response of human umbilical artery to bradykinin (0.2 microgram/ml) and adrenalin (0.8 microgram/ml) was studied by an in vitro perfusion method.	Estriol	14-21	kininogen 1	Homo sapiens	67-77
624845-9	1978	The data suggest that antisera for bradykinin radioimmunoassay be tested with several radioactive iodobradykinins to maximize their usefulness.	iodobradykinins	98-113	kininogen 1	Homo sapiens	35-45
200263-4	1977	The enzyme requires chloride ion for activity and is inhibited by ethylenediaminetetraacetic acid, angiotensin II, bradykinin, bradykinin potentiating factor nonapeptide, and 3-mercapto-2-D-methylpropanoyl-L-proline (SQ-14,225).	Chlorides	20-28	kininogen 1	Homo sapiens	115-125
204962-1	1978	Bradykinin, a potent inflammatory mediator, induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the synthesis and release of 3H-arachidonic acid and 3H-E prostaglandins from these cells pre-labeled in their phospholipids.	3h-e prostaglandins	202-221	kininogen 1	Homo sapiens	0-10
204962-0	1978	The effect of 7-oxa-13 prostynoic acid on the mechanism of action of bradykinin in human synovial fibroblasts.	7-oxa-13-prostynoic acid	14-38	kininogen 1	Homo sapiens	69-79
204962-1	1978	Bradykinin, a potent inflammatory mediator, induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the synthesis and release of 3H-arachidonic acid and 3H-E prostaglandins from these cells pre-labeled in their phospholipids.	Cyclic AMP	82-92	kininogen 1	Homo sapiens	0-10
200263-4	1977	The enzyme requires chloride ion for activity and is inhibited by ethylenediaminetetraacetic acid, angiotensin II, bradykinin, bradykinin potentiating factor nonapeptide, and 3-mercapto-2-D-methylpropanoyl-L-proline (SQ-14,225).	Chlorides	20-28	kininogen 1	Homo sapiens	127-137
204962-1	1978	Bradykinin, a potent inflammatory mediator, induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the synthesis and release of 3H-arachidonic acid and 3H-E prostaglandins from these cells pre-labeled in their phospholipids.	3h-arachidonic acid	178-197	kininogen 1	Homo sapiens	0-10
204962-1	1978	Bradykinin, a potent inflammatory mediator, induces an increment in intracellular cyclic AMP concentrations of human synovial fibroblasts and evokes the synthesis and release of 3H-arachidonic acid and 3H-E prostaglandins from these cells pre-labeled in their phospholipids.	Phospholipids	260-273	kininogen 1	Homo sapiens	0-10
200263-4	1977	The enzyme requires chloride ion for activity and is inhibited by ethylenediaminetetraacetic acid, angiotensin II, bradykinin, bradykinin potentiating factor nonapeptide, and 3-mercapto-2-D-methylpropanoyl-L-proline (SQ-14,225).	sq-14	217-222	kininogen 1	Homo sapiens	115-125
204962-2	1978	Fetal calf serum in the media also stimulates the synthesis and release of these labeled lipids from pre-labeled human synovial fibroblasts and potentiates the bradykinin-induced cyclic AMP response.	Cyclic AMP	179-189	kininogen 1	Homo sapiens	160-170
204962-3	1978	The PGE1 analogue, 7-oxa-13 prostynoic acid, completely abrogates both the bradykinin-induced cyclic AMP response and the bradykinin- and fetal calf serum-evoked release of labeled E-prostaglandins from pre-labeled cells.	Alprostadil	4-8	kininogen 1	Homo sapiens	75-85
204962-3	1978	The PGE1 analogue, 7-oxa-13 prostynoic acid, completely abrogates both the bradykinin-induced cyclic AMP response and the bradykinin- and fetal calf serum-evoked release of labeled E-prostaglandins from pre-labeled cells.	Alprostadil	4-8	kininogen 1	Homo sapiens	122-132
204962-3	1978	The PGE1 analogue, 7-oxa-13 prostynoic acid, completely abrogates both the bradykinin-induced cyclic AMP response and the bradykinin- and fetal calf serum-evoked release of labeled E-prostaglandins from pre-labeled cells.	7-oxa-13-prostynoic acid	19-43	kininogen 1	Homo sapiens	75-85
204962-3	1978	The PGE1 analogue, 7-oxa-13 prostynoic acid, completely abrogates both the bradykinin-induced cyclic AMP response and the bradykinin- and fetal calf serum-evoked release of labeled E-prostaglandins from pre-labeled cells.	7-oxa-13-prostynoic acid	19-43	kininogen 1	Homo sapiens	122-132
204962-3	1978	The PGE1 analogue, 7-oxa-13 prostynoic acid, completely abrogates both the bradykinin-induced cyclic AMP response and the bradykinin- and fetal calf serum-evoked release of labeled E-prostaglandins from pre-labeled cells.	Cyclic AMP	94-104	kininogen 1	Homo sapiens	75-85
204962-3	1978	The PGE1 analogue, 7-oxa-13 prostynoic acid, completely abrogates both the bradykinin-induced cyclic AMP response and the bradykinin- and fetal calf serum-evoked release of labeled E-prostaglandins from pre-labeled cells.	e-prostaglandins	181-197	kininogen 1	Homo sapiens	122-132
200263-4	1977	The enzyme requires chloride ion for activity and is inhibited by ethylenediaminetetraacetic acid, angiotensin II, bradykinin, bradykinin potentiating factor nonapeptide, and 3-mercapto-2-D-methylpropanoyl-L-proline (SQ-14,225).	sq-14	217-222	kininogen 1	Homo sapiens	127-137
915004-1	1977	Factor XI and high molecular weight kininogen were found associated in normal human plasma at mol wt 380,000 as assessed by gel filtration on Sephadex G-200.	sephadex	142-156	kininogen 1	Homo sapiens	14-45
597666-4	1977	These paradoxical effects were brought about by that portion of the high dose of histamine which re-entered the cat"s systemic circulation.4 The order of potency of the vasodilators was the same for their potentiating effect on the acetylcholine-induced contractile responses as for their enhancing effect on muscle blood flow: bradykinin &gt;histamine&gt;&gt;papaverine&gt;&gt;NaH(2)PO(4) &gt;KCl.	Histamine	81-90	kininogen 1	Homo sapiens	328-338
597666-4	1977	These paradoxical effects were brought about by that portion of the high dose of histamine which re-entered the cat"s systemic circulation.4 The order of potency of the vasodilators was the same for their potentiating effect on the acetylcholine-induced contractile responses as for their enhancing effect on muscle blood flow: bradykinin &gt;histamine&gt;&gt;papaverine&gt;&gt;NaH(2)PO(4) &gt;KCl.	Acetylcholine	232-245	kininogen 1	Homo sapiens	328-338
596228-0	1977	Inhibition of bradykinin induced macromolecular leakage from post-capillary venules by a beta2-adrenoreceptor stimulant, terbutaline.	Terbutaline	121-132	kininogen 1	Homo sapiens	14-24
197839-1	1977	Human synovial fibroblasts in culture respond to bradykinin (8 X 10(-9) M) with an increment in intracellular cyclic AMP concentration.	Cyclic AMP	110-120	kininogen 1	Homo sapiens	49-59
907100-0	1977	SP-Sephadex equilibrium chromatography of bradykinin and related peptides: application to trypsin-treated human plasma.	sp-sephadex	0-11	kininogen 1	Homo sapiens	42-52
197839-9	1977	Indomethacin (IM) inhibits the BK evoked cyclic AMP response unless cell cultures are pretreated with PGE1.	Cyclic AMP	41-51	kininogen 1	Homo sapiens	31-33
197839-9	1977	Indomethacin (IM) inhibits the BK evoked cyclic AMP response unless cell cultures are pretreated with PGE1.	Alprostadil	102-106	kininogen 1	Homo sapiens	31-33
197839-10	1977	The PGE1 analog, 7-oxa-13-prostynoic acid, is a better inhibitor of the cyclic AMP response induced by BK than by PGE1.	Alprostadil	4-8	kininogen 1	Homo sapiens	103-105
197839-10	1977	The PGE1 analog, 7-oxa-13-prostynoic acid, is a better inhibitor of the cyclic AMP response induced by BK than by PGE1.	7-oxa-13-prostynoic acid	17-41	kininogen 1	Homo sapiens	103-105
197839-10	1977	The PGE1 analog, 7-oxa-13-prostynoic acid, is a better inhibitor of the cyclic AMP response induced by BK than by PGE1.	Cyclic AMP	72-82	kininogen 1	Homo sapiens	103-105
197839-11	1977	BK does not elicit a cyclic AMP response solely by elaborating PGE1, yet the prostaglandin pathway and its products seem to have a role in the degree of the cyclic AMP response to BK challenge.	Prostaglandins	77-90	kininogen 1	Homo sapiens	180-182
197839-11	1977	BK does not elicit a cyclic AMP response solely by elaborating PGE1, yet the prostaglandin pathway and its products seem to have a role in the degree of the cyclic AMP response to BK challenge.	Cyclic AMP	157-167	kininogen 1	Homo sapiens	180-182
887505-1	1977	The influence of bradykinin on the action of compounds affecting predominantly the dopaminergic receptor was studied in behavioral tests (Lat test and sterotypy) and biochemically (estimation of the level of biogenic amines--noradrenaline, dopamine and serotonin, and their metabolites--normetanephrine, homovanillic and 5-hydroxyindoleacetic acids in the brain tissue).	Dopamine	83-91	kininogen 1	Homo sapiens	17-27
887505-1	1977	The influence of bradykinin on the action of compounds affecting predominantly the dopaminergic receptor was studied in behavioral tests (Lat test and sterotypy) and biochemically (estimation of the level of biogenic amines--noradrenaline, dopamine and serotonin, and their metabolites--normetanephrine, homovanillic and 5-hydroxyindoleacetic acids in the brain tissue).	Serotonin	253-262	kininogen 1	Homo sapiens	17-27
887505-1	1977	The influence of bradykinin on the action of compounds affecting predominantly the dopaminergic receptor was studied in behavioral tests (Lat test and sterotypy) and biochemically (estimation of the level of biogenic amines--noradrenaline, dopamine and serotonin, and their metabolites--normetanephrine, homovanillic and 5-hydroxyindoleacetic acids in the brain tissue).	Normetanephrine	285-302	kininogen 1	Homo sapiens	17-27
887505-1	1977	The influence of bradykinin on the action of compounds affecting predominantly the dopaminergic receptor was studied in behavioral tests (Lat test and sterotypy) and biochemically (estimation of the level of biogenic amines--noradrenaline, dopamine and serotonin, and their metabolites--normetanephrine, homovanillic and 5-hydroxyindoleacetic acids in the brain tissue).	5-hydroxyindoleacetic acids	321-348	kininogen 1	Homo sapiens	17-27
887505-2	1977	Bradykinin potentiated the action of nialamide with L-dopa, dopamine, 1,3-dimethyl-5-aminoadamantane, apomorphine and noradrenaline.	Nialamide	37-46	kininogen 1	Homo sapiens	0-10
887505-2	1977	Bradykinin potentiated the action of nialamide with L-dopa, dopamine, 1,3-dimethyl-5-aminoadamantane, apomorphine and noradrenaline.	Levodopa	52-58	kininogen 1	Homo sapiens	0-10
887505-2	1977	Bradykinin potentiated the action of nialamide with L-dopa, dopamine, 1,3-dimethyl-5-aminoadamantane, apomorphine and noradrenaline.	Dopamine	60-68	kininogen 1	Homo sapiens	0-10
887505-2	1977	Bradykinin potentiated the action of nialamide with L-dopa, dopamine, 1,3-dimethyl-5-aminoadamantane, apomorphine and noradrenaline.	Memantine	70-100	kininogen 1	Homo sapiens	0-10
887505-2	1977	Bradykinin potentiated the action of nialamide with L-dopa, dopamine, 1,3-dimethyl-5-aminoadamantane, apomorphine and noradrenaline.	Apomorphine	102-113	kininogen 1	Homo sapiens	0-10
887505-2	1977	Bradykinin potentiated the action of nialamide with L-dopa, dopamine, 1,3-dimethyl-5-aminoadamantane, apomorphine and noradrenaline.	Norepinephrine	118-131	kininogen 1	Homo sapiens	0-10
887505-3	1977	Spiroperidol abolished potentializing effect of bradykinin on the central action of nialamide with L-DOPA and of noradrenaline.	Spiperone	0-12	kininogen 1	Homo sapiens	48-58
887505-3	1977	Spiroperidol abolished potentializing effect of bradykinin on the central action of nialamide with L-DOPA and of noradrenaline.	Nialamide	84-93	kininogen 1	Homo sapiens	48-58
887505-3	1977	Spiroperidol abolished potentializing effect of bradykinin on the central action of nialamide with L-DOPA and of noradrenaline.	Levodopa	99-105	kininogen 1	Homo sapiens	48-58
887505-3	1977	Spiroperidol abolished potentializing effect of bradykinin on the central action of nialamide with L-DOPA and of noradrenaline.	Norepinephrine	113-126	kininogen 1	Homo sapiens	48-58
887505-4	1977	In animals receiving spiroperidol with bradykinin psychostimulatory action of noradrenaline was also not observed.	Spiperone	21-33	kininogen 1	Homo sapiens	39-49
887505-4	1977	In animals receiving spiroperidol with bradykinin psychostimulatory action of noradrenaline was also not observed.	Norepinephrine	78-91	kininogen 1	Homo sapiens	39-49
887505-5	1977	FLA-63--inhibitor of dopamine beta-hydroxylase--increased the potentializing effect of bradykinin on the central action of dopamine.	Bis(4-Methyl-1-Homopiperazinylthiocarbonyl)disulfide	0-6	kininogen 1	Homo sapiens	87-97
887505-5	1977	FLA-63--inhibitor of dopamine beta-hydroxylase--increased the potentializing effect of bradykinin on the central action of dopamine.	Dopamine	21-29	kininogen 1	Homo sapiens	87-97
887505-6	1977	Most significant biochemical changes between the group receiving nialamide alone and the group given nialamide together with bradykinin have been observed in corpus striatum, where the level of dopamine and its metabolite--homovanillic acid--increased.	Dopamine	194-202	kininogen 1	Homo sapiens	125-135
887505-6	1977	Most significant biochemical changes between the group receiving nialamide alone and the group given nialamide together with bradykinin have been observed in corpus striatum, where the level of dopamine and its metabolite--homovanillic acid--increased.	Homovanillic Acid	223-240	kininogen 1	Homo sapiens	125-135
558755-0	1977	Circular dichroism spectra of bradykinin analogs containing beta-homoamino acids.	beta-homoamino acids	60-80	kininogen 1	Homo sapiens	30-40
403030-8	1977	After indomethacin, the renal dilator response to bradykinin was enhanced; however, dilator responses to nitroglycerin were unaltered.	Indomethacin	6-18	kininogen 1	Homo sapiens	50-60
870748-0	1977	[Effect of bradykinin on muscular glucose uptake in man (author"s transl)].	Glucose	34-41	kininogen 1	Homo sapiens	11-21
870748-1	1977	Glucose metabolism of the human forearm was studied in 4 healthy volunteers by monitoring arterial deepvenous glucose concentration differences and by the determination of muscle blood flow, using 133xenon as a tracer, during 25 min intra-brachial-arterial infusion of bradykinin (13.3 ng per min).	Glucose	0-7	kininogen 1	Homo sapiens	269-279
69390-1	1977	Some authors succeded in binding the bradykinin in form of a haptene by an azo-bridge to the human gammaglobulin as a vehicle.	anthrone	75-79	kininogen 1	Homo sapiens	37-47
69390-4	1977	If such animals receive an intravenous or intracardiac injection of a 1% Evans blue solution, there is a strong blue colouring in the place where the bradykinin has been applied.	Evans Blue	73-83	kininogen 1	Homo sapiens	150-160
69390-5	1977	The guinea pigs and the rabbits which had been immunized by bradykinin-azo-protein showed a significant decrease in the local accumulation of the Evans blue-solution,, which must be attributed to the immunologic neutralization of the intradermally injected bradykinin by an anti-bradykinin-antibody.	Evans Blue	146-156	kininogen 1	Homo sapiens	60-70
69390-5	1977	The guinea pigs and the rabbits which had been immunized by bradykinin-azo-protein showed a significant decrease in the local accumulation of the Evans blue-solution,, which must be attributed to the immunologic neutralization of the intradermally injected bradykinin by an anti-bradykinin-antibody.	Evans Blue	146-156	kininogen 1	Homo sapiens	257-267
69390-5	1977	The guinea pigs and the rabbits which had been immunized by bradykinin-azo-protein showed a significant decrease in the local accumulation of the Evans blue-solution,, which must be attributed to the immunologic neutralization of the intradermally injected bradykinin by an anti-bradykinin-antibody.	Evans Blue	146-156	kininogen 1	Homo sapiens	257-267
602510-8	1977	The reaction of another important pharmacological substance bradykinin (BRS), has been closely associated with oxygen saturation of the perfusion solution.	Oxygen	111-117	kininogen 1	Homo sapiens	60-70
12529-2	1976	It was shown that bradykinin in a dose of 4 mug decreased the content of norepinephrine in corpus striatum, midbrain, and cerebellum.	Norepinephrine	73-87	kininogen 1	Homo sapiens	18-28
12529-6	1976	Bradykinin, in a dose of 4 mug, decreased the level of normetanephrine in corpus striatum, hippocampus, and midbrain and the level of homovanillic acid in corpus striatum, and increased the level of 5-hydroxyindoloacetic acid in corpus striatum and hippocampus.	Normetanephrine	55-70	kininogen 1	Homo sapiens	0-10
12529-6	1976	Bradykinin, in a dose of 4 mug, decreased the level of normetanephrine in corpus striatum, hippocampus, and midbrain and the level of homovanillic acid in corpus striatum, and increased the level of 5-hydroxyindoloacetic acid in corpus striatum and hippocampus.	Homovanillic Acid	134-151	kininogen 1	Homo sapiens	0-10
12529-6	1976	Bradykinin, in a dose of 4 mug, decreased the level of normetanephrine in corpus striatum, hippocampus, and midbrain and the level of homovanillic acid in corpus striatum, and increased the level of 5-hydroxyindoloacetic acid in corpus striatum and hippocampus.	5-hydroxyindoloacetic acid	199-225	kininogen 1	Homo sapiens	0-10
12529-7	1976	It was also shown that bradykinin increased norepinephrine uptake by the blood platelets when its level in the platelets was low, and released the absorbed norepinephrine into the medium when the level of norepinephrine was higher.	Norepinephrine	44-58	kininogen 1	Homo sapiens	23-33
12529-7	1976	It was also shown that bradykinin increased norepinephrine uptake by the blood platelets when its level in the platelets was low, and released the absorbed norepinephrine into the medium when the level of norepinephrine was higher.	Norepinephrine	156-170	kininogen 1	Homo sapiens	23-33
12529-7	1976	It was also shown that bradykinin increased norepinephrine uptake by the blood platelets when its level in the platelets was low, and released the absorbed norepinephrine into the medium when the level of norepinephrine was higher.	Norepinephrine	156-170	kininogen 1	Homo sapiens	23-33
1012987-1	1976	Bradykinin (2 mug ivc) or kallikrein (40 U/kg) inhibited the stimulatory psychomotoric action of a low (0.5 mg/kg) dose of amphetamine, and potentiated the action of a high (2 mg/kg) dose of the drug.	Amphetamine	123-134	kininogen 1	Homo sapiens	0-10
1012987-2	1976	A treatment with bradykinin and the low dose of amphetamine reduced the noradrenaline and enhanced the serotonin level in the striatum, and lowered the dopamine content in the cortex, while a combined treatment with the high dose of amphetamine elevated the dopamine level in the striatum and hypothalamus and depressed the serotonin level in the midbrain.	Norepinephrine	72-85	kininogen 1	Homo sapiens	17-27
1012987-2	1976	A treatment with bradykinin and the low dose of amphetamine reduced the noradrenaline and enhanced the serotonin level in the striatum, and lowered the dopamine content in the cortex, while a combined treatment with the high dose of amphetamine elevated the dopamine level in the striatum and hypothalamus and depressed the serotonin level in the midbrain.	Serotonin	103-112	kininogen 1	Homo sapiens	17-27
1012987-2	1976	A treatment with bradykinin and the low dose of amphetamine reduced the noradrenaline and enhanced the serotonin level in the striatum, and lowered the dopamine content in the cortex, while a combined treatment with the high dose of amphetamine elevated the dopamine level in the striatum and hypothalamus and depressed the serotonin level in the midbrain.	Dopamine	152-160	kininogen 1	Homo sapiens	17-27
1012987-2	1976	A treatment with bradykinin and the low dose of amphetamine reduced the noradrenaline and enhanced the serotonin level in the striatum, and lowered the dopamine content in the cortex, while a combined treatment with the high dose of amphetamine elevated the dopamine level in the striatum and hypothalamus and depressed the serotonin level in the midbrain.	Amphetamine	233-244	kininogen 1	Homo sapiens	17-27
1012987-2	1976	A treatment with bradykinin and the low dose of amphetamine reduced the noradrenaline and enhanced the serotonin level in the striatum, and lowered the dopamine content in the cortex, while a combined treatment with the high dose of amphetamine elevated the dopamine level in the striatum and hypothalamus and depressed the serotonin level in the midbrain.	Dopamine	258-266	kininogen 1	Homo sapiens	17-27
1012987-2	1976	A treatment with bradykinin and the low dose of amphetamine reduced the noradrenaline and enhanced the serotonin level in the striatum, and lowered the dopamine content in the cortex, while a combined treatment with the high dose of amphetamine elevated the dopamine level in the striatum and hypothalamus and depressed the serotonin level in the midbrain.	Serotonin	324-333	kininogen 1	Homo sapiens	17-27
786740-7	1976	Other evidence also suggests that prostaglandins participate in a variety of vascular responses, including the mediation of bradykinin vasodilation, functional hyperemia, and reactive hyperemia.	Prostaglandins	34-48	kininogen 1	Homo sapiens	124-134
828748-2	1976	Bradykinin was applied either locally, in the organ bath, in doses of 9 microng, or by superfusion in doses of 0.8 - 0.9 microng/ml saline.	Sodium Chloride	132-138	kininogen 1	Homo sapiens	0-10
970286-1	1976	Human high molecular weight kininogen was isolated by a rapid procedure, using anion exchange chromatography on QAE-Sephadex, ammonium sulfate precipitation and cation exchange chromatography on CM-Sephadex.	qae-sephadex	112-124	kininogen 1	Homo sapiens	6-37
970286-1	1976	Human high molecular weight kininogen was isolated by a rapid procedure, using anion exchange chromatography on QAE-Sephadex, ammonium sulfate precipitation and cation exchange chromatography on CM-Sephadex.	Ammonium Sulfate	126-142	kininogen 1	Homo sapiens	6-37
970286-1	1976	Human high molecular weight kininogen was isolated by a rapid procedure, using anion exchange chromatography on QAE-Sephadex, ammonium sulfate precipitation and cation exchange chromatography on CM-Sephadex.	sephadex	116-124	kininogen 1	Homo sapiens	6-37
983720-0	1976	Influence of bradykinin and drugs blocking alpha and beta-adrenergic receptor on the stimulating effect of nialamide and L--DOPA.	Nialamide	107-116	kininogen 1	Homo sapiens	13-23
983720-0	1976	Influence of bradykinin and drugs blocking alpha and beta-adrenergic receptor on the stimulating effect of nialamide and L--DOPA.	Levodopa	121-128	kininogen 1	Homo sapiens	13-23
983720-2	1976	Phentolamine and propranolol decrease stimulatory effects of Nialamide and L-DOPA only when they are given jointly with bradykinin.	Phentolamine	0-12	kininogen 1	Homo sapiens	120-130
983720-2	1976	Phentolamine and propranolol decrease stimulatory effects of Nialamide and L-DOPA only when they are given jointly with bradykinin.	Propranolol	17-28	kininogen 1	Homo sapiens	120-130
983720-2	1976	Phentolamine and propranolol decrease stimulatory effects of Nialamide and L-DOPA only when they are given jointly with bradykinin.	Nialamide	61-70	kininogen 1	Homo sapiens	120-130
983720-2	1976	Phentolamine and propranolol decrease stimulatory effects of Nialamide and L-DOPA only when they are given jointly with bradykinin.	Levodopa	75-81	kininogen 1	Homo sapiens	120-130
593429-0	1977	Mechanism of action of bradykinin-induced release of prostaglandin E.	Prostaglandins E	53-68	kininogen 1	Homo sapiens	23-33
927556-0	1977	Influence of changed calcium and potassium concentration on the algesic effect of bradykinin and acetylcholine.	Calcium	21-28	kininogen 1	Homo sapiens	82-92
927556-0	1977	Influence of changed calcium and potassium concentration on the algesic effect of bradykinin and acetylcholine.	Potassium	33-42	kininogen 1	Homo sapiens	82-92
912443-1	1977	Under light to moderate sodium pentobarbital anesthesia one half of the thalamic neurons displaying place and modality specific responses to low intensity mechanical stimulation of contralateral receptive fields also responded, by excitation or by inhibition, to bradykinin injections into somatic and visceral arteries.	Pentobarbital	24-44	kininogen 1	Homo sapiens	263-273
18587-0	1977	Bradykinin relaxes contracted airways through prostaglandin production.	Prostaglandins	46-59	kininogen 1	Homo sapiens	0-10
870233-3	1977	In normal subjects, angiotensin II at 3 ng/kg per min or potassium at 20 mEq/hour infused intravenously for 2 hours both significantly increased plasma aldosterone levels, yet neither stimulus altered plasma bradykinin.	Potassium	57-66	kininogen 1	Homo sapiens	208-218
887505-1	1977	The influence of bradykinin on the action of compounds affecting predominantly the dopaminergic receptor was studied in behavioral tests (Lat test and sterotypy) and biochemically (estimation of the level of biogenic amines--noradrenaline, dopamine and serotonin, and their metabolites--normetanephrine, homovanillic and 5-hydroxyindoleacetic acids in the brain tissue).	Amines	217-223	kininogen 1	Homo sapiens	17-27
191471-8	1977	Endothelial cells also inactivate longer analogs of bradykinin, such as kallidin, methionyl-lysyl bradykinin, and bradykinin coupled covalently to 500,000 mol wt dextran.	Dextrans	162-169	kininogen 1	Homo sapiens	52-62
191875-0	1977	Hydrocortisone inhibition of the bradykinin activation of human synovial fibroblasts.	Hydrocortisone	0-14	kininogen 1	Homo sapiens	33-43
191875-1	1977	Human synovial fibroblasts in culture respond to bradykinin with a 20-fold increment in intracellular cyclic AMP concentrations, however bradykinin does not directly activate adenylate cyclase activity in a particulate fraction derived from these cells.	Cyclic AMP	102-112	kininogen 1	Homo sapiens	49-59
191875-2	1977	Bradykinin evokes a release of labeled arachidonic acid and prostaglandins E and F from synovial fibroblasts pre-labeled with 3H-arachidonic acid.	Arachidonic Acid	39-55	kininogen 1	Homo sapiens	0-10
191875-2	1977	Bradykinin evokes a release of labeled arachidonic acid and prostaglandins E and F from synovial fibroblasts pre-labeled with 3H-arachidonic acid.	prostaglandins e and f	60-82	kininogen 1	Homo sapiens	0-10
191875-2	1977	Bradykinin evokes a release of labeled arachidonic acid and prostaglandins E and F from synovial fibroblasts pre-labeled with 3H-arachidonic acid.	3h-arachidonic acid	126-145	kininogen 1	Homo sapiens	0-10
191875-3	1977	Hydrocortisone inhibits the bradykinin induced increment in cyclic AMP and the release of arachidonic acid and prostaglandins E and F from synovial fibroblasts.	Hydrocortisone	0-14	kininogen 1	Homo sapiens	28-38
191875-3	1977	Hydrocortisone inhibits the bradykinin induced increment in cyclic AMP and the release of arachidonic acid and prostaglandins E and F from synovial fibroblasts.	Cyclic AMP	60-70	kininogen 1	Homo sapiens	28-38
191875-3	1977	Hydrocortisone inhibits the bradykinin induced increment in cyclic AMP and the release of arachidonic acid and prostaglandins E and F from synovial fibroblasts.	Arachidonic Acid	90-106	kininogen 1	Homo sapiens	28-38
191875-3	1977	Hydrocortisone inhibits the bradykinin induced increment in cyclic AMP and the release of arachidonic acid and prostaglandins E and F from synovial fibroblasts.	prostaglandins e and f	111-133	kininogen 1	Homo sapiens	28-38
191875-4	1977	Indomethacin, which also inhibits the cyclic AMP response to bradykinin, has no effect on the release of arachidonic acid from synovial fibroblasts.	Indomethacin	0-12	kininogen 1	Homo sapiens	61-71
191875-4	1977	Indomethacin, which also inhibits the cyclic AMP response to bradykinin, has no effect on the release of arachidonic acid from synovial fibroblasts.	Cyclic AMP	38-48	kininogen 1	Homo sapiens	61-71
191875-6	1977	These studies support the hypothesis that bradykinin does not activate human synovial fibroblast adenylate cyclase, but presumably activates a phospholipase whose products in turn result in the synthesis of prostaglandins.	Prostaglandins	207-221	kininogen 1	Homo sapiens	42-52
562351-0	1977	Synthesis of analogues of bradykinin with replacement of the arginine residues by 4-guanidinophenyl-l-alanine.	Arginine	61-69	kininogen 1	Homo sapiens	26-36
562351-0	1977	Synthesis of analogues of bradykinin with replacement of the arginine residues by 4-guanidinophenyl-l-alanine.	4-guanidinophenyl-l-alanine	82-109	kininogen 1	Homo sapiens	26-36
1013700-4	1976	The central and autonomous nervous systems, the renin-angiotensin system, the mineralocorticoids, the antidiuretic hormone and the kallikrein-bradykinin-prostaglandin system all affect this regulation and are closely interrelated.	Prostaglandins	153-166	kininogen 1	Homo sapiens	142-152
1000085-5	1976	Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin.	Warfarin	431-439	kininogen 1	Homo sapiens	0-17
1027487-1	1976	A preparation of high-molecular weight kininogen (HMWK) was isolated from rabbit citrate blood plasma and purified using chromatography on DEAE-Sephadex A-50 and CM-Sephadex C-50.	deae-sephadex a	139-154	kininogen 1	Homo sapiens	50-54
1027487-1	1976	A preparation of high-molecular weight kininogen (HMWK) was isolated from rabbit citrate blood plasma and purified using chromatography on DEAE-Sephadex A-50 and CM-Sephadex C-50.	sephadex c	165-175	kininogen 1	Homo sapiens	50-54
1027487-2	1976	From 1 mg HMWK, trypsin or kallikreine of human blood plasma release 10 mkg bradykinine.	Bradykinin	76-87	kininogen 1	Homo sapiens	10-14
1027487-3	1976	The HMWK preparation is homogeneous during electrophoresis in 7.5% polyacrylamide gel in tris-glycine buffer, pH 8.3; its electrophoretic mobility corresponds to that of alpha2-globulins.	polyacrylamide	67-81	kininogen 1	Homo sapiens	4-8
1027487-3	1976	The HMWK preparation is homogeneous during electrophoresis in 7.5% polyacrylamide gel in tris-glycine buffer, pH 8.3; its electrophoretic mobility corresponds to that of alpha2-globulins.	glycyl-glycyl-glycine	89-101	kininogen 1	Homo sapiens	4-8
1027487-4	1976	The molecular weight of HMWK estimated using the collumn with Sephadex G-200, is 130.000--150.000; the sedimentation constant S20w is 7.6.	sephadex	62-76	kininogen 1	Homo sapiens	24-28
1027487-6	1976	0.05 M 2-mercaptoethanol and 8 M urea induce HMWK splitting into 2 fragments with respective molecular weights of 80.000 and 30.000, the kinine-containing group being localized in the low-molecular weight fragment.	Mercaptoethanol	7-24	kininogen 1	Homo sapiens	45-49
1027487-6	1976	0.05 M 2-mercaptoethanol and 8 M urea induce HMWK splitting into 2 fragments with respective molecular weights of 80.000 and 30.000, the kinine-containing group being localized in the low-molecular weight fragment.	Urea	33-37	kininogen 1	Homo sapiens	45-49
6719-4	1976	The effects of bradykinin, A I and A II have been shown to be inhibited by aspirin but not by propranolol, metiamide, SC 19220 or a specific, competitive antagonist of A II.	Aspirin	75-82	kininogen 1	Homo sapiens	15-25
3198-2	1976	N-acetyl-L-phenylalaninamide, support our previous conclusion (Biochemistry 12, 3780, 1973) that the positive 221-nm CD band of bradykinin is a composite of bands due to two chromophores, the 217-nm band characteristic of the Phe residues overlying the 223-nm band of the N-terminal sequence, Arg-Pro-Pro.	N-acetyl-L-phenylalanine amide	0-28	kininogen 1	Homo sapiens	128-138
3198-2	1976	N-acetyl-L-phenylalaninamide, support our previous conclusion (Biochemistry 12, 3780, 1973) that the positive 221-nm CD band of bradykinin is a composite of bands due to two chromophores, the 217-nm band characteristic of the Phe residues overlying the 223-nm band of the N-terminal sequence, Arg-Pro-Pro.	Phenylalanine	226-229	kininogen 1	Homo sapiens	128-138
3198-2	1976	N-acetyl-L-phenylalaninamide, support our previous conclusion (Biochemistry 12, 3780, 1973) that the positive 221-nm CD band of bradykinin is a composite of bands due to two chromophores, the 217-nm band characteristic of the Phe residues overlying the 223-nm band of the N-terminal sequence, Arg-Pro-Pro.	Arginine	293-296	kininogen 1	Homo sapiens	128-138
3198-2	1976	N-acetyl-L-phenylalaninamide, support our previous conclusion (Biochemistry 12, 3780, 1973) that the positive 221-nm CD band of bradykinin is a composite of bands due to two chromophores, the 217-nm band characteristic of the Phe residues overlying the 223-nm band of the N-terminal sequence, Arg-Pro-Pro.	Proline	297-300	kininogen 1	Homo sapiens	128-138
3198-2	1976	N-acetyl-L-phenylalaninamide, support our previous conclusion (Biochemistry 12, 3780, 1973) that the positive 221-nm CD band of bradykinin is a composite of bands due to two chromophores, the 217-nm band characteristic of the Phe residues overlying the 223-nm band of the N-terminal sequence, Arg-Pro-Pro.	Proline	301-304	kininogen 1	Homo sapiens	128-138
1244922-0	1976	Evidence that Fitzgerald factor counteracts inhibition by kaolin or ellagic acid of the amidolytic properties of a plasma kallikrein.	Ellagic Acid	68-80	kininogen 1	Homo sapiens	14-31
1244922-5	1976	Addition of preparations of Fitzgerald factor to kaolin or to solutions of ellagic acid counteracted their inhibitory properties.	Ellagic Acid	75-87	kininogen 1	Homo sapiens	28-45
197839-3	1977	The cyclic AMP response to BK is enhanced by a heat stable factor(s) in fetal calf serum (FCS) and by the addition of arachidonic acid (AA) to monolayer cultures incubated in serum-free media.	Cyclic AMP	4-14	kininogen 1	Homo sapiens	27-29
197839-3	1977	The cyclic AMP response to BK is enhanced by a heat stable factor(s) in fetal calf serum (FCS) and by the addition of arachidonic acid (AA) to monolayer cultures incubated in serum-free media.	Arachidonic Acid	118-134	kininogen 1	Homo sapiens	27-29
197839-5	1977	These BK refractory cells do respond with significant increment in cyclic AMP to challenge with prostaglandin E1 (PGE1).	Cyclic AMP	67-77	kininogen 1	Homo sapiens	6-8
937136-0	1976	Cardiovascular and respiratory reflexes elicited by bradykinin acting on receptor sites (K &amp; P) in the muscular circulatory area.	k &amp	89-95	kininogen 1	Homo sapiens	52-62
197839-5	1977	These BK refractory cells do respond with significant increment in cyclic AMP to challenge with prostaglandin E1 (PGE1).	Alprostadil	96-112	kininogen 1	Homo sapiens	6-8
197839-5	1977	These BK refractory cells do respond with significant increment in cyclic AMP to challenge with prostaglandin E1 (PGE1).	Alprostadil	114-118	kininogen 1	Homo sapiens	6-8
197839-6	1977	Cells that have become refractory to PGE1 stimulation respond to BK.	Alprostadil	37-41	kininogen 1	Homo sapiens	65-67
197839-7	1977	this suggests that a receptor or activator system different from the one for PGE1 and PGE2 exists for BK.	Dinoprostone	86-90	kininogen 1	Homo sapiens	102-104
197839-8	1977	When both BK and PGE1 are incubated together with synovial fibroblasts, the cyclic AMP response elicited is more than additive as compared to the response of each hormone separately.	Cyclic AMP	76-86	kininogen 1	Homo sapiens	10-12
197839-9	1977	Indomethacin (IM) inhibits the BK evoked cyclic AMP response unless cell cultures are pretreated with PGE1.	Indomethacin	0-12	kininogen 1	Homo sapiens	31-33
999466-3	1976	The influence of bradykinin and kallikrein on the action of norepinephrine, epinephrine, isoprenaline, phentolamine, propranolol, aminophylline and theophylline on blood pressure was studied.	Norepinephrine	60-74	kininogen 1	Homo sapiens	17-27
790919-9	1976	Bradykinin stimulates phospholipase A2, thereby making available prostaglandin precursors.	Prostaglandins	65-78	kininogen 1	Homo sapiens	0-10
939322-0	1976	[Use of oximinoiminopyrrazoline esters in the synthesis of solids phase peptides: synthesis of bradykinin].	oximinoiminopyrrazoline esters	8-38	kininogen 1	Homo sapiens	95-105
172888-2	1975	Agonist that cause contraction (bradykinin, histamine, and serotonin) cause accumulation of guanosine 3":5"-monophosphate (cGMP) without altering adenosine 3":5"-monophosphate (cAMP).	Cyclic GMP	92-121	kininogen 1	Homo sapiens	32-42
1203628-6	1975	5 Dexamethasone reduced the activity of bradykinin but not that of 5-hydroxytryptamine or acetylcholine.	Dexamethasone	2-15	kininogen 1	Homo sapiens	40-50
172070-1	1975	[[125I]Tyr8]Bradykinin is degraded by angiotensin-converting enzyme to [125I]Tyr-Arg.	Iodine-125	1-7	kininogen 1	Homo sapiens	12-22
48505-2	1975	The peptides, derived from human or porcine complement proteins C3 and C5, were less potent than 48/80 but more potent than bradykinin in stimulating release of histamine from mast cells.	Histamine	161-170	kininogen 1	Homo sapiens	124-134
172888-2	1975	Agonist that cause contraction (bradykinin, histamine, and serotonin) cause accumulation of guanosine 3":5"-monophosphate (cGMP) without altering adenosine 3":5"-monophosphate (cAMP).	Cyclic GMP	123-127	kininogen 1	Homo sapiens	32-42
172888-2	1975	Agonist that cause contraction (bradykinin, histamine, and serotonin) cause accumulation of guanosine 3":5"-monophosphate (cGMP) without altering adenosine 3":5"-monophosphate (cAMP).	adenosine 3"	146-158	kininogen 1	Homo sapiens	32-42
172888-2	1975	Agonist that cause contraction (bradykinin, histamine, and serotonin) cause accumulation of guanosine 3":5"-monophosphate (cGMP) without altering adenosine 3":5"-monophosphate (cAMP).	5"-monophosphate	105-121	kininogen 1	Homo sapiens	32-42
172888-2	1975	Agonist that cause contraction (bradykinin, histamine, and serotonin) cause accumulation of guanosine 3":5"-monophosphate (cGMP) without altering adenosine 3":5"-monophosphate (cAMP).	Cyclic AMP	177-181	kininogen 1	Homo sapiens	32-42
172888-6	1975	O2 was required for demonstration of the Ca++-dependent accumulation of cGMP in response to bradykinin, histamine, and ionophore A23187.	Oxygen	0-2	kininogen 1	Homo sapiens	92-102
172888-6	1975	O2 was required for demonstration of the Ca++-dependent accumulation of cGMP in response to bradykinin, histamine, and ionophore A23187.	Cyclic GMP	72-76	kininogen 1	Homo sapiens	92-102
172888-7	1975	The effect of the phosphodiesterase inhibitor 3-isobutyl-1-methyl xanthine on basal cGMP content and on the bradykinin-induced accumulation was also dependent on the presence of O2.	1-Methyl-3-isobutylxanthine	46-74	kininogen 1	Homo sapiens	108-118
172888-7	1975	The effect of the phosphodiesterase inhibitor 3-isobutyl-1-methyl xanthine on basal cGMP content and on the bradykinin-induced accumulation was also dependent on the presence of O2.	Cyclic GMP	84-88	kininogen 1	Homo sapiens	108-118
172888-7	1975	The effect of the phosphodiesterase inhibitor 3-isobutyl-1-methyl xanthine on basal cGMP content and on the bradykinin-induced accumulation was also dependent on the presence of O2.	Oxygen	178-180	kininogen 1	Homo sapiens	108-118
1122682-7	1975	It is suggested that the late response is similar to that observed in reactive hyperemia and following injection of bradykinin and, therefore, may be related to local release of vasoactive substances by glucagon.	Glucagon	203-211	kininogen 1	Homo sapiens	116-126
235559-6	1975	In subjects receiving saline, plasma bradykinin fell from 3.9 plus or minus 1.5 (SEM) ng/ml at 0 min to 0.93 plus or minus 0.2 at 30 min and 0.95 plus or minus 0.3 at 120 min.	Sodium Chloride	22-28	kininogen 1	Homo sapiens	37-47
235566-5	1975	(b) Bradykinin, histamine, serotonin, acetylcholine, and K+ ion, which cause umbilical artery constriction, can increase the cGMP content of the artery segments within 30 s of exposure without altering the cAMP content.	Cyclic GMP	125-129	kininogen 1	Homo sapiens	4-14
235559-18	1975	Thus, in sodium-depleted individuals, saline infusion produces a rapid fall of plasma bradykinin at a rate similar to that observed for a II and PRA.	Sodium	9-15	kininogen 1	Homo sapiens	86-96
235559-18	1975	Thus, in sodium-depleted individuals, saline infusion produces a rapid fall of plasma bradykinin at a rate similar to that observed for a II and PRA.	Sodium Chloride	38-44	kininogen 1	Homo sapiens	86-96
235559-19	1975	Conversely, in sodium-loaded individuals, assumption of upright posture leads to a parallel rise in A II, TPRA, and bradykinin.	Sodium	15-21	kininogen 1	Homo sapiens	116-126
235559-20	1975	These studies indicate that there is a close correlation of bradykinin levels with renin activity and angiotensin II, in both acute sodium loading and assumption of upright posture, suggesting that these two systems may be physiologically interrelated.	Sodium	132-138	kininogen 1	Homo sapiens	60-70
1092549-5	1975	The modifications induced by bradykinin administration were suppressed by Ketamin and Thiopental.	Ketamine	74-81	kininogen 1	Homo sapiens	29-39
1092549-5	1975	The modifications induced by bradykinin administration were suppressed by Ketamin and Thiopental.	Thiopental	86-96	kininogen 1	Homo sapiens	29-39
4421042-0	1974	Cortical synchronization evoked by noxious bradykinin stimulation under barbiturate anesthesia.	barbituric acid	72-83	kininogen 1	Homo sapiens	43-53
1184280-3	1975	Two tripeptides and one dipeptide, protected except at the carboxyl ends, have been prepared in solution and used as intermediates in a new synthesis of bradykinin on a solid support.	tripeptides	4-15	kininogen 1	Homo sapiens	153-163
1184280-3	1975	Two tripeptides and one dipeptide, protected except at the carboxyl ends, have been prepared in solution and used as intermediates in a new synthesis of bradykinin on a solid support.	Dipeptides	24-33	kininogen 1	Homo sapiens	153-163
4452211-0	1974	Syntheses of [Phe(4NO-2)5, Tyr(Me)8]- and [Tyr(Me)5, Phe(4NO-2)8]- bradykinin.	4no-2)8	57-64	kininogen 1	Homo sapiens	67-77
4377109-1	1974	The hydrolysis of bradykinin and its higher homologues by angiotensin-converting enzyme has been investigated by using an automated ninhydrin technique.	Ninhydrin	132-141	kininogen 1	Homo sapiens	18-28
4441169-0	1974	Reversal of bradykinin action by a high molecular weight ethylene oxide polymer.	Ethylene Oxide	57-71	kininogen 1	Homo sapiens	12-22
4451769-0	1974	Proceedings: the concomitant release of bradykinin and prostaglandin in the inflammatory response to carrageenin.	Carrageenan	101-112	kininogen 1	Homo sapiens	40-50
4458701-0	1974	[Effects of acetylsalicylic acid on reflex cardiocirculatory and respiratory responses induced by injection of bradykinin into the femoral artery].	Aspirin	12-32	kininogen 1	Homo sapiens	111-121
4604234-0	1974	Clinical trial of a new anti-bradykinin, anti-inflammatory drug, ketoprofen (19.583 r.p.)	Ketoprofen	65-75	kininogen 1	Homo sapiens	29-39
4830258-0	1974	Hydroxyproline analogs of bradykinin.	Hydroxyproline	0-14	kininogen 1	Homo sapiens	26-36
4797302-0	1973	Histamine, norepinephrine, and bradykinin stimulation of fibroblast growth and modification of serotonin response.	Serotonin	95-104	kininogen 1	Homo sapiens	31-41
4211479-0	1974	[Interaction of a biological preparation (Lysocorticone) against serotonin in vivo and against serotonin, bradykinin and prostaglandin in vitro].	lysocorticone	42-55	kininogen 1	Homo sapiens	106-116
4283109-0	1974	[Arachidonic acid release by bradykinin].	Arachidonic Acid	1-17	kininogen 1	Homo sapiens	29-39
4128894-0	1973	Bradykinin inactivation by rabbit serum and butylated hydroxyanisole.	Butylated Hydroxyanisole	44-68	kininogen 1	Homo sapiens	0-10
4362593-7	1973	Under similar experimental conditions the vasodilator, bradykinin, 0.001-1 mug/kg, and procedures which produce a local increase in nutritive capillary blood flow also enhanced acetylcholine-evoked contractile responses of the anterior tibialis, whereas the vasoconstrictor, angiotensin, 0.001-1 mug/kg, inhibited them.5.	Acetylcholine	177-190	kininogen 1	Homo sapiens	55-65
4745509-0	1973	Synthesis of bradykinin via oximinopyrazoline active esters (OPmp).	oximinopyrazoline active esters	28-59	kininogen 1	Homo sapiens	13-23
4148513-0	1973	Letter: Prostaglandins as regulators of bradykinin responses.	Prostaglandins	8-22	kininogen 1	Homo sapiens	40-50
4745509-0	1973	Synthesis of bradykinin via oximinopyrazoline active esters (OPmp).	opmp	61-65	kininogen 1	Homo sapiens	13-23
4355709-0	1973	[The antagonism exercised by Sandomigran (BC 105) on some properties of bradykinin].	Pizotyline	29-40	kininogen 1	Homo sapiens	72-82
4752265-0	1973	[Effect of aspirin on the response to the intradermal injection of bradykinin].	Aspirin	11-18	kininogen 1	Homo sapiens	67-77
4655267-10	1972	Gallamine only slightly reduced the effect of bradykinin.4.	Gallamine Triethiodide	0-9	kininogen 1	Homo sapiens	46-56
4766561-0	1973	The effect of pyridinolcarbamate on the vasodilator action of bradykinin in the human forearm.	Pyridinolcarbamate	14-32	kininogen 1	Homo sapiens	62-72
4786554-0	1973	[Effects of general anesthesia and morphine analgesia on the reflex cardiocirculatory and respiratory responses to injection of bradykinin into the common carotid and femoral arteries].	Morphine	35-43	kininogen 1	Homo sapiens	128-138
1247511-0	1976	Vespulakinins: new carbohydrate-containing bradykinin derivatives.	Carbohydrates	19-31	kininogen 1	Homo sapiens	43-53
4655267-16	1972	On the other hand, the effect of ACh was depressed when given immediately after a big dose of bradykinin (10-15 mug).7.	Acetylcholine	33-36	kininogen 1	Homo sapiens	94-104
4337940-0	1972	Potentiation of the bradykinin response by cysteine: mechanism of action.	Cysteine	43-51	kininogen 1	Homo sapiens	20-30
4656611-4	1972	Bradykinin-insensitive vein and aortic strips responded with substantial increases in contractile tension when exposed to prostaglandin E(2), noradrenaline, histamine and KC1.	Dinoprostone	122-140	kininogen 1	Homo sapiens	0-10
4656611-4	1972	Bradykinin-insensitive vein and aortic strips responded with substantial increases in contractile tension when exposed to prostaglandin E(2), noradrenaline, histamine and KC1.	Norepinephrine	142-155	kininogen 1	Homo sapiens	0-10
4656611-4	1972	Bradykinin-insensitive vein and aortic strips responded with substantial increases in contractile tension when exposed to prostaglandin E(2), noradrenaline, histamine and KC1.	Histamine	157-166	kininogen 1	Homo sapiens	0-10
4656611-4	1972	Bradykinin-insensitive vein and aortic strips responded with substantial increases in contractile tension when exposed to prostaglandin E(2), noradrenaline, histamine and KC1.	kc1	171-174	kininogen 1	Homo sapiens	0-10
4656611-5	1972	However, bradykinin (0.1,mug/ml) was, capable of relaxing human vein strips, which had contracted in response to prostaglandin E(2).	Prostaglandins E	113-128	kininogen 1	Homo sapiens	9-19
5036570-0	1972	The relationship of the renal vasodilator action of bradykinin to the release of a prostaglandin E-like substance.	Prostaglandins E	83-98	kininogen 1	Homo sapiens	52-62
5046102-2	1972	Norepinephrine release by bradykinin.	Norepinephrine	0-14	kininogen 1	Homo sapiens	26-36
4338183-0	1972	Inhibition of pressor effects of angiotensin I and augmentation of depressor effects of bradykinin by synthetic peptides.	Peptides	112-120	kininogen 1	Homo sapiens	88-98
5029445-0	1972	[Sensitization of posterior root fibers to the stimulating action of potassium ions caused by bradykinin and acetylcholine].	Potassium	69-78	kininogen 1	Homo sapiens	94-104
4672445-2	1972	The synthesis of analogues of bradykinin by the picolyl ester method.	picolyl ester	48-61	kininogen 1	Homo sapiens	30-40
4331917-2	1972	Synthesis and properties of p-(N,N-)-bis(2-chloroethyl)amino)phenylbutyryl derivatives of bradykinin and bradykinin potentiating factor.	p-(n,n-)-bis(2-chloroethyl)amino)phenylbutyryl	28-74	kininogen 1	Homo sapiens	90-100
4331917-2	1972	Synthesis and properties of p-(N,N-)-bis(2-chloroethyl)amino)phenylbutyryl derivatives of bradykinin and bradykinin potentiating factor.	p-(n,n-)-bis(2-chloroethyl)amino)phenylbutyryl	28-74	kininogen 1	Homo sapiens	105-115
5277513-0	1970	[Effects of ethylcysteine on bradykininase and on bradykinin action].	ethyl cysteine	12-25	kininogen 1	Homo sapiens	29-39
5131849-0	1971	A prostaglandin may mediate the renal vasodilator action of bradykinin.	Prostaglandins	2-15	kininogen 1	Homo sapiens	60-70
5140004-0	1971	Analogs of bradykinin containing  -2-thienyl-L-alanine.	2-thienyl-l-alanine	35-54	kininogen 1	Homo sapiens	11-21
4355304-0	1971	Bradykinin potentiating peptide PCA-Lys-Trp-Ala-Pro.	Lysine	36-39	kininogen 1	Homo sapiens	0-10
4355304-0	1971	Bradykinin potentiating peptide PCA-Lys-Trp-Ala-Pro.	Tryptophan	40-43	kininogen 1	Homo sapiens	0-10
4355304-0	1971	Bradykinin potentiating peptide PCA-Lys-Trp-Ala-Pro.	alanylproline	44-51	kininogen 1	Homo sapiens	0-10
5117532-0	1971	The substrate recognition site of collagen proline hydroxylase: the hydroxylation of -X-Pro-Gly- sequences in bradykinin analogs and other peptides.	Glycine	92-95	kininogen 1	Homo sapiens	110-120
5542742-0	1971	[Anti-bradykinin activity of Lysoartrosi].	lysoartrosi	29-40	kininogen 1	Homo sapiens	6-16
33639628-2	2021	The underlying mechanism in HAE is related to bradykinin dysregulation which causes these attacks not to respond to common treatment strategies including epinephrine/corticosteroid or adrenaline.	Epinephrine	154-165	kininogen 1	Homo sapiens	46-56
4317724-0	1970	[Release of catecholamines from the adrenal gland by bradykinin].	Catecholamines	12-26	kininogen 1	Homo sapiens	53-63
4392995-0	1970	Action of rare earth metal complexes on neurogenic as well as on bradykinin-induced inflammation.	Metals	21-26	kininogen 1	Homo sapiens	65-75
5417050-0	1970	Bradykinin inhibition by butylated hydroxyanisole.	Butylated Hydroxyanisole	25-49	kininogen 1	Homo sapiens	0-10
5417050-1	1970	Concentrations of butylated hydroxyanisole as low as 8 x 10(-9) mole per liter can inhibit detectably the contraction of smooth muscle elicited by bradykinin.	Butylated Hydroxyanisole	18-42	kininogen 1	Homo sapiens	147-157
4314857-0	1970	Cyclic AMP mediation of bradykinin-induced stimulation of mitotic activity and DNA synthesis in thymocytes.	Cyclic AMP	0-10	kininogen 1	Homo sapiens	24-34
5527210-0	1970	Bradykinin induced release of serotonin in man.	Serotonin	30-39	kininogen 1	Homo sapiens	0-10
5366278-8	1969	Production by the tumour of serotonin or other derivatives of tryptophan or of kallikrein, which activates bradykinin, is rare.	Serotonin	28-37	kininogen 1	Homo sapiens	107-117
5822045-0	1969	Substrate specificity of collagen proline hydroxylase: hydroxylation of a specific proline residue in bradykinin.	Proline	34-41	kininogen 1	Homo sapiens	102-112
5823240-0	1969	[Inactivation of bradykinin by cortisone-released protease preparation].	Cortisone	31-40	kininogen 1	Homo sapiens	17-27
5784642-0	1969	Effect of acetylsalicylic acid and morphine on pressor responses produced by bradykinin.	Aspirin	10-30	kininogen 1	Homo sapiens	77-87
5784642-0	1969	Effect of acetylsalicylic acid and morphine on pressor responses produced by bradykinin.	Morphine	35-43	kininogen 1	Homo sapiens	77-87
5780001-0	1969	The mitogenic action of bradykinin on thymic lymphocytes and its dependence on calcium.	Calcium	79-86	kininogen 1	Homo sapiens	24-34
5766195-0	1969	Radioimmunoassay of bradykinin: chemical modification to enable use of radioactive iodine.	radioactive iodine	71-89	kininogen 1	Homo sapiens	20-30
4388191-0	1969	Bradykinin antagonism by dimethothiazine.	fonazine	25-40	kininogen 1	Homo sapiens	0-10
5375730-0	1969	Release of serotonin during bradykinin infusion.	Serotonin	11-20	kininogen 1	Homo sapiens	28-38
4175672-0	1968	[Study of the characterization of bradykinin as a histamine liberator].	Histamine	50-59	kininogen 1	Homo sapiens	34-44
4385509-1	1968	Interaction between oxygen and bradykinin.	Oxygen	20-26	kininogen 1	Homo sapiens	31-41
5690111-1	1968	Bradykinin is a potent constrictor of the human umbilical artery and vein and the ductus arteriosus of the lamb in vitro at oxygen tensions above 40 mm Hg (comparable to those in the newborn infant).	Oxygen	124-130	kininogen 1	Homo sapiens	0-10
4386532-0	1968	N-(3-benzythio-2,6-dichlorophenyl)anthramyl acid (ASD 30): a non-competitive antagonist of bradykinin.	n-(3-benzythio-2,6-dichlorophenyl)anthramyl acid	0-48	kininogen 1	Homo sapiens	91-101
4295887-0	1968	Inflammatory changes in newly formed vessels of carrageenin-induced granulomas after systemic 5-hydroxytryptamine, bradykinin, kallikrein, or lysolecithin.	Carrageenan	48-59	kininogen 1	Homo sapiens	115-125
5735039-0	1968	[Role of bradykinin in the alcohol medication vasomotor reaction].	Alcohols	27-34	kininogen 1	Homo sapiens	9-19
5583800-0	1967	Synthesis of 4-L-valine-6-L-threonine-, 4-L-isoleucine-6-L-threonine-, 4-L-leucine-6-L-threonine-, 4-L-valine-, and 4-L-isoleucine-bradykinin and their O-acetyl compounds.	4-l-valine-6-l-threonine	13-37	kininogen 1	Homo sapiens	131-141
5583800-0	1967	Synthesis of 4-L-valine-6-L-threonine-, 4-L-isoleucine-6-L-threonine-, 4-L-leucine-6-L-threonine-, 4-L-valine-, and 4-L-isoleucine-bradykinin and their O-acetyl compounds.	4-l-leucine-6-l-threonine	71-96	kininogen 1	Homo sapiens	131-141
5583800-0	1967	Synthesis of 4-L-valine-6-L-threonine-, 4-L-isoleucine-6-L-threonine-, 4-L-leucine-6-L-threonine-, 4-L-valine-, and 4-L-isoleucine-bradykinin and their O-acetyl compounds.	4-l-valine	13-23	kininogen 1	Homo sapiens	131-141
5633534-0	1967	[Blocking effect of atropine on fibrinolysis induced by acetylcholine and bradykinin].	Atropine	20-28	kininogen 1	Homo sapiens	74-84
5235628-0	1967	[Effects of tranexamic acid on bradykinin action].	Tranexamic Acid	12-27	kininogen 1	Homo sapiens	31-41
6073550-0	1967	Synthesis of 3-L-lysine-bradykinin and its O-acetyl compound.	3-l-lysine	13-23	kininogen 1	Homo sapiens	24-34
5610046-0	1967	[Increase in the sensitivity of afferent fibers to the stimulating action of potassium ions induced by bradykinin.	Potassium	77-86	kininogen 1	Homo sapiens	103-113
6040967-0	1967	Syntheses of bradykinin analogs containing sarcosine residues and their biological activities.	Sarcosine	43-52	kininogen 1	Homo sapiens	13-23
4291730-4	1967	Acetylcholine depolarized the chromaffin cells and so did various other substances known to evoke catecholamine secretion: nicotine, pilocarpine, histamine, 5-hydroxytryptamine, angiotensin, and bradykinin.3.	Acetylcholine	0-13	kininogen 1	Homo sapiens	195-205
6064255-0	1967	[Treatment of experimental and human athero- sclerosis by a bradykinin antagonist, pyridinol carbamate.	Pyridinolcarbamate	83-102	kininogen 1	Homo sapiens	60-70
5967019-0	1966	Sulphuric esters of polysaccharides as activators of a bradykinin-forming system in plasma.	sulphuric esters	0-16	kininogen 1	Homo sapiens	55-65
5967019-0	1966	Sulphuric esters of polysaccharides as activators of a bradykinin-forming system in plasma.	Polysaccharides	20-35	kininogen 1	Homo sapiens	55-65
5298721-0	1966	Tranexamic acid enhances bradykinin--induced venoconstriction.	Tranexamic Acid	0-15	kininogen 1	Homo sapiens	25-35
4382078-0	1966	Methixene: a non-competitive antagonist of bradykinin.	methixene	0-9	kininogen 1	Homo sapiens	43-53
5976508-0	1966	Synthesis of beta-alanine-containing analogs of bradykinin.	beta-Alanine	13-25	kininogen 1	Homo sapiens	48-58
5964088-0	1966	Synthesis of phyllokinin, a natural bradykinin analogue.	Phyllokinin	13-24	kininogen 1	Homo sapiens	36-46
5905444-0	1966	Pyridinolcarbamate, a bradykinin antagonist in veins.	Pyridinolcarbamate	0-18	kininogen 1	Homo sapiens	22-32
5904790-0	1966	[Synthesis of bradykinin analogs with D-amino acids (all-D-bradykinin and all-D-retro-bradykinin)].	d-amino acids	38-51	kininogen 1	Homo sapiens	14-24
5904790-0	1966	[Synthesis of bradykinin analogs with D-amino acids (all-D-bradykinin and all-D-retro-bradykinin)].	d-amino acids	38-51	kininogen 1	Homo sapiens	59-69
5904790-0	1966	[Synthesis of bradykinin analogs with D-amino acids (all-D-bradykinin and all-D-retro-bradykinin)].	d-amino acids	38-51	kininogen 1	Homo sapiens	59-69
5938558-0	1966	Effects of bradykinin on the movement of water and sodium in some isolated living membranes.	Water	41-46	kininogen 1	Homo sapiens	11-21
5938558-0	1966	Effects of bradykinin on the movement of water and sodium in some isolated living membranes.	Sodium	51-57	kininogen 1	Homo sapiens	11-21
6004860-0	1966	Fenamates as antagonists of bronchoconstriction and nociception induced by bradykinin and other substances.	Fenamates	0-9	kininogen 1	Homo sapiens	75-85
5909493-0	1966	The effect of aspirin on pain and hand blood flow responses to intra-arterial injection of bradykinin in man.	Aspirin	14-21	kininogen 1	Homo sapiens	91-101
5866720-0	1965	Potentiation of some bradykinin effects by thiol compounds.	Sulfhydryl Compounds	43-48	kininogen 1	Homo sapiens	21-31
5858825-0	1965	The antagonism of chloroform-epinephrine induced cardiac arrhythmia by bradykinin and 6-glycine bradykinin.	chloroform-epinephrine	18-40	kininogen 1	Homo sapiens	71-81
5858825-0	1965	The antagonism of chloroform-epinephrine induced cardiac arrhythmia by bradykinin and 6-glycine bradykinin.	chloroform-epinephrine	18-40	kininogen 1	Homo sapiens	96-106
5841424-1	1965	Relations to seroagglutination of latex-bradykinin, latex-serotonin, latex-acetylcholine and latex-heparin complexes].	Latex	34-39	kininogen 1	Homo sapiens	40-50
5835405-0	1965	Inactivation of bradykinin in urea solutions.	Urea	30-34	kininogen 1	Homo sapiens	16-26
14341617-0	1964	THE ANTAGONISTIC EFFECT OF NORAMIDOPYRINE METHANESULFONATE ON SOME PHARMACOLOGICAL ACTIONS OF THE SYNTHETIC BRADYKININ.	Dipyrone	27-58	kininogen 1	Homo sapiens	108-118
14193641-0	1964	THREONINE ANALOGS OF BRADYKININ DESIGNED AS ANTIMETABOLITES.	Threonine	0-9	kininogen 1	Homo sapiens	21-31
14170148-1	1964	RELEASE OF ADRENALINE BY BRADYKININ AND ANGIOTENSIN.	Epinephrine	11-21	kininogen 1	Homo sapiens	25-35
14190467-0	1964	THE PRESERVATION OF BRADYKININ BY PHENOTHIAZINES IN VITRO.	Phenothiazines	34-48	kininogen 1	Homo sapiens	20-30
14190467-1	1964	Chlorpromazine and phenoxybenzamine have been shown to potentiate the actions of bradykinin in vivo.	Chlorpromazine	0-14	kininogen 1	Homo sapiens	81-91
14190467-1	1964	Chlorpromazine and phenoxybenzamine have been shown to potentiate the actions of bradykinin in vivo.	Phenoxybenzamine	19-35	kininogen 1	Homo sapiens	81-91
14096072-0	1963	ACTION OF PROSTAGLANDIN E1 ON TISSUES WHICH RESPOND TO BRADYKININ.	Alprostadil	10-26	kininogen 1	Homo sapiens	55-65
14062112-0	1963	[LACK OF EFFECTIVENESS OF ANTIPHLOGISTICS (DEXAMETHASONE AND ISOPYRIN) ON THE PERMEABILITY-INCREASING ACTION OF BRADYKININ].	Dexamethasone	43-56	kininogen 1	Homo sapiens	112-122
14062112-0	1963	[LACK OF EFFECTIVENESS OF ANTIPHLOGISTICS (DEXAMETHASONE AND ISOPYRIN) ON THE PERMEABILITY-INCREASING ACTION OF BRADYKININ].	isopyrin	61-69	kininogen 1	Homo sapiens	112-122
13944892-0	1962	Potentiation of bradykinin by dimercaptopropanol (bal) and other inhibitors of its destroying enzyme in plasma.	Dimercaprol	30-48	kininogen 1	Homo sapiens	16-26
13944892-0	1962	Potentiation of bradykinin by dimercaptopropanol (bal) and other inhibitors of its destroying enzyme in plasma.	Dimercaprol	50-53	kininogen 1	Homo sapiens	16-26
14486338-0	1962	Potentiation of bradykinin action on smooth-muscle by cysteine.	Cysteine	54-62	kininogen 1	Homo sapiens	16-26
13753032-4	1960	An octapeptide with the following structure: H-L-Arg-L-Pro-Gly-L-Phe-L-Ser-L-Pro-L-Phe-L-Arg-OH also exerted bradykinin-like effects but was 50 to 100 times less active than the nonapeptide.	Arg-pro-gly-phe-ser-pro-phe-arg	45-95	kininogen 1	Homo sapiens	109-119
14426973-0	1960	Synthesis and biological properties of L-arginyl-Lprolyl-glycyl-L-phenylalanyl-L-seryl-L-phenylalanyl-L-arginine, an octapeptide related to bradykinin.	l-arginyl-lprolyl-glycyl-l-phenylalanyl-l-seryl-l-phenylalanyl-l-arginine	39-112	kininogen 1	Homo sapiens	140-150
14438050-0	1960	Potentiation of duration of the vasodilator effect of bradykinin by sympatholytic drugs and by reserpine.	Reserpine	95-104	kininogen 1	Homo sapiens	54-64
13660879-0	1959	[Effect of tetraethylammonium on isolated contractions of the isolated muscles induced by bradykinin].	Tetraethylammonium	11-29	kininogen 1	Homo sapiens	90-100
13629568-0	1958	[Effect of tetraethylammonium bromide on contractions induced by bradykinin].	Tetraethylammonium	11-37	kininogen 1	Homo sapiens	65-75
34007408-5	2021	And the direct effects of bradykinin on prostate cells were detected by MTT experiment.	monooxyethylene trimethylolpropane tristearate	72-75	kininogen 1	Homo sapiens	26-36
33907665-0	2021	Indomethacin: Can It Counteract Bradykinin Effects in COVID-19 Patients?	Indomethacin	0-12	kininogen 1	Homo sapiens	32-42
33907665-11	2021	The choice of indomethacin was based on its ability to suppress the cyclooxygenase enzyme while also lowering the level of the inflammatory mediator bradykinin.	Indomethacin	14-26	kininogen 1	Homo sapiens	149-159
33918267-0	2021	Hypersensitivity Induced by Intrathecal Bradykinin Administration Is Enhanced by N-oleoyldopamine (OLDA) and Prevented by TRPV1 Antagonist.	N-oleoyldopamine	81-97	kininogen 1	Homo sapiens	40-50
33918267-0	2021	Hypersensitivity Induced by Intrathecal Bradykinin Administration Is Enhanced by N-oleoyldopamine (OLDA) and Prevented by TRPV1 Antagonist.	N-oleoyldopamine	99-103	kininogen 1	Homo sapiens	40-50
33599029-11	2021	Proposed mechanisms include temporary stabilization of the negative-positive interactions of the dextran sulfate filter leading to a reduction of circulating bradykinin, reduction of nitric oxide, and reduction of the sympathetic response to LA.	Dextran Sulfate	97-112	kininogen 1	Homo sapiens	158-168
14821302-0	1951	Analysis of certain interactions of nicotine with bradykinin and histamine.	Nicotine	36-44	kininogen 1	Homo sapiens	50-60
33164754-1	2021	Tranexamic acid (TXA) is an antifibrinolytic agent which inhibits conversion of plasminogen to plasmin, a key step in kallikrein activation and bradykinin formation.	Tranexamic Acid	0-15	kininogen 1	Homo sapiens	144-154
33164754-1	2021	Tranexamic acid (TXA) is an antifibrinolytic agent which inhibits conversion of plasminogen to plasmin, a key step in kallikrein activation and bradykinin formation.	Tranexamic Acid	17-20	kininogen 1	Homo sapiens	144-154
33847403-9	2021	Anaphylactoid reaction, often with angioedema, occurred in 4/6 patients undergoing DSA and was attributed to bradykinin activation.	dsa	83-86	kininogen 1	Homo sapiens	109-119
33319474-4	2021	Blockers of the renin-angiotensin-aldosterone system, colesevelam, ranolazine and verapamil through slowing breakdown of bradykinin, vasodilation, increasing cholecystokinin levels, blocking sodium channels, and decreasing beta cell apoptosis may improve glycemic control and avoid the development of diabetes.	Aldosterone	34-45	kininogen 1	Homo sapiens	121-131
33319474-4	2021	Blockers of the renin-angiotensin-aldosterone system, colesevelam, ranolazine and verapamil through slowing breakdown of bradykinin, vasodilation, increasing cholecystokinin levels, blocking sodium channels, and decreasing beta cell apoptosis may improve glycemic control and avoid the development of diabetes.	Colesevelam Hydrochloride	54-65	kininogen 1	Homo sapiens	121-131
33319474-4	2021	Blockers of the renin-angiotensin-aldosterone system, colesevelam, ranolazine and verapamil through slowing breakdown of bradykinin, vasodilation, increasing cholecystokinin levels, blocking sodium channels, and decreasing beta cell apoptosis may improve glycemic control and avoid the development of diabetes.	Ranolazine	67-77	kininogen 1	Homo sapiens	121-131
33319474-4	2021	Blockers of the renin-angiotensin-aldosterone system, colesevelam, ranolazine and verapamil through slowing breakdown of bradykinin, vasodilation, increasing cholecystokinin levels, blocking sodium channels, and decreasing beta cell apoptosis may improve glycemic control and avoid the development of diabetes.	Verapamil	82-91	kininogen 1	Homo sapiens	121-131
33067882-1	2021	Angiotensin-1 converting enzyme (ACE) is a key enzyme in the renin-angiotensin-aldosterone and kinin systems where it cleaves angiotensin I and bradykinin peptides, respectively.	Aldosterone	79-90	kininogen 1	Homo sapiens	144-154
33645996-2	2021	This paper describes an application of attenuated total reflection Fourier transform infrared spectroscopy (ATR-FTIR) and surface-enhanced infrared spectroscopy (SEIRA) to characterize the selective adsorption of four peptides present in body fluids such as neuromedin B (NMB), bombesin (BN), neurotensin (NT), and bradykinin (BK), which are known as markers for various human carcinomas.	Peptides	218-226	kininogen 1	Homo sapiens	315-325
33645996-2	2021	This paper describes an application of attenuated total reflection Fourier transform infrared spectroscopy (ATR-FTIR) and surface-enhanced infrared spectroscopy (SEIRA) to characterize the selective adsorption of four peptides present in body fluids such as neuromedin B (NMB), bombesin (BN), neurotensin (NT), and bradykinin (BK), which are known as markers for various human carcinomas.	Peptides	218-226	kininogen 1	Homo sapiens	327-329
33639628-2	2021	The underlying mechanism in HAE is related to bradykinin dysregulation which causes these attacks not to respond to common treatment strategies including epinephrine/corticosteroid or adrenaline.	Epinephrine	184-194	kininogen 1	Homo sapiens	46-56
33542252-2	2021	Viral blockade of the angiotensin-converting enzyme 2 impedes degradation of the active kinin des-Arg(9)-bradykinin, which thus increasingly activates bradykinin receptors known to promote inflammation, cough, and edema-symptoms that are commonly observed in COVID-19.	des-arg	94-101	kininogen 1	Homo sapiens	105-115
33646555-2	2021	The inhibition of kallikrein by berotralstat decreases the production of bradykinin, which prevents the localised tissue oedema that occurs during attacks of HAE.	Berotralstat	32-44	kininogen 1	Homo sapiens	73-83
33599139-3	2021	Bradykinin is generated from high- and low-molecular-weight kininogen by the serine protease kallikrein-1.	Serine	77-83	kininogen 1	Homo sapiens	0-10
33238712-3	2020	The potential of ROS/RNS generated by two different plasma sources (kINPen and COST-Jet) to introduce post-translational modifications (PTMs) in the peptides angiotensin and bradykinin was explored.	Reactive Oxygen Species	17-20	kininogen 1	Homo sapiens	174-184
33052508-2	2021	In this study, a series of six-membered heterocycle-substituted (piperidine, morpholine, 1-methyl piperazine) bdk ligands and boron complexes were synthesized, and their luminescent properties were investigated.	piperidine	65-75	kininogen 1	Homo sapiens	110-113
33052508-2	2021	In this study, a series of six-membered heterocycle-substituted (piperidine, morpholine, 1-methyl piperazine) bdk ligands and boron complexes were synthesized, and their luminescent properties were investigated.	morpholine	77-87	kininogen 1	Homo sapiens	110-113
33052508-2	2021	In this study, a series of six-membered heterocycle-substituted (piperidine, morpholine, 1-methyl piperazine) bdk ligands and boron complexes were synthesized, and their luminescent properties were investigated.	1-methylpiperazine	89-108	kininogen 1	Homo sapiens	110-113
33052508-2	2021	In this study, a series of six-membered heterocycle-substituted (piperidine, morpholine, 1-methyl piperazine) bdk ligands and boron complexes were synthesized, and their luminescent properties were investigated.	Boron	126-131	kininogen 1	Homo sapiens	110-113
33052508-4	2021	In response to solubility changes in water/tetrahydrofuran mixtures, while the piperazine bdk ligand showed aggregation caused quenching, the piperidine and morpholine bdks displayed enhanced emission upon aggregation.	Water	37-42	kininogen 1	Homo sapiens	90-93
33052508-4	2021	In response to solubility changes in water/tetrahydrofuran mixtures, while the piperazine bdk ligand showed aggregation caused quenching, the piperidine and morpholine bdks displayed enhanced emission upon aggregation.	tetrahydrofuran	43-58	kininogen 1	Homo sapiens	90-93
33052508-4	2021	In response to solubility changes in water/tetrahydrofuran mixtures, while the piperazine bdk ligand showed aggregation caused quenching, the piperidine and morpholine bdks displayed enhanced emission upon aggregation.	Piperazine	79-89	kininogen 1	Homo sapiens	90-93
33052508-4	2021	In response to solubility changes in water/tetrahydrofuran mixtures, while the piperazine bdk ligand showed aggregation caused quenching, the piperidine and morpholine bdks displayed enhanced emission upon aggregation.	morpholine	157-167	kininogen 1	Homo sapiens	90-93
33489085-8	2020	Sacubitril/valsartan concomitantly blocks the renin-angiotensin system and inhibits neprilysin, a ubiquitous enzyme responsible for the breakdown of more than 50 vasoactive peptides, including the biologically active natriuretic peptides, bradykinin, angiotensin I and II, endothelin 1, glucagon, glucagon-like peptide-1, insulin-B chain, and others.	sacubitril and valsartan sodium hydrate drug combination	0-10	kininogen 1	Homo sapiens	239-249
33489085-8	2020	Sacubitril/valsartan concomitantly blocks the renin-angiotensin system and inhibits neprilysin, a ubiquitous enzyme responsible for the breakdown of more than 50 vasoactive peptides, including the biologically active natriuretic peptides, bradykinin, angiotensin I and II, endothelin 1, glucagon, glucagon-like peptide-1, insulin-B chain, and others.	Valsartan	11-20	kininogen 1	Homo sapiens	239-249
33276216-2	2021	Despite a very similar clinical presentation among subtypes, the differential diagnosis is limited by the difficulty to identify bradykinin-mediated PA and the lack of specific biomarkers.	Protactinium	149-151	kininogen 1	Homo sapiens	129-139
33383825-0	2020	Discovery of a Bradykinin B2 Partial Agonist Profile of Raloxifene in a Drug Repurposing Campaign.	Raloxifene Hydrochloride	56-66	kininogen 1	Homo sapiens	15-25
33383825-3	2020	In the scope of a drug repurposing campaign undertaken to identify bradykinin antagonists, raloxifene was identified as prospective compound in a virtual screening process.	Raloxifene Hydrochloride	91-101	kininogen 1	Homo sapiens	67-77
33383825-4	2020	The pharmacodynamics profile of raloxifene towards bradykinin receptors is reported in the present work, showing a weak selective partial agonist profile at the B2 receptor.	Raloxifene Hydrochloride	32-42	kininogen 1	Homo sapiens	51-61
33109319-2	2020	C1 inhibitor (C1-INH) is a serine protease inhibitor, which, under normal circumstances, is the regulator of critical enzymes that are active in the cascades that result in bradykinin generation.	Serine	27-33	kininogen 1	Homo sapiens	173-183
33109319-12	2020	The alterations in FXII and plasminogen (also a serine protease inhibited by C1-INH) like with classic HAE are the result of dysregulation of bradykinin generation.	Serine	48-54	kininogen 1	Homo sapiens	142-152
32337769-7	2020	Noscapine, a medication used for the treatment of cough, has been shown to inhibit bradykinin enhanced cough response in man.	Noscapine	0-9	kininogen 1	Homo sapiens	83-93
32220499-6	2020	This antidepressant effect seemed to be independent of the renin-angiotensin system, but dependent on the bradykinin (BK) system, since the decreased BK detected in the stressed mice could be reversed by captopril.	Captopril	204-213	kininogen 1	Homo sapiens	106-116
32938990-2	2020	We tested whether inhaled prostaglandin-E2 (PGE2) and bradykinin (BK) regulate TRPV-1 activity in vivo by changing cough response to capsaicin (CPS) and affecting heart rate variability (HRV), while also taking into account the influence of TRPV-1 polymorphisms (SNPs).	Capsaicin	133-142	kininogen 1	Homo sapiens	54-64
32938990-2	2020	We tested whether inhaled prostaglandin-E2 (PGE2) and bradykinin (BK) regulate TRPV-1 activity in vivo by changing cough response to capsaicin (CPS) and affecting heart rate variability (HRV), while also taking into account the influence of TRPV-1 polymorphisms (SNPs).	Capsaicin	133-142	kininogen 1	Homo sapiens	66-68
32938990-2	2020	We tested whether inhaled prostaglandin-E2 (PGE2) and bradykinin (BK) regulate TRPV-1 activity in vivo by changing cough response to capsaicin (CPS) and affecting heart rate variability (HRV), while also taking into account the influence of TRPV-1 polymorphisms (SNPs).	Capsaicin	144-147	kininogen 1	Homo sapiens	54-64
32938990-2	2020	We tested whether inhaled prostaglandin-E2 (PGE2) and bradykinin (BK) regulate TRPV-1 activity in vivo by changing cough response to capsaicin (CPS) and affecting heart rate variability (HRV), while also taking into account the influence of TRPV-1 polymorphisms (SNPs).	Capsaicin	144-147	kininogen 1	Homo sapiens	66-68
32908455-3	2020	Moreover, TXA has been approved as second-line prophylactic therapy for hereditary angioedema and further data have been published about a possible use of TXA as maintenance treatment for nonhistaminergic angioedema and treatment for episodes of bradykinin-mediated angioedema induced by ACE inhibitors.	Tranexamic Acid	155-158	kininogen 1	Homo sapiens	246-256
32984222-6	2020	Bradykinin and corticosteroids also induce ductal constriction by attenuating the sensitivity of the ductus to PGE2.	Dinoprostone	111-115	kininogen 1	Homo sapiens	0-10
32843685-9	2020	Moreover, penicillin not only directly activated contact system FXII-dependently, but also promoted bradykinin release in plasma incubated-human umbilical vein endothelial cells.	Penicillins	10-20	kininogen 1	Homo sapiens	100-110
32742410-11	2020	On the whole, the findings of the present study indicate that rivastigmine hydrogen tartrate used in combination with donepezil hydrochloride relieves the symptoms and improves the quality of life of patients with AD more effectively, which may be related to the reduction of the bradykinin level in these patients.	Rivastigmine	62-92	kininogen 1	Homo sapiens	280-290
32742410-11	2020	On the whole, the findings of the present study indicate that rivastigmine hydrogen tartrate used in combination with donepezil hydrochloride relieves the symptoms and improves the quality of life of patients with AD more effectively, which may be related to the reduction of the bradykinin level in these patients.	Donepezil	118-141	kininogen 1	Homo sapiens	280-290
32633718-4	2020	Bradykinin is a potent part of the vasopressor system that induces hypotension and vasodilation and is degraded by ACE and enhanced by the angiotensin1-9 produced by ACE2.	angiotensin1-9	139-153	kininogen 1	Homo sapiens	0-10
32766265-3	2020	The half-life of BK (100 nM) added to normal plasma was 34 s, a value that was increased ~12-fold when the angiotensin converting enzyme (ACE) inhibitor enalaprilat (130 nM) was added (enzyme immunoassay measurements).	Enalaprilat	153-164	kininogen 1	Homo sapiens	17-19
32766265-4	2020	The BK half-life was similarly increased ~5-fold following 2 daily oral doses of enalapril maleate in healthy volunteers, finding of possible relevance for the most common form of drug-associated AE.	Enalapril	81-98	kininogen 1	Homo sapiens	4-6
32510214-9	2020	At the "softest" settings where the benzylammonium thermometer ions have an effective average energy of 1.73 eV, we observe the majority of bradykinin in the compact state.	phenylmethanaminium	36-50	kininogen 1	Homo sapiens	140-150
32685383-2	2020	The assay was developed based on the predecessor assay using bradykinin (JPBA 2017).	jpba	73-77	kininogen 1	Homo sapiens	61-71
32685383-6	2020	Dabsylated Substance P and bradykinin are substrates of angiotensin-converting enzyme and other proteases.	dabsylated	0-10	kininogen 1	Homo sapiens	27-37
32510214-10	2020	Under more extreme operating conditions where the energy of the benzylammonium ions varies from 1.83 to 1.86 eV, the bradykinin transitions from the compact to the elongated state.	phenylmethanaminium	64-78	kininogen 1	Homo sapiens	117-127
32463805-0	2020	Avicularin Reduces the Expression of Mediators of Inflammation and Oxidative Stress in Bradykinin-Treated MG-63 Human Osteoblastic Osteosarcoma Cells.	avicularin	0-10	kininogen 1	Homo sapiens	87-97
31784929-10	2020	The results confirmed that PBM have beneficial effects in the early phases of the healing process playing a role in modulation of BK, EGF, and VEGF in gingival crevicular fluid levels; both groups had significant clinical improvement over control but there was no significant difference between them, only a trend for PBM group.	pbm	27-30	kininogen 1	Homo sapiens	130-132
32297487-7	2020	In contrast, proteins associated with energy metabolism are significantly expressed after HMWK hydrogel treatment at day 1, and these play an important role in cellular growth and reactive oxygen species scavenging at day 7.	Reactive Oxygen Species	180-203	kininogen 1	Homo sapiens	90-94
32144755-2	2020	This clinical transformation started just over 50 years ago, with the unexpected identification of a bradykinin potentiating peptide from snake venom, as a potent inhibitor of angiotensin converting enzyme which led to the development of the first synthetic inhibitor, captopril, followed by the angiotensin receptor blockers.	Captopril	269-278	kininogen 1	Homo sapiens	101-111
32463805-3	2020	This study aimed to investigate the effects of avicularin on bradykinin-treated MG-63 human osteoblastic osteosarcoma cells in vitro.	avicularin	47-57	kininogen 1	Homo sapiens	61-71
32518694-8	2020	One of the inflammatory proteins that was identified to be induced by BK treatment is Prostaglandin (PG) H Synthase-2 (Cyclooxygenase-2, COX-2).	prostaglandin (pg	86-103	kininogen 1	Homo sapiens	70-72
32518694-9	2020	In addition, BK significantly induced the production and release of PGE2 and this effect was inhibited by both COX-2 and MEK Kinase inhibitors, demonstrating that the production of PGE2 by BK is mediated via COX-2 and MAPK-dependent mechanisms.	Dinoprostone	68-72	kininogen 1	Homo sapiens	13-15
32463805-9	2020	Avicularin significantly upregulated the expression levels IL-1ss, IL-6, and TNF-alpha in the bradykinin treated group in a dose-dependent manner.	avicularin	0-10	kininogen 1	Homo sapiens	94-104
32518694-9	2020	In addition, BK significantly induced the production and release of PGE2 and this effect was inhibited by both COX-2 and MEK Kinase inhibitors, demonstrating that the production of PGE2 by BK is mediated via COX-2 and MAPK-dependent mechanisms.	Dinoprostone	68-72	kininogen 1	Homo sapiens	189-191
32518694-9	2020	In addition, BK significantly induced the production and release of PGE2 and this effect was inhibited by both COX-2 and MEK Kinase inhibitors, demonstrating that the production of PGE2 by BK is mediated via COX-2 and MAPK-dependent mechanisms.	Dinoprostone	181-185	kininogen 1	Homo sapiens	13-15
32463805-10	2020	Avicularin reduced the level of MDA and the activity of SOD and catalase in the bradykinin treated MG-63 cells, reduced p-p38, p-p65, iNOS, and COX-2 expression, and decreased the p-p38/p38 ratio and the p-p65/p65 ratio in bradykinin treated MG-63 cells in a dose-dependent manner.	avicularin	0-10	kininogen 1	Homo sapiens	80-90
32518694-9	2020	In addition, BK significantly induced the production and release of PGE2 and this effect was inhibited by both COX-2 and MEK Kinase inhibitors, demonstrating that the production of PGE2 by BK is mediated via COX-2 and MAPK-dependent mechanisms.	Dinoprostone	181-185	kininogen 1	Homo sapiens	189-191
32463805-10	2020	Avicularin reduced the level of MDA and the activity of SOD and catalase in the bradykinin treated MG-63 cells, reduced p-p38, p-p65, iNOS, and COX-2 expression, and decreased the p-p38/p38 ratio and the p-p65/p65 ratio in bradykinin treated MG-63 cells in a dose-dependent manner.	avicularin	0-10	kininogen 1	Homo sapiens	223-233
32301440-1	2021	BACKGROUND AND OBJECTIVE: Hereditary angioedema with C1-inhibitor deficiency (C1-INH-HAE) and acquired angioedema related to ACE inhibitors (ACEI-AAE) are types of bradykinin-mediated angioedema without wheals characterized by recurrent swelling episodes.	acei-aae	141-149	kininogen 1	Homo sapiens	164-174
32359101-3	2020	In this paper, we use established and emerging evidence to propose a testable hypothesis that, a vicious positive feedback loop of des-Arg(9)-bradykinin- and bradykinin-mediated inflammation   injury   inflammation, likely precipitates life threatening respiratory complications in COVID-19.	des-arg	131-138	kininogen 1	Homo sapiens	142-152
32359101-3	2020	In this paper, we use established and emerging evidence to propose a testable hypothesis that, a vicious positive feedback loop of des-Arg(9)-bradykinin- and bradykinin-mediated inflammation   injury   inflammation, likely precipitates life threatening respiratory complications in COVID-19.	des-arg	131-138	kininogen 1	Homo sapiens	158-168
32114020-2	2020	We explored bradykinin effects on prostaglandin E2 (PGE2) release from fibroblasts derived from human skeletal muscular biopsies.	Dinoprostone	34-50	kininogen 1	Homo sapiens	12-22
32114020-2	2020	We explored bradykinin effects on prostaglandin E2 (PGE2) release from fibroblasts derived from human skeletal muscular biopsies.	Dinoprostone	52-56	kininogen 1	Homo sapiens	12-22
32114020-3	2020	Bradykinin induced PGE2 release through bradykinin B2 receptors, since PGE2 release was blocked by the bradykinin B2 receptor selective antagonist FR173657 and B2 receptor agonist (Hyp3)-bradykinin showed effects comparable to bradykinin.	Dinoprostone	19-23	kininogen 1	Homo sapiens	0-10
32114020-3	2020	Bradykinin induced PGE2 release through bradykinin B2 receptors, since PGE2 release was blocked by the bradykinin B2 receptor selective antagonist FR173657 and B2 receptor agonist (Hyp3)-bradykinin showed effects comparable to bradykinin.	Dinoprostone	19-23	kininogen 1	Homo sapiens	40-50
32114020-3	2020	Bradykinin induced PGE2 release through bradykinin B2 receptors, since PGE2 release was blocked by the bradykinin B2 receptor selective antagonist FR173657 and B2 receptor agonist (Hyp3)-bradykinin showed effects comparable to bradykinin.	Dinoprostone	19-23	kininogen 1	Homo sapiens	103-113
32114020-3	2020	Bradykinin induced PGE2 release through bradykinin B2 receptors, since PGE2 release was blocked by the bradykinin B2 receptor selective antagonist FR173657 and B2 receptor agonist (Hyp3)-bradykinin showed effects comparable to bradykinin.	Dinoprostone	71-75	kininogen 1	Homo sapiens	0-10
32114020-3	2020	Bradykinin induced PGE2 release through bradykinin B2 receptors, since PGE2 release was blocked by the bradykinin B2 receptor selective antagonist FR173657 and B2 receptor agonist (Hyp3)-bradykinin showed effects comparable to bradykinin.	Dinoprostone	71-75	kininogen 1	Homo sapiens	40-50
32114020-3	2020	Bradykinin induced PGE2 release through bradykinin B2 receptors, since PGE2 release was blocked by the bradykinin B2 receptor selective antagonist FR173657 and B2 receptor agonist (Hyp3)-bradykinin showed effects comparable to bradykinin.	Dinoprostone	71-75	kininogen 1	Homo sapiens	103-113
32114020-6	2020	The release of PGE2 by bradykinin could be blocked inhibiting COX-2 and p65/NF-kB, ERK1/2 or p38 activation.	Dinoprostone	15-19	kininogen 1	Homo sapiens	23-33
32114020-8	2020	Thus, bradykinin, acting via B2 receptors, induced PGE2 release through ERK1/2 and p38-dependent pathways and consequent p65/NF-kB translocation to nucleus.	Dinoprostone	51-55	kininogen 1	Homo sapiens	6-16
32114020-10	2020	The release of PGE2 provide a possible explanation for the role of bradykinin in inflammatory diseases.	Dinoprostone	15-19	kininogen 1	Homo sapiens	67-77
32182968-3	2020	Bradykinin functionally prompts calcium influx via activation of bradykinin receptor B1/B2 (BDKRB1/2).	Calcium	32-39	kininogen 1	Homo sapiens	0-10
32182968-7	2020	Successively, bradykinin stimulated influx of calcium, phosphorylation of MEK1 and extracellular signal-regulated kinase (ERK)1/2, translocation and transactivation of nuclear factor-kappaB (NF-kappaB), and expressions of AQP4 mRNA and protein.	Calcium	46-53	kininogen 1	Homo sapiens	14-24
32182968-11	2020	Therefore, bradykinin can induce AQP4 expression and subsequent migration and invasion through BDKRB1-mediated calcium influx and subsequent activation of a MEK1-ERK1/2-NF-kappaB pathway.	Calcium	111-118	kininogen 1	Homo sapiens	11-21
31550055-14	2020	Bradykinin-induced bradykinin-2-receptor signaling through intracellular calcium mobilization and reduction in cAMP levels, triggered changes in solute permeability and cellular junction expression.	Bradykinin	19-29	kininogen 1	Homo sapiens	0-10
31933486-5	2020	We also aimed to assess the effect of bradykinin on ROS levels.	Reactive Oxygen Species	52-55	kininogen 1	Homo sapiens	38-48
31933486-10	2020	Bradykinin reduced basal and H2O2-induced ROS generation in PBMCs only in patients with HAE (P = 0.03).	Hydrogen Peroxide	29-33	kininogen 1	Homo sapiens	0-10
31933486-12	2020	However, by reducing basal and H2O2-induced ROS levels, bradykinin shows antioxidant action in this disorder.	Hydrogen Peroxide	31-35	kininogen 1	Homo sapiens	56-66
32157838-3	2020	This report describes a patient with a bradykinin-mediated angioedema soon after the initiation of perindopril, with laryngeal involvement requiring orotracheal intubation in emergency.	Perindopril	99-110	kininogen 1	Homo sapiens	39-49
32180811-1	2020	We describe a case of new onset angioedema likely due to Ezetimibe therapy in an elderly patient with a prior history of drug-induced bradykinin reactions who had been on the medication for multiple years.	Ezetimibe	57-66	kininogen 1	Homo sapiens	134-144
31550055-14	2020	Bradykinin-induced bradykinin-2-receptor signaling through intracellular calcium mobilization and reduction in cAMP levels, triggered changes in solute permeability and cellular junction expression.	Calcium	73-80	kininogen 1	Homo sapiens	0-10
31550055-14	2020	Bradykinin-induced bradykinin-2-receptor signaling through intracellular calcium mobilization and reduction in cAMP levels, triggered changes in solute permeability and cellular junction expression.	Cyclic AMP	111-115	kininogen 1	Homo sapiens	0-10
31877149-1	2019	BACKGROUND: Pulmonary vascular endothelium is the main metabolic site for Angiotensin I-Converting Enzyme (ACE)-mediated degradation of several biologically-active peptides (angiotensin I, bradykinin, hemo-regulatory peptide Ac-SDKP).	Peptides	164-172	kininogen 1	Homo sapiens	189-199
31857655-6	2019	In the brown adipose tissue, a major thermoregulator, WIN 64338 increased expression of the mitochondrial regulator Pgc1a and the bradykinin precursor gene Kng2 was upregulated after cold stress.	WIN 64338	54-63	kininogen 1	Homo sapiens	130-140
31487785-2	2019	Kv7 channels interact functionally with transient receptor potential vanilloid 1 (TRPV1) channels activated by endogenous and/or exogenous pain-inducing substances, such as bradykinin (BK) or capsaicin (CAP), respectively; however, whether Kv7 channels of specific molecular composition provide a dominant contribution in BK- or CAP-evoked responses is yet unknown.	Capsaicin	192-201	kininogen 1	Homo sapiens	322-324
31638249-1	2019	It has been reported recently that bradykinin (BK) is involved in the regulation of various processes in cancer cells.	Bradykinin	35-45	kininogen 1	Homo sapiens	47-49
31638249-4	2019	Furthermore, it was confirmed that overexpression of bradykinin B2 receptor (B2R) facilitated the proliferation, migration, and invasion of BK-treated CC cells, while knockdown of B2R had the opposite effect.	Bradykinin	53-63	kininogen 1	Homo sapiens	140-142
31726468-11	2019	A pathway analysis revealed enrichment in steroid metabolites related to sex hormones, caffeine metabolites, lysolipids, dipeptides, and polypeptide bradykinin derivatives (all, FDR < 0.1).	Steroids	42-49	kininogen 1	Homo sapiens	149-159
31659032-6	2019	We show that this antibody blocks dextran sodium sulfate-induced HK cleavage and bradykinin production.	dextran sodium sulfate	34-56	kininogen 1	Homo sapiens	81-91
31119778-0	2019	Bradykinin protects cardiac c-kit positive cells from high-glucose-induced senescence through B2 receptor signaling pathway.	Glucose	59-66	kininogen 1	Homo sapiens	0-10
31119778-4	2019	However, whether bradykinin prevents cardiac c-kit positive cells from high-glucose-induced senescence is unknown.	Glucose	76-83	kininogen 1	Homo sapiens	17-27
31119778-6	2019	Bradykinin B2 receptor (B2R) expression was declined by glucose-induced senescence.	Glucose	56-63	kininogen 1	Homo sapiens	0-10
31119778-7	2019	Bradykinin treatment inhibited senescence and reduced intracellular oxygen radicals according to senescence-associated beta-galactosidase staining and 2",7"-dichlorodihydrofluorescein diacetate staining.	Reactive Oxygen Species	68-83	kininogen 1	Homo sapiens	0-10
31119778-7	2019	Bradykinin treatment inhibited senescence and reduced intracellular oxygen radicals according to senescence-associated beta-galactosidase staining and 2",7"-dichlorodihydrofluorescein diacetate staining.	2',7'-dichlorodihydrofluorescein diacetate	151-193	kininogen 1	Homo sapiens	0-10
31119778-10	2019	The concentration of superoxide was decreased, and the concentration of intracellular adenosine triphosphate was increased after bradykinin treatment.	Adenosine Triphosphate	86-108	kininogen 1	Homo sapiens	129-139
31119778-11	2019	Western blot showed that bradykinin leads to AKT and mammalian target of rapamycin (mTOR) phosphorylation and decreased levels of P53 and P16 when compared with glucose treatment alone.	Glucose	161-168	kininogen 1	Homo sapiens	25-35
31119778-14	2019	In conclusion, bradykinin prevents the glucose-induced premature senescence of cardiac c-kit positive cells through the B2R/PI3K/AKT/mTOR/P53 signal pathways.	Glucose	39-46	kininogen 1	Homo sapiens	15-25
31401267-7	2019	Bbeta15-42 inhibited the enzymatic activity of CBPM and modified the impact of CBPM on bradykinin signaling.	bbeta15-42	0-10	kininogen 1	Homo sapiens	87-97
31487785-2	2019	Kv7 channels interact functionally with transient receptor potential vanilloid 1 (TRPV1) channels activated by endogenous and/or exogenous pain-inducing substances, such as bradykinin (BK) or capsaicin (CAP), respectively; however, whether Kv7 channels of specific molecular composition provide a dominant contribution in BK- or CAP-evoked responses is yet unknown.	Capsaicin	203-206	kininogen 1	Homo sapiens	322-324
31158660-6	2019	FD exposure impaired vasorelaxation in response to bradykinin and activated the local angiotensin system (LAS), which was inhibited by treatment with the antioxidant N-acetyl cysteine (NAC) and angiotensin II receptor type 1 (AT1) antagonist losartan (LOS).	Acetylcysteine	166-183	kininogen 1	Homo sapiens	51-61
31071434-6	2019	Bradykinin, chosen as a model, was incubated with increasing concentrations of 1,2,3,4,6-penta-O-galloyl-beta-d-glucose and tannic acid selected as reference of tannic compounds.	beta-penta-O-galloyl-glucose	79-119	kininogen 1	Homo sapiens	0-10
31422672-7	2019	Maximal endothelium-dependent vasorelaxation to BK (bradykinin; 10-6-10-10 M) was blunted (P<0.05) in arteries from patients with ICM compared with non-ICM and donor controls, whereas responses to sodium nitroprusside (10-4-10-9 M) were similar among the groups.	Nitroprusside	197-217	kininogen 1	Homo sapiens	48-50
31422672-9	2019	Of these patients, an exploratory subgroup analysis revealed that BK-induced coronary artery vasorelaxation was greater (P<0.05) after (87+-6%) versus before (54+-14%) CF-LVAD intervention in ICM patients, whereas sodium nitroprusside-evoked responses were similar.	Nitroprusside	214-234	kininogen 1	Homo sapiens	66-68
31234673-2	2019	Kallikreins are serine proteases that cleave kininogens to produce bradykinin leading to inflammation.	Serine	16-22	kininogen 1	Homo sapiens	67-77
31071434-6	2019	Bradykinin, chosen as a model, was incubated with increasing concentrations of 1,2,3,4,6-penta-O-galloyl-beta-d-glucose and tannic acid selected as reference of tannic compounds.	Tannins	124-135	kininogen 1	Homo sapiens	0-10
31071434-6	2019	Bradykinin, chosen as a model, was incubated with increasing concentrations of 1,2,3,4,6-penta-O-galloyl-beta-d-glucose and tannic acid selected as reference of tannic compounds.	tannic compounds	161-177	kininogen 1	Homo sapiens	0-10
31025294-5	2019	Our data indicate that non-covalent bradykinin assemblies are largely preserved in TIMS-TIMS under carefully selected operating conditions.	tims-tims	83-92	kininogen 1	Homo sapiens	36-46
30712581-11	2019	As demonstrated by deuterium retention of bradykinin, these features serve to reduce experimental error normally associated with conventional deuterium exchange experiments.	Deuterium	19-28	kininogen 1	Homo sapiens	42-52
31298304-12	2019	BK significantly inhibited the proliferation of hRECs cells, enhanced Caspase-3 activity, decreased the content of LDH and ROS, increased SOD activity, reduced the expressions of HMGB-1 and NF-kappaB protein, attenuated the expression of VEGF, and restrained the secretion of TNF-alpha and IL-1beta compared with high glucose group (p &lt; 0.05).	ros	123-126	kininogen 1	Homo sapiens	0-2
31298304-12	2019	BK significantly inhibited the proliferation of hRECs cells, enhanced Caspase-3 activity, decreased the content of LDH and ROS, increased SOD activity, reduced the expressions of HMGB-1 and NF-kappaB protein, attenuated the expression of VEGF, and restrained the secretion of TNF-alpha and IL-1beta compared with high glucose group (p &lt; 0.05).	Glucose	318-325	kininogen 1	Homo sapiens	0-2
31006328-7	2019	At LA, the NO synthase inhibitor L-NG-nitroarginine methyl ester decreased both acetylcholine and bradykinin vasodilation by 56% and 33%, respectively.	NG-Nitroarginine Methyl Ester	33-64	kininogen 1	Homo sapiens	98-108
31006328-8	2019	L-NG-nitroarginine methyl ester plus the COX (cyclooxygenase) inhibitor indomethacin had similar effects on acetylcholine and bradykinin vasodilation (68% and 42% reduction, respectively) as did removing the endothelium (78% and 50% decrease, respectively), suggesting a predominantly NO-dependent vasodilation at LA.	NG-Nitroarginine Methyl Ester	0-31	kininogen 1	Homo sapiens	126-136
31006328-8	2019	L-NG-nitroarginine methyl ester plus the COX (cyclooxygenase) inhibitor indomethacin had similar effects on acetylcholine and bradykinin vasodilation (68% and 42% reduction, respectively) as did removing the endothelium (78% and 50% decrease, respectively), suggesting a predominantly NO-dependent vasodilation at LA.	Indomethacin	72-84	kininogen 1	Homo sapiens	126-136
30712581-11	2019	As demonstrated by deuterium retention of bradykinin, these features serve to reduce experimental error normally associated with conventional deuterium exchange experiments.	Deuterium	142-151	kininogen 1	Homo sapiens	42-52
30987055-6	2019	RESULTS: Bradykinin (BK) increased NOX-derived cytosolic ROS.	nox	35-38	kininogen 1	Homo sapiens	9-19
30987055-6	2019	RESULTS: Bradykinin (BK) increased NOX-derived cytosolic ROS.	nox	35-38	kininogen 1	Homo sapiens	21-23
30987055-6	2019	RESULTS: Bradykinin (BK) increased NOX-derived cytosolic ROS.	Reactive Oxygen Species	57-60	kininogen 1	Homo sapiens	9-19
30987055-6	2019	RESULTS: Bradykinin (BK) increased NOX-derived cytosolic ROS.	Reactive Oxygen Species	57-60	kininogen 1	Homo sapiens	21-23
30987055-7	2019	When cells were exposed to BK with either a nominal Ca2+-free or 1 mM of extracellular Ca2+ concentration modified Tyrode"s solution, no difference in BK-induced ROS production was observed; however, chelating of cytosolic Ca2+ by BAPTA/AM or the depletion of ER Ca2+ contents by thapsigargin eliminated BK-induced ROS production.	tyrode"s	115-123	kininogen 1	Homo sapiens	27-29
30987055-8	2019	BK-induced ROS production was inhibited by a CaM inhibitor; however, a Ca2+/CaM-dependent protein kinase II (CaMKII) inhibitor did not affect BK-induced ROS production.	Reactive Oxygen Species	11-14	kininogen 1	Homo sapiens	0-2
30987055-10	2019	CONCLUSIONS: BK-induced NOX-derived ROS production was mediated via a Ca2+/CaM-dependent pathway; however, it was independent from NOX phosphorylation.	nox	24-27	kininogen 1	Homo sapiens	13-15
30987055-10	2019	CONCLUSIONS: BK-induced NOX-derived ROS production was mediated via a Ca2+/CaM-dependent pathway; however, it was independent from NOX phosphorylation.	Reactive Oxygen Species	36-39	kininogen 1	Homo sapiens	13-15
30987055-10	2019	CONCLUSIONS: BK-induced NOX-derived ROS production was mediated via a Ca2+/CaM-dependent pathway; however, it was independent from NOX phosphorylation.	cafestol palmitate	75-78	kininogen 1	Homo sapiens	13-15
30987055-10	2019	CONCLUSIONS: BK-induced NOX-derived ROS production was mediated via a Ca2+/CaM-dependent pathway; however, it was independent from NOX phosphorylation.	nox	131-134	kininogen 1	Homo sapiens	13-15
30899997-4	2019	The specificity of thiol-gold interaction was demonstrated over allyl-rich thiol-ene surfaces and the robustness of the CHT-IMERs at different flow rates and reaction temperatures using bradykinin hydrolysis as the model reaction.	Sulfhydryl Compounds	19-24	kininogen 1	Homo sapiens	186-196
30886671-4	2019	We have found that H2O2 in concentration range 10-100 muM increases the rise of [Ca2+]i induced by 5-hydroxytryptamine (5-HT) and carbachol and does not affect the calcium signals of ATP, agonist of type 1 protease-activated receptor SFLLRN, histamine and bradykinin.	Hydrogen Peroxide	19-23	kininogen 1	Homo sapiens	256-266
30876891-1	2019	Plasma kallikrein (pKal) is a serine protease responsible for cleaving high-molecular-weight kininogen to produce the pro-inflammatory peptide, bradykinin.	Serine	30-36	kininogen 1	Homo sapiens	144-154
30756324-4	2019	Both bradykinin and insulin show mass resolution increases of ~ 90% allowing baseline resolution of the [insulin+5H]5+ isotopes after only 300 ms of data acquisition.	5h	113-115	kininogen 1	Homo sapiens	5-15
30393270-6	2018	In the 10 patients whose SVGs were taken without electrocautery, endothelial-dependent relaxation with bradykinin was apparently increased in the CON group more than in the NT group.	nt	173-175	kininogen 1	Homo sapiens	103-113
30814538-6	2019	Pre-treatment of HGF for 24 h with Pam2CSK4 resulted in increased PGE2 release in response to BK and DALBK.	Dinoprostone	66-70	kininogen 1	Homo sapiens	94-96
29796990-0	2019	Neuroprotective Effects of Dehydroepiandrosterone Sulfate Through Inhibiting Expression of Matrix Metalloproteinase-9 from Bradykinin-Challenged Astroglia.	Dehydroepiandrosterone Sulfate	27-57	kininogen 1	Homo sapiens	123-133
30312677-11	2019	Moreover, the normal endothelial function in danazol-treated patients with pro-atherogenic lipid profile suggests that elevated bradykinin level or other factor(s) involved in the pathogenesis of edematous attacks may have a protective role against endothelial dysfunction and atherosclerosis.	Danazol	45-52	kininogen 1	Homo sapiens	128-138
31526514-9	2019	It was considered to be mediated by bradykinin, as the patient had already had two similar episodes and was on regular medication (enalapril).	Enalapril	131-140	kininogen 1	Homo sapiens	36-46
30033381-2	2018	This study investigated vasomotor responses after direct exposure of human subcutaneous arteries to food-grade TiO2 (E171) (14 or 140 mug/ml) for 30 min and 18 h. Vasomotor responses to bradykinin, 5-hydroxytryptamine (5-HT), sarafotoxin 6c (S6c) and nitroglycerin were recorded in wire-myographs.	titanium dioxide	111-115	kininogen 1	Homo sapiens	186-196
30283089-0	2018	A gender-specific association of the polymorphism Ile197Met in the kininogen 1 gene with plasma irbesartan concentrations in Chinese patients with essential hypertension.	ile197met	50-59	kininogen 1	Homo sapiens	67-78
30283089-0	2018	A gender-specific association of the polymorphism Ile197Met in the kininogen 1 gene with plasma irbesartan concentrations in Chinese patients with essential hypertension.	Irbesartan	96-106	kininogen 1	Homo sapiens	67-78
30283089-1	2018	This study was conducted to explore interactions in the association of the kininogen (KNG1) Ile197Met polymorphism and gender with plasma concentrations of irbesartan in Chinese patients with essential hypertension.	Irbesartan	156-166	kininogen 1	Homo sapiens	86-90
30283089-9	2018	A further test for a multiplicative interaction between the KNG1 Ile197Met polymorphism and gender in association with ln-plasma irbesartan concentrations in a multiple linear regression model was also significant (P for interaction = 0.033).	Irbesartan	129-139	kininogen 1	Homo sapiens	60-64
30283089-10	2018	This is the first study to suggest that gender may influence the association of the Ile197Met variant of KNG1 with ln-plasma irbesartan concentration.	Irbesartan	125-135	kininogen 1	Homo sapiens	105-109
30283089-11	2018	This finding may indicate that the interaction of gender and the KNG1 Ile197Met gene polymorphism can influence plasma trough irbesartan concentrations, which may contribute to a better development of personalized hypertensive treatment in Chinese patients.	Irbesartan	126-136	kininogen 1	Homo sapiens	65-69
30333824-6	2018	The angiotensin converting enzyme inhibitor enalaprilat, without any effect per se, increased immunoreactive BK (iBK) concentration under active stimulation of blood.	Enalaprilat	44-55	kininogen 1	Homo sapiens	109-111
30427893-4	2018	Sumanirole, a specific D2R agonist, was shown to diminish the excessive production of reactive oxygen species induced by bradykinin, a proinflammatory B2R-activating peptide.	U 95666E	0-10	kininogen 1	Homo sapiens	121-131
30427893-4	2018	Sumanirole, a specific D2R agonist, was shown to diminish the excessive production of reactive oxygen species induced by bradykinin, a proinflammatory B2R-activating peptide.	Reactive Oxygen Species	86-109	kininogen 1	Homo sapiens	121-131
30117680-3	2018	It was found that bradykinin increased cytosolic free Ca2+ ( Cai2+ ) by triggering a transient Ca2+ release from ER IP3Rs followed by sustained Ca2+ influx through store-operated Ca2+ entry (SOCE) channel.	cai2+	61-66	kininogen 1	Homo sapiens	18-28
30117680-7	2018	These results demonstrate for the first time that bradykinin-mediated increase in free Cai2+ via ER-IP3R3 Ca2+ release followed by Ca2+ influx through SOCE channel plays a crucial role in regulating cell growth and migration via activating pAkt, pERK1/2 and cyclin D1 in human cardiac c-Kit+ progenitor cells.	cai2+	87-92	kininogen 1	Homo sapiens	50-60
29735174-0	2018	[Tranexamic acid as first-line emergency treatment for episodes of bradykinin-mediated angioedema induced by ACE inhibitors].	Tranexamic Acid	1-16	kininogen 1	Homo sapiens	67-77
30074774-4	2018	Here, we developed a simple, membrane-free, electrokinetic, on-line, integrated SDS removal-ESI-MS device that was able to enhance ESI-MS signals of bradykinin and peptides from trypsin-digested bovine serum albumin (BSA) in samples that contained SDS micelles.	Sodium Dodecyl Sulfate	80-83	kininogen 1	Homo sapiens	149-159
30074774-4	2018	Here, we developed a simple, membrane-free, electrokinetic, on-line, integrated SDS removal-ESI-MS device that was able to enhance ESI-MS signals of bradykinin and peptides from trypsin-digested bovine serum albumin (BSA) in samples that contained SDS micelles.	Sodium Dodecyl Sulfate	248-251	kininogen 1	Homo sapiens	149-159
29424931-5	2018	The responsiveness of the stellate cells to bradykinin was markedly reduced in experimental alcohol-related acute pancreatitis, but they became sensitive to stimulation with trypsin.	Alcohols	92-99	kininogen 1	Homo sapiens	44-54
30028131-1	2018	Ion mobility and mass spectrometry techniques are used to investigate the stabilities of different conformations of bradykinin (BK, Arg1-Pro2-Pro3-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9).	glycyl-glycyl-glycyl-glycine	147-151	kininogen 1	Homo sapiens	116-126
30028131-2	2018	At elevated solution temperatures, we observe a slow protonation reaction, i.e., [BK+2H]2++H+   [BK+3H]3+, that is regulated by trans   cis isomerization of Arg1-Pro2, resulting in the Arg1- cis-Pro2- cis-Pro3-Gly4-Phe5-Ser6- cis-Pro7-Phe8-Arg9 (all- cis) configuration.	Deuterium	85-87	kininogen 1	Homo sapiens	82-84
30028131-2	2018	At elevated solution temperatures, we observe a slow protonation reaction, i.e., [BK+2H]2++H+   [BK+3H]3+, that is regulated by trans   cis isomerization of Arg1-Pro2, resulting in the Arg1- cis-Pro2- cis-Pro3-Gly4-Phe5-Ser6- cis-Pro7-Phe8-Arg9 (all- cis) configuration.	Deuterium	85-87	kininogen 1	Homo sapiens	97-99
30028131-2	2018	At elevated solution temperatures, we observe a slow protonation reaction, i.e., [BK+2H]2++H+   [BK+3H]3+, that is regulated by trans   cis isomerization of Arg1-Pro2, resulting in the Arg1- cis-Pro2- cis-Pro3-Gly4-Phe5-Ser6- cis-Pro7-Phe8-Arg9 (all- cis) configuration.	Tritium	100-102	kininogen 1	Homo sapiens	82-84
30028131-2	2018	At elevated solution temperatures, we observe a slow protonation reaction, i.e., [BK+2H]2++H+   [BK+3H]3+, that is regulated by trans   cis isomerization of Arg1-Pro2, resulting in the Arg1- cis-Pro2- cis-Pro3-Gly4-Phe5-Ser6- cis-Pro7-Phe8-Arg9 (all- cis) configuration.	Tritium	100-102	kininogen 1	Homo sapiens	97-99
30028131-2	2018	At elevated solution temperatures, we observe a slow protonation reaction, i.e., [BK+2H]2++H+   [BK+3H]3+, that is regulated by trans   cis isomerization of Arg1-Pro2, resulting in the Arg1- cis-Pro2- cis-Pro3-Gly4-Phe5-Ser6- cis-Pro7-Phe8-Arg9 (all- cis) configuration.	arg1-pro2	157-166	kininogen 1	Homo sapiens	82-84
30028131-2	2018	At elevated solution temperatures, we observe a slow protonation reaction, i.e., [BK+2H]2++H+   [BK+3H]3+, that is regulated by trans   cis isomerization of Arg1-Pro2, resulting in the Arg1- cis-Pro2- cis-Pro3-Gly4-Phe5-Ser6- cis-Pro7-Phe8-Arg9 (all- cis) configuration.	arg1-pro2	157-166	kininogen 1	Homo sapiens	97-99
30028131-2	2018	At elevated solution temperatures, we observe a slow protonation reaction, i.e., [BK+2H]2++H+   [BK+3H]3+, that is regulated by trans   cis isomerization of Arg1-Pro2, resulting in the Arg1- cis-Pro2- cis-Pro3-Gly4-Phe5-Ser6- cis-Pro7-Phe8-Arg9 (all- cis) configuration.	ser6- cis-pro7-phe8-arg9	220-244	kininogen 1	Homo sapiens	82-84
30028131-2	2018	At elevated solution temperatures, we observe a slow protonation reaction, i.e., [BK+2H]2++H+   [BK+3H]3+, that is regulated by trans   cis isomerization of Arg1-Pro2, resulting in the Arg1- cis-Pro2- cis-Pro3-Gly4-Phe5-Ser6- cis-Pro7-Phe8-Arg9 (all- cis) configuration.	ser6- cis-pro7-phe8-arg9	220-244	kininogen 1	Homo sapiens	97-99
30028131-3	2018	Once formed, the all- cis [BK+3H]3+ spontaneously cleaves the bond between Pro2-Pro3 with perfect specificity, a bond that is biologically resistant to cleavage by any human enzyme.	Tritium	30-32	kininogen 1	Homo sapiens	27-29
30263036-6	2018	Non-histamine mediated angioedema is largely driven by bradykinin and can be hereditary, acquired or drug-induced, such as with angiotensin-converting enzyme inhibitors.	Histamine	4-13	kininogen 1	Homo sapiens	55-65
29557886-0	2018	Multiple Inhibitory Mechanisms of Lidocaine on Bradykinin Receptor Activity in Model Sensory Neurons.	Lidocaine	34-43	kininogen 1	Homo sapiens	47-57
29557886-4	2018	METHODS: ND/7 sensory neurons were stimulated by different concentrations of BK in the presence or absence of LAs, with transient increases in intracellular calcium (Delta[Ca]in) detected fluorometrically in fields of cells.	Calcium	157-164	kininogen 1	Homo sapiens	77-79
29557886-6	2018	RESULTS: Responses to low BK (5 nM) were inhibited by lidocaine at 1 mM (approximately 35% inhibition) and 10 mM (approximately 70% inhibition), whereas responses to high BK (100 nM) were unaffected by 1 mM yet inhibited (approximately 75%) by 10 mM lidocaine.	Lidocaine	54-63	kininogen 1	Homo sapiens	26-28
29557886-6	2018	RESULTS: Responses to low BK (5 nM) were inhibited by lidocaine at 1 mM (approximately 35% inhibition) and 10 mM (approximately 70% inhibition), whereas responses to high BK (100 nM) were unaffected by 1 mM yet inhibited (approximately 75%) by 10 mM lidocaine.	Lidocaine	250-259	kininogen 1	Homo sapiens	26-28
29557886-9	2018	Saturation binding of BK showed that lidocaine lowered the binding capacity (Bmax) without changing the KD, consistent with noncompetitive inhibition.	Lidocaine	37-46	kininogen 1	Homo sapiens	22-24
29557886-10	2018	CONCLUSIONS: At subclinical concentrations, lidocaine suppresses BK"s activation of model sensory neurons.	Lidocaine	44-53	kininogen 1	Homo sapiens	65-67
29775649-3	2018	B1R and B2R are induced by proinflammatory cytokines and their activation by bradykinin (BK: B2R agonist) or des-arg-kallidin (DAKD: B1R agonist), induces NO and PGI2 production which is key for reducing collagen I levels.	Epoprostenol	162-166	kininogen 1	Homo sapiens	77-87
29727795-6	2018	The endothelium-dependent vasodilation to acetylcholine and bradykinin as well as the relaxation responses to the nitric oxide donor sodium nitroprusside are impaired in MA of fructose- but not glucose-supplemented rats.	Fructose	176-184	kininogen 1	Homo sapiens	60-70
29424931-14	2018	The principal agent evoking Ca2+ signals in the stellate cells is bradykinin, but in experimental alcohol-related acute pancreatitis, these cells become much less responsive to bradykinin and then acquire sensitivity to trypsin.	Alcohols	98-105	kininogen 1	Homo sapiens	66-76
29424931-14	2018	The principal agent evoking Ca2+ signals in the stellate cells is bradykinin, but in experimental alcohol-related acute pancreatitis, these cells become much less responsive to bradykinin and then acquire sensitivity to trypsin.	Alcohols	98-105	kininogen 1	Homo sapiens	177-187
29424931-16	2018	Initial release of the proteases kallikrein and trypsin from dying acinar cells can, via bradykinin generation and protease-activated receptors, induce Ca2+ signals in stellate cells which can then, possibly via nitric oxide generation, damage more acinar cells and thereby cause additional release of proteases, generating a vicious circle.	Nitric Oxide	212-224	kininogen 1	Homo sapiens	89-99
29867151-1	2018	The proinflammatory mediator bradykinin stimulated cyclooxygenase-2 (COX-2) expression and subsequently prostaglandin E2 synthesis in dermal fibroblasts.	Dinoprostone	104-120	kininogen 1	Homo sapiens	29-39
29940605-10	2018	Moreover, BK-induced up-regulation of p-p38, NF-kappaB p-p65, NLRP3, ASC, caspase-1, and COX-2 was dose-dependently down-regulated by propofol treatment.	Propofol	134-142	kininogen 1	Homo sapiens	10-12
29867151-2	2018	The involvement of B2 receptors and Galphaq in the role of bradykinin was suggested by using pharmacological inhibitors.	galphaq	36-43	kininogen 1	Homo sapiens	59-69
29867151-13	2018	Consequently, we concluded that bradykinin activates PKCepsilon via the PLD/PDK-1 pathway, which subsequently induces activation and translocation of ERK1 into the nucleus, and contributes to COX-2 expression for prostaglandin E2 synthesis in dermal fibroblasts.	Dinoprostone	213-229	kininogen 1	Homo sapiens	32-42
29867502-3	2018	We show for first time that bradykinin augmented chemotactic responsiveness of neuroblastoma cells to SDF-1 and ATP concentrations, encountered under physiological conditions.	Adenosine Triphosphate	112-115	kininogen 1	Homo sapiens	28-38
29550336-5	2018	The relaxations by the latter 2 and bradykinin, but not those by H2O2, were prevented by the soluble guanylyl cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one.	1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one	134-177	kininogen 1	Homo sapiens	36-46
29240458-9	2018	These targeted DEMs were significantly enriched in D-Arginine and D-ornithine metabolism and glycerolipid metabolism of Kyoto Encyclopedia of Genes and Genomes pathways, and enriched in bradykinin receptor activity and haptoglobin binding of gene ontology biological processes.	D-Arginine	51-61	kininogen 1	Homo sapiens	186-196
29389319-6	2018	The space charge effect by SDS on bradykinin was also reduced, increasing the signal for bradykinin 12x in the presence of gamma-CD.	Sodium Dodecyl Sulfate	27-30	kininogen 1	Homo sapiens	34-44
29389319-6	2018	The space charge effect by SDS on bradykinin was also reduced, increasing the signal for bradykinin 12x in the presence of gamma-CD.	Sodium Dodecyl Sulfate	27-30	kininogen 1	Homo sapiens	89-99
29389319-6	2018	The space charge effect by SDS on bradykinin was also reduced, increasing the signal for bradykinin 12x in the presence of gamma-CD.	gamma-cyclodextrin	123-131	kininogen 1	Homo sapiens	34-44
29389319-6	2018	The space charge effect by SDS on bradykinin was also reduced, increasing the signal for bradykinin 12x in the presence of gamma-CD.	gamma-cyclodextrin	123-131	kininogen 1	Homo sapiens	89-99
29649319-2	2018	Treatment of HPASMC with vasoactive peptides, endothelin-1 (ET-1) and bradykinin (BK) but not angiotensin II, induced a temporal decrease in the electrical impedance profile mirroring constrictive morphological change of the cells which typically was more robust in PAH as opposed to non-PAH cells.	p-Aminohippuric Acid	266-269	kininogen 1	Homo sapiens	70-80
29649319-2	2018	Treatment of HPASMC with vasoactive peptides, endothelin-1 (ET-1) and bradykinin (BK) but not angiotensin II, induced a temporal decrease in the electrical impedance profile mirroring constrictive morphological change of the cells which typically was more robust in PAH as opposed to non-PAH cells.	p-Aminohippuric Acid	266-269	kininogen 1	Homo sapiens	82-84
29649319-2	2018	Treatment of HPASMC with vasoactive peptides, endothelin-1 (ET-1) and bradykinin (BK) but not angiotensin II, induced a temporal decrease in the electrical impedance profile mirroring constrictive morphological change of the cells which typically was more robust in PAH as opposed to non-PAH cells.	p-Aminohippuric Acid	288-291	kininogen 1	Homo sapiens	70-80
29649319-2	2018	Treatment of HPASMC with vasoactive peptides, endothelin-1 (ET-1) and bradykinin (BK) but not angiotensin II, induced a temporal decrease in the electrical impedance profile mirroring constrictive morphological change of the cells which typically was more robust in PAH as opposed to non-PAH cells.	p-Aminohippuric Acid	288-291	kininogen 1	Homo sapiens	82-84
29333632-1	2018	The intrinsic binding ability of 7 natural peptides (oxytocin, arg8 -vasopressin, bradykinin, angiotensin-I, substance-P, somatostatin, and neurotensin) with copper in 2 different oxidation states (CuI/II ) derived from different Cu+/2+ precursor sources have been investigated for their charge-dependent binding characteristics.	Copper	158-164	kininogen 1	Homo sapiens	82-92
29214395-1	2018	Hereditary angioedema with C1-inhibitor deficiency (C1-INH-HAE) is a form of bradykinin-mediated angioedema.	c1-inh-hae	52-62	kininogen 1	Homo sapiens	77-87
29676873-8	2018	In the pharmacological class of ACE-Is, perindopril likely produces the strongest effects on bradykinin, which may explain, at least in part, the documented superiority of this drug in the prevention and treatment of cardiovascular disease.	Perindopril	40-51	kininogen 1	Homo sapiens	93-103
29605732-0	2018	Bradykinin-potentiating PEPTIDE-10C, an argininosuccinate synthetase activator, protects against H2O2-induced oxidative stress in SH-SY5Y neuroblastoma cells.	Hydrogen Peroxide	97-101	kininogen 1	Homo sapiens	0-10
29605732-1	2018	Bradykinin-potentiating peptides (BPPs - 5a, 7a, 9a, 10c, 11e, and 12b) of Bothrops jararaca (Bj) were described as argininosuccinate synthase (AsS) activators, improving l-arginine availability.	Arginine	171-181	kininogen 1	Homo sapiens	0-10
29649319-9	2018	However, inhibiting the activity of the sarcoplasmic reticulum Ca2+ ATPase blunted ET-1 and BK induced HPASMC contraction in both PAH and non-PAH derived HPASMC.	p-Aminohippuric Acid	130-133	kininogen 1	Homo sapiens	92-94
29649319-9	2018	However, inhibiting the activity of the sarcoplasmic reticulum Ca2+ ATPase blunted ET-1 and BK induced HPASMC contraction in both PAH and non-PAH derived HPASMC.	p-Aminohippuric Acid	142-145	kininogen 1	Homo sapiens	92-94
29240458-9	2018	These targeted DEMs were significantly enriched in D-Arginine and D-ornithine metabolism and glycerolipid metabolism of Kyoto Encyclopedia of Genes and Genomes pathways, and enriched in bradykinin receptor activity and haptoglobin binding of gene ontology biological processes.	Ornithine	66-77	kininogen 1	Homo sapiens	186-196
29240458-9	2018	These targeted DEMs were significantly enriched in D-Arginine and D-ornithine metabolism and glycerolipid metabolism of Kyoto Encyclopedia of Genes and Genomes pathways, and enriched in bradykinin receptor activity and haptoglobin binding of gene ontology biological processes.	glycerolipid	93-105	kininogen 1	Homo sapiens	186-196
29141443-5	2018	Three derived photodissociation models were used to interpret the experimental results and show that while protonated 3-iodo-l-tyrosine and Fe(II) attached to 1,2-dioleoyl-sn-glycero-3-phosphocholine most likely dissociates via a single-photon process, fragmentation of doubly charged bradykinin ions was found to be most consistent with sequential two-photon dissociation (213 nm).	3-iodotyrosine	118-135	kininogen 1	Homo sapiens	285-295
29141443-5	2018	Three derived photodissociation models were used to interpret the experimental results and show that while protonated 3-iodo-l-tyrosine and Fe(II) attached to 1,2-dioleoyl-sn-glycero-3-phosphocholine most likely dissociates via a single-photon process, fragmentation of doubly charged bradykinin ions was found to be most consistent with sequential two-photon dissociation (213 nm).	ammonium ferrous sulfate	140-146	kininogen 1	Homo sapiens	285-295
29141443-5	2018	Three derived photodissociation models were used to interpret the experimental results and show that while protonated 3-iodo-l-tyrosine and Fe(II) attached to 1,2-dioleoyl-sn-glycero-3-phosphocholine most likely dissociates via a single-photon process, fragmentation of doubly charged bradykinin ions was found to be most consistent with sequential two-photon dissociation (213 nm).	1,2-oleoylphosphatidylcholine	159-199	kininogen 1	Homo sapiens	285-295
29226721-1	2018	INTRODUCTION: Hereditary angioedema (HAE) with C1-inhibitor deficiency (C1-INH-HAE) is a rare bradykinin-mediated disease characterized by recurrent subcutaneous and/or submucosal angioedematous attacks (HAE attacks), which occur unpredictably.	c1-inh-hae	72-82	kininogen 1	Homo sapiens	94-104
29360776-0	2018	Involvement of Bradykinin B2 Receptor in Pathological Vascularization in Oxygen-Induced Retinopathy in Mice and Rabbit Cornea.	Oxygen	73-79	kininogen 1	Homo sapiens	15-25
29351301-3	2018	The plasma kinin, bradykinin, was used as the substrate to conduct enzymatic activity analyses and to determine the Michaelis constant (Km) of 174 muM and the catalytic rate constant (kcat) of 10.8 s-1 for hcAMPP.	hcampp	206-212	kininogen 1	Homo sapiens	18-28
30148510-5	2018	Bradykinin, the main B2R agonist, significantly increased cell adhesion, and this effect was reversed when the endothelial cells were additionally co-treated with a selective D2R agonist, sumanirole.	U 95666E	188-198	kininogen 1	Homo sapiens	0-10
28686356-1	2018	In human pericardial resistance arteries, effects of the endothelium-dependent vasodilator bradykinin are mediated by NO during contraction induced by K+ or the TxA2 analogue U46619 and by H2 O2 during contraction by endothelin-1 (ET-1), respectively.	Hydrogen Peroxide	189-194	kininogen 1	Homo sapiens	91-101
29071730-10	2018	In hASMCs, acute treatment with BK triggered subcellular translocation of ARHGEF1 and RhoA and enhanced auto-phosphorylation of SrcFK and phosphorylation of MYPT1 and MLC20 , but induced de-phosphorylation of cofilin.	hasmcs	3-9	kininogen 1	Homo sapiens	32-34
29071730-12	2018	In hASMCs, an ARHGEF1 small interfering RNA suppressed the effects of BK and TGF-beta on RhoA-GTP content, RhoA translocation and MYPT1 and MLC20 phosphorylation, but minimally influenced the effects of TGF-beta on cofilin expression and phosphorylation.	hasmcs	3-9	kininogen 1	Homo sapiens	70-72
29071730-12	2018	In hASMCs, an ARHGEF1 small interfering RNA suppressed the effects of BK and TGF-beta on RhoA-GTP content, RhoA translocation and MYPT1 and MLC20 phosphorylation, but minimally influenced the effects of TGF-beta on cofilin expression and phosphorylation.	Guanosine Triphosphate	94-97	kininogen 1	Homo sapiens	70-72
29071730-14	2018	Our data indicate that TGF-beta enhances BK-induced contraction, RhoA translocation and Rho-kinase activity in airway smooth muscle largely via ARHGEF1, but independently of SrcFK and total RhoA-GTP content.	Guanosine Triphosphate	195-198	kininogen 1	Homo sapiens	41-43
28939029-2	2017	Captopril dilates blood vessels, reducing blood pressure clinically and bradykinin, as the downstream signaling moiety of captopril, is capable of dilating blood vessels and effectively increasing vessel permeability.	Captopril	0-9	kininogen 1	Homo sapiens	72-82
28939029-2	2017	Captopril dilates blood vessels, reducing blood pressure clinically and bradykinin, as the downstream signaling moiety of captopril, is capable of dilating blood vessels and effectively increasing vessel permeability.	Captopril	122-131	kininogen 1	Homo sapiens	72-82
28939029-7	2017	Immunofluorescence-staining of tumor slices demonstrated that captopril significantly increased bradykinin expression, possibly explaining tumor perfusion improvements and endothelial gap enlargement.	Captopril	62-71	kininogen 1	Homo sapiens	96-106
29059213-8	2017	In cultured endothelial cells, bradykinin treatment produced the anticipated rapid influx of Ca2+ and transient CaMKII and eNOS activation, whereas CaMKII inhibition blocked eNOS phosphorylation on Ser-1179 and dephosphorylation at Thr-497.	Serine	198-201	kininogen 1	Homo sapiens	31-41
29187192-9	2017	Identified metabolites were related to the bradykinin system, involved in oxidative stress (e.g., glutamine or pipecolate) or linked to the urea cycle (e.g., ornithine or citrulline).	Glutamine	98-107	kininogen 1	Homo sapiens	43-53
29187192-9	2017	Identified metabolites were related to the bradykinin system, involved in oxidative stress (e.g., glutamine or pipecolate) or linked to the urea cycle (e.g., ornithine or citrulline).	pipecolic acid	111-121	kininogen 1	Homo sapiens	43-53
29187192-9	2017	Identified metabolites were related to the bradykinin system, involved in oxidative stress (e.g., glutamine or pipecolate) or linked to the urea cycle (e.g., ornithine or citrulline).	Ornithine	158-167	kininogen 1	Homo sapiens	43-53
29187192-9	2017	Identified metabolites were related to the bradykinin system, involved in oxidative stress (e.g., glutamine or pipecolate) or linked to the urea cycle (e.g., ornithine or citrulline).	Citrulline	171-181	kininogen 1	Homo sapiens	43-53
28587989-2	2017	Bradykinin (BK) is an endothelium-dependent agonist that induces relaxation followed by contraction of the porcine basilar artery through release of NO and PGF2alpha, respectively.	Dinoprost	156-165	kininogen 1	Homo sapiens	0-10
28587989-2	2017	Bradykinin (BK) is an endothelium-dependent agonist that induces relaxation followed by contraction of the porcine basilar artery through release of NO and PGF2alpha, respectively.	Dinoprost	156-165	kininogen 1	Homo sapiens	12-14
28587989-8	2017	In vitro, BK-induced endothelium-dependent dilation of isolated basilar artery specimens was abolished and BK-induced contraction was significantly increased (Emax: 15.85+-2.42% and 56.54+-2.71% of 60mM KCl in control and Ang II group respectively at 10-7M concentration of BK; P&lt;0.01; n=5) in Ang II-infused MMPigs.	Potassium Chloride	203-206	kininogen 1	Homo sapiens	10-12
28587989-8	2017	In vitro, BK-induced endothelium-dependent dilation of isolated basilar artery specimens was abolished and BK-induced contraction was significantly increased (Emax: 15.85+-2.42% and 56.54+-2.71% of 60mM KCl in control and Ang II group respectively at 10-7M concentration of BK; P&lt;0.01; n=5) in Ang II-infused MMPigs.	Potassium Chloride	203-206	kininogen 1	Homo sapiens	107-109
28587989-8	2017	In vitro, BK-induced endothelium-dependent dilation of isolated basilar artery specimens was abolished and BK-induced contraction was significantly increased (Emax: 15.85+-2.42% and 56.54+-2.71% of 60mM KCl in control and Ang II group respectively at 10-7M concentration of BK; P&lt;0.01; n=5) in Ang II-infused MMPigs.	Potassium Chloride	203-206	kininogen 1	Homo sapiens	107-109
28587989-8	2017	In vitro, BK-induced endothelium-dependent dilation of isolated basilar artery specimens was abolished and BK-induced contraction was significantly increased (Emax: 15.85+-2.42% and 56.54+-2.71% of 60mM KCl in control and Ang II group respectively at 10-7M concentration of BK; P&lt;0.01; n=5) in Ang II-infused MMPigs.	mmpigs	312-318	kininogen 1	Homo sapiens	10-12
28587989-8	2017	In vitro, BK-induced endothelium-dependent dilation of isolated basilar artery specimens was abolished and BK-induced contraction was significantly increased (Emax: 15.85+-2.42% and 56.54+-2.71% of 60mM KCl in control and Ang II group respectively at 10-7M concentration of BK; P&lt;0.01; n=5) in Ang II-infused MMPigs.	mmpigs	312-318	kininogen 1	Homo sapiens	107-109
28587989-8	2017	In vitro, BK-induced endothelium-dependent dilation of isolated basilar artery specimens was abolished and BK-induced contraction was significantly increased (Emax: 15.85+-2.42% and 56.54+-2.71% of 60mM KCl in control and Ang II group respectively at 10-7M concentration of BK; P&lt;0.01; n=5) in Ang II-infused MMPigs.	mmpigs	312-318	kininogen 1	Homo sapiens	107-109
28587989-9	2017	Ang II stimulation of the endothelial cells significantly decreased (54.15% at 24h; P&lt;0.05; n=three independent experiment performed in triplicate) the amount of BK-elicited NO and increased (44.27% at 24h; P&lt;0.05; n=three independent experiment performed in triplicate) the amount of BK-elicited PGF2alpha.	Dinoprost	303-312	kininogen 1	Homo sapiens	165-167
29059213-8	2017	In cultured endothelial cells, bradykinin treatment produced the anticipated rapid influx of Ca2+ and transient CaMKII and eNOS activation, whereas CaMKII inhibition blocked eNOS phosphorylation on Ser-1179 and dephosphorylation at Thr-497.	Threonine	232-235	kininogen 1	Homo sapiens	31-41
28797641-7	2017	Therefore, the anti-escape effect of opiorphin in the dPAG seems to be mediated by endogenous bradykinin, acting on kinin B2 receptors, which previous results have shown to interact synergistically with MOR in the dPAG to restrain escape in two animal models of panic.	dpag	54-58	kininogen 1	Homo sapiens	94-104
28689178-8	2017	Second, this review explores other hormones that are augmented by sacubitril/valsartan such as bradykinin, substance P and adrenomedullin that may contribute to the efficacy of sacubitril/valsartan in HF.	sacubitril and valsartan sodium hydrate drug combination	66-76	kininogen 1	Homo sapiens	95-105
28689178-8	2017	Second, this review explores other hormones that are augmented by sacubitril/valsartan such as bradykinin, substance P and adrenomedullin that may contribute to the efficacy of sacubitril/valsartan in HF.	Valsartan	77-86	kininogen 1	Homo sapiens	95-105
28689178-8	2017	Second, this review explores other hormones that are augmented by sacubitril/valsartan such as bradykinin, substance P and adrenomedullin that may contribute to the efficacy of sacubitril/valsartan in HF.	sacubitril and valsartan sodium hydrate drug combination	177-187	kininogen 1	Homo sapiens	95-105
28689178-8	2017	Second, this review explores other hormones that are augmented by sacubitril/valsartan such as bradykinin, substance P and adrenomedullin that may contribute to the efficacy of sacubitril/valsartan in HF.	Valsartan	188-197	kininogen 1	Homo sapiens	95-105
28797641-7	2017	Therefore, the anti-escape effect of opiorphin in the dPAG seems to be mediated by endogenous bradykinin, acting on kinin B2 receptors, which previous results have shown to interact synergistically with MOR in the dPAG to restrain escape in two animal models of panic.	dpag	214-218	kininogen 1	Homo sapiens	94-104
28928655-7	2017	Moreover, simvastatin oral treatment was able to reduce the nociception induced by acidified saline [an acid-sensing ion channels (ASICs) activator] and bradykinin (BK) stimulus, but not by TRPA1, TRPV1 or prostaglandin-E2 (PGE2).	Simvastatin	10-21	kininogen 1	Homo sapiens	153-163
28928655-7	2017	Moreover, simvastatin oral treatment was able to reduce the nociception induced by acidified saline [an acid-sensing ion channels (ASICs) activator] and bradykinin (BK) stimulus, but not by TRPA1, TRPV1 or prostaglandin-E2 (PGE2).	Simvastatin	10-21	kininogen 1	Homo sapiens	165-167
28928655-9	2017	These results indicate that simvastatin consistently inhibits mechanical hyperalgesia during neuropathic and inflammatory disorders, possibly by modulating the ascending pain signaling (TRPM8/ASIC/BK pathways expressed in the primary sensory neuron).	Simvastatin	28-39	kininogen 1	Homo sapiens	197-199
28985857-8	2017	In the DM arterioles, not the ND vessels, bradykinin-induced relaxation response was inhibited in the presence of the specific COX-2 inhibitor NS398 at baseline (P &lt; 0.05).	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	143-148	kininogen 1	Homo sapiens	42-52
28985857-9	2017	After CPB, bradykinin-induced relaxation response of the ND and DM arterioles was inhibited in the presence of the specific COX-2 inhibitor NS398, but this effect was more pronounced in the diabetic patients (P &lt; 0.05).	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	140-145	kininogen 1	Homo sapiens	11-21
28554847-3	2017	A similar inhibitory effect has also been reported after local administration of bradykinin (BK), which is blocked by the non-selective opioid receptor antagonist naloxone.	Naloxone	163-171	kininogen 1	Homo sapiens	81-91
27167682-4	2017	RESULTS: In smooth muscle strips obtained from human urethra, bradykinin induced contraction, which was inhibited by FK3657 in a concentration-dependent manner.	FR 173657	117-123	kininogen 1	Homo sapiens	62-72
27167682-6	2017	FK3657 shifted the intraurethral pressure dose-response curve for bradykinin to the right in rats.	FR 173657	0-6	kininogen 1	Homo sapiens	66-76
28554847-3	2017	A similar inhibitory effect has also been reported after local administration of bradykinin (BK), which is blocked by the non-selective opioid receptor antagonist naloxone.	Naloxone	163-171	kininogen 1	Homo sapiens	93-95
28554847-4	2017	The latter evidence, points to an interaction between BK and opioids in the dPAG.	dpag	76-80	kininogen 1	Homo sapiens	54-56
28554847-6	2017	We also investigated whether intra-dPAG injection of captopril, an inhibitor of the angiotensin-converting enzyme (ACE) that also degrades BK, causes a panicolytic-like effect.	Captopril	53-62	kininogen 1	Homo sapiens	139-141
28554847-7	2017	Our results showed that intra-dPAG injection of BK inhibited escape performance in a dose-dependent way, and this panicolytic-like effect was blocked by the BK type 2 receptor (B2R) antagonist HOE-140, and by the selective MOR antagonist CTOP.	dpag	30-34	kininogen 1	Homo sapiens	48-50
28554847-9	2017	Finally, intra-dPAG injection of captopril also impaired escape in a dose-dependent way, and this panicolytic-like effect was blocked by pretreatment with HOE-140, suggesting mediation by endogenous BK.	dpag	15-19	kininogen 1	Homo sapiens	199-201
28554847-9	2017	Finally, intra-dPAG injection of captopril also impaired escape in a dose-dependent way, and this panicolytic-like effect was blocked by pretreatment with HOE-140, suggesting mediation by endogenous BK.	Captopril	33-42	kininogen 1	Homo sapiens	199-201
28223053-6	2017	RESULTS: In the diabetes arterioles, bradykinin-induced relaxation response was inhibited by the selective COX-2 inhibitor NS398 at baseline (p &lt; 0.05).	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	123-128	kininogen 1	Homo sapiens	37-47
28223053-8	2017	After CP/CPB, bradykinin-induced responses in all groups were inhibited by NS398, but this effect was more pronounced in the UDM patients (p &lt; 0.05).	cpb	9-12	kininogen 1	Homo sapiens	14-24
28223053-8	2017	After CP/CPB, bradykinin-induced responses in all groups were inhibited by NS398, but this effect was more pronounced in the UDM patients (p &lt; 0.05).	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	75-80	kininogen 1	Homo sapiens	14-24
28528204-6	2017	Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1.	Aspirin	10-17	kininogen 1	Homo sapiens	157-161
28700653-8	2017	In longitudinal analyses, higher bradykinin was associated with preservation of surface density of the peripheral glomerular basement membrane (partial r = 0.162, P = 0.013), and for participants randomized to losartan, higher hyp3-bradykinin (1-8) was associated with more limited increase in cortical interstitial fractional volume (partial r = -0.291, P = 0.033).	Losartan	210-218	kininogen 1	Homo sapiens	33-43
28370444-1	2017	BACKGROUND: Hereditary angioedema (HAE) due to C1-inhibitor deficiency (C1-INH-HAE) is a rare, potentially fatal, bradykinin-mediated disease.	c1-inh-hae	72-82	kininogen 1	Homo sapiens	114-124
28091811-1	2017	1+, 2+, and 3+ precursors of substance P and bradykinin were subjected to helium cation irradiation in a 3D ion trap mass spectrometer.	Helium	74-80	kininogen 1	Homo sapiens	45-55
28539578-11	2017	The patient also had regular treatment with saxagliptin, a dipeptidyl peptidase 4 inhibitor, so we assumed that the simultaneous inhibition of two bradykinin degrading enzymes led to a treatment-refractory course of angioedema.	saxagliptin	44-55	kininogen 1	Homo sapiens	147-157
28032559-9	2017	RESULTS: BK stimulated myofibroblast migration over 24 h. BK also led to rapid and sustained phosphorylation of PKD at Ser-916, rapid phosphorylation of Hsp27 at Ser-82, and increased COX-2 expression over 4 h. BK-mediated COX-2 expression and Hsp27 phosphorylation were both inhibited by the PKD inhibitor CID755673.	Serine	119-122	kininogen 1	Homo sapiens	58-60
28499726-0	2017	Inhibitory effect of donepezil on bradykinin-induced increase in the intracellular calcium concentration in cultured cortical astrocytes.	Donepezil	21-30	kininogen 1	Homo sapiens	34-44
28499726-0	2017	Inhibitory effect of donepezil on bradykinin-induced increase in the intracellular calcium concentration in cultured cortical astrocytes.	Calcium	83-90	kininogen 1	Homo sapiens	34-44
28499726-3	2017	Bradykinin induced a transient increase of intracellular calcium concentration ([Ca2+]i) in cultured astrocytes.	Calcium	57-64	kininogen 1	Homo sapiens	0-10
28499726-4	2017	Bradykinin-induced [Ca2+]i increase was inhibited by the exposure to thapsigargin, which depletes Ca2+ stores on endoplasmic reticulum, but not by the exclusion of extracellular Ca2+.	Thapsigargin	69-81	kininogen 1	Homo sapiens	0-10
28499726-5	2017	Twenty four hours pretreatment of donepezil reduced the bradykinin-induced [Ca2+]i increase.	Donepezil	34-43	kininogen 1	Homo sapiens	56-66
28499726-7	2017	In addition, donepezil inhibited bradykinin-induced increase of the intracellular reactive oxygen species level in astrocytes.	Donepezil	13-22	kininogen 1	Homo sapiens	33-43
28499726-7	2017	In addition, donepezil inhibited bradykinin-induced increase of the intracellular reactive oxygen species level in astrocytes.	Reactive Oxygen Species	82-105	kininogen 1	Homo sapiens	33-43
28499726-8	2017	These results suggest that donepezil inhibits the inflammatory response induced by bradykinin via nAChR and PI3K-Akt pathway in astrocytes.	Donepezil	27-36	kininogen 1	Homo sapiens	83-93
27923785-9	2017	The obtained results might be used in estimation of resistance to hypoxia of any origin in human beings or in a medical practice.NEW &amp; NOTEWORTHY Our study demonstrates that the vascular reactions in response to the diving reflex are genetically determined and depend on gene polymorphisms of the kinin-bradykinin and the renin-angiotensin systems.	Adenosine Monophosphate	134-137	kininogen 1	Homo sapiens	307-317
28288820-0	2017	Resveratrol inhibits BK-induced COX-2 transcription by suppressing acetylation of AP-1 and NF-kappaB in human rheumatoid arthritis synovial fibroblasts.	Resveratrol	0-11	kininogen 1	Homo sapiens	21-23
28288820-3	2017	Here, we investigated the mechanisms underlying BK-induced COX-2 expression which is modulated by resveratrol/Sirt1 in human rheumatoid arthritis synovial fibroblasts (RASFs).	Resveratrol	98-109	kininogen 1	Homo sapiens	48-50
28288820-4	2017	We found that BK-induced COX-2 protein and mRNA expression associated with PGE2 synthesis, and promoter activity was mediated through B2R receptors, which were attenuated by selective B2R antagonist Hoe140 or transfection with B2R siRNA.	Dinoprostone	75-79	kininogen 1	Homo sapiens	14-16
28288820-6	2017	Up-regulation of Sirt1 by resveratrol suppressed the BK-induced COX-2/PGE2 production through inhibiting the interaction of AP-1 and NF-kappaB with COX-2 promoter in RASFs.	Resveratrol	26-37	kininogen 1	Homo sapiens	53-55
28288820-6	2017	Up-regulation of Sirt1 by resveratrol suppressed the BK-induced COX-2/PGE2 production through inhibiting the interaction of AP-1 and NF-kappaB with COX-2 promoter in RASFs.	Dinoprostone	70-74	kininogen 1	Homo sapiens	53-55
28288820-7	2017	BK-induced COX-2/PGE2 expression is mediated through a B2R-PKCmu-dependent MAPKs, AP-1, and NF-kappaB cascade.	Dinoprostone	17-21	kininogen 1	Homo sapiens	0-2
28435263-1	2017	A drug delivery system of quercetin (QU)-encapsulated liposomes (LS) grafted with RMP-7, a bradykinin analog, and lactoferrin (Lf) was developed to permeate the blood-brain barrier (BBB) and rescue degenerated neurons, acting as an Alzheimer"s disease (AD) pharmacotherapy.	Quercetin	26-35	kininogen 1	Homo sapiens	91-101
28032559-9	2017	RESULTS: BK stimulated myofibroblast migration over 24 h. BK also led to rapid and sustained phosphorylation of PKD at Ser-916, rapid phosphorylation of Hsp27 at Ser-82, and increased COX-2 expression over 4 h. BK-mediated COX-2 expression and Hsp27 phosphorylation were both inhibited by the PKD inhibitor CID755673.	Serine	119-122	kininogen 1	Homo sapiens	58-60
28032559-9	2017	RESULTS: BK stimulated myofibroblast migration over 24 h. BK also led to rapid and sustained phosphorylation of PKD at Ser-916, rapid phosphorylation of Hsp27 at Ser-82, and increased COX-2 expression over 4 h. BK-mediated COX-2 expression and Hsp27 phosphorylation were both inhibited by the PKD inhibitor CID755673.	Serine	162-165	kininogen 1	Homo sapiens	58-60
28032559-9	2017	RESULTS: BK stimulated myofibroblast migration over 24 h. BK also led to rapid and sustained phosphorylation of PKD at Ser-916, rapid phosphorylation of Hsp27 at Ser-82, and increased COX-2 expression over 4 h. BK-mediated COX-2 expression and Hsp27 phosphorylation were both inhibited by the PKD inhibitor CID755673.	Serine	162-165	kininogen 1	Homo sapiens	58-60
28032559-9	2017	RESULTS: BK stimulated myofibroblast migration over 24 h. BK also led to rapid and sustained phosphorylation of PKD at Ser-916, rapid phosphorylation of Hsp27 at Ser-82, and increased COX-2 expression over 4 h. BK-mediated COX-2 expression and Hsp27 phosphorylation were both inhibited by the PKD inhibitor CID755673.	CID755673	307-316	kininogen 1	Homo sapiens	58-60
28032559-9	2017	RESULTS: BK stimulated myofibroblast migration over 24 h. BK also led to rapid and sustained phosphorylation of PKD at Ser-916, rapid phosphorylation of Hsp27 at Ser-82, and increased COX-2 expression over 4 h. BK-mediated COX-2 expression and Hsp27 phosphorylation were both inhibited by the PKD inhibitor CID755673.	CID755673	307-316	kininogen 1	Homo sapiens	58-60
28032559-10	2017	Similarly, BK-induced myofibroblast migration was significantly inhibited by CID755673 (P &lt; 0.05), by the direct COX-2 inhibitor NS398 (P &lt; 0.05), and by Hsp27 small interfering RNA (P &lt; 0.05).	CID755673	77-86	kininogen 1	Homo sapiens	11-13
28032559-10	2017	Similarly, BK-induced myofibroblast migration was significantly inhibited by CID755673 (P &lt; 0.05), by the direct COX-2 inhibitor NS398 (P &lt; 0.05), and by Hsp27 small interfering RNA (P &lt; 0.05).	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	132-137	kininogen 1	Homo sapiens	11-13
28299349-4	2017	We found that gabapentin significantly reduced PKCepsilon translocation induced by the pronociceptive peptides bradykinin and prokineticin 2, involved in both inflammatory and chronic pain.	Gabapentin	14-24	kininogen 1	Homo sapiens	111-121
28099911-7	2017	The increase of pAkt, pERK1/2 and cyclin D1 by bradykinin was prevented by the PI3K inhibitor Ly294002, the PLC inhibitors U73122 and neomycin, and/or the PKC inhibitor chelerythrine and the MAPK inhibitor PD98059.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	94-102	kininogen 1	Homo sapiens	47-57
28099911-7	2017	The increase of pAkt, pERK1/2 and cyclin D1 by bradykinin was prevented by the PI3K inhibitor Ly294002, the PLC inhibitors U73122 and neomycin, and/or the PKC inhibitor chelerythrine and the MAPK inhibitor PD98059.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	123-129	kininogen 1	Homo sapiens	47-57
28099911-7	2017	The increase of pAkt, pERK1/2 and cyclin D1 by bradykinin was prevented by the PI3K inhibitor Ly294002, the PLC inhibitors U73122 and neomycin, and/or the PKC inhibitor chelerythrine and the MAPK inhibitor PD98059.	Neomycin	134-142	kininogen 1	Homo sapiens	47-57
28099911-7	2017	The increase of pAkt, pERK1/2 and cyclin D1 by bradykinin was prevented by the PI3K inhibitor Ly294002, the PLC inhibitors U73122 and neomycin, and/or the PKC inhibitor chelerythrine and the MAPK inhibitor PD98059.	chelerythrine	169-182	kininogen 1	Homo sapiens	47-57
28099911-7	2017	The increase of pAkt, pERK1/2 and cyclin D1 by bradykinin was prevented by the PI3K inhibitor Ly294002, the PLC inhibitors U73122 and neomycin, and/or the PKC inhibitor chelerythrine and the MAPK inhibitor PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	206-213	kininogen 1	Homo sapiens	47-57
28044232-0	2017	Lipid Emulsions Containing Medium Chain Triacylglycerols Blunt Bradykinin-Induced Endothelium-Dependent Relaxation in Porcine Coronary Artery Rings.	Triglycerides	40-56	kininogen 1	Homo sapiens	63-73
27881662-5	2017	Moreover, cells lacking PC1 expression use less O2 and show less mitochondrial Ca2+ uptake in response to bradykinin-induced ER Ca2+ release, indicating that PC1 can modulate mitochondrial function.	Oxygen	48-50	kininogen 1	Homo sapiens	106-116
28566000-5	2017	Treatment with the KV7 opener retigabine almost completely abolished visceral afferent firing evoked by the algogen bradykinin, in agreement with significant co-expression of mRNA transcripts by single-cell qualitative real-time polymerase chain reaction for KCNQ subtypes and the B2 bradykinin receptor in retrogradely labelled extrinsic sensory neurons from the colon.	ezogabine	30-40	kininogen 1	Homo sapiens	116-126
28566000-7	2017	In human bowel tissues, KV7.3 and KV7.5 were expressed in neuronal varicosities co-labelled with synaptophysin and CGRP, and retigabine inhibited bradykinin-induced afferent activation in afferent recordings from human colon.	ezogabine	125-135	kininogen 1	Homo sapiens	146-156
27533118-3	2016	The renin inhibitor aliskiren was recently shown to increase cardiac tissue kallikrein expression and bradykinin levels, and to reduce myocardial ischemia-reperfusion injury by bradykinin B2 receptor- and angiotensin AT2 receptor-mediated mechanisms.	aliskiren	20-29	kininogen 1	Homo sapiens	102-112
27533118-3	2016	The renin inhibitor aliskiren was recently shown to increase cardiac tissue kallikrein expression and bradykinin levels, and to reduce myocardial ischemia-reperfusion injury by bradykinin B2 receptor- and angiotensin AT2 receptor-mediated mechanisms.	aliskiren	20-29	kininogen 1	Homo sapiens	177-187
27693494-3	2016	In our study, we found that bradykinin (BK) could upregulate the expression of TRPM7 and dynamically regulate the phosphorylation of non-muscle myosin IIA heavy chain (NMHC-IIA) Ser-1943 in HepG2 cells.	Serine	178-181	kininogen 1	Homo sapiens	28-38
27693494-3	2016	In our study, we found that bradykinin (BK) could upregulate the expression of TRPM7 and dynamically regulate the phosphorylation of non-muscle myosin IIA heavy chain (NMHC-IIA) Ser-1943 in HepG2 cells.	Serine	178-181	kininogen 1	Homo sapiens	40-42
27040396-6	2016	Co-activation of Gi-coupled alpha2-adrenoceptor and Gq-coupled bradykinin receptor resulted in a synergistic CXCL8 production, with Gbetagamma-responsive PLCbeta2/3, Src, ERK, and STAT3 serving as critical signaling intermediates.	gbetagamma	132-142	kininogen 1	Homo sapiens	63-73
27755983-7	2016	Another had symptoms of nausea, hypotension, and bradycardia with increased levels of serum bradykinin during a dextran sulfate cellulose absorption-based LA procedure.	dextran sulfate cellulose	112-137	kininogen 1	Homo sapiens	92-102
27406326-5	2016	Bile acid-mediated pancreatic damage can be further escalated by bradykinin-induced signals in stellate cells and thus killing of stellate cells by bile acids might have important implications in acute biliary pancreatitis.	Bile Acids and Salts	0-9	kininogen 1	Homo sapiens	65-75
27406326-5	2016	Bile acid-mediated pancreatic damage can be further escalated by bradykinin-induced signals in stellate cells and thus killing of stellate cells by bile acids might have important implications in acute biliary pancreatitis.	Bile Acids and Salts	148-158	kininogen 1	Homo sapiens	65-75
27273087-6	2016	The complex of prekallikrein-HK acquires an inducible active site not present in prekallikrein which in Tris-type buffers cleaves HK stoichiometrically to release bradykinin, or in phosphate buffer auto-activates to generate kallikrein and bradykinin.	Tromethamine	104-108	kininogen 1	Homo sapiens	163-173
27273087-7	2016	Thus immunologic depletion of C1 inhibitor from factor XII-deficient plasma (phosphate is the natural buffer) auto-activates on incubation to release bradykinin.	Phosphates	77-86	kininogen 1	Homo sapiens	150-160
27579517-6	2016	A second exosite, which is involved in the regulation of enzymatic processing by IDE of all substrates investigated (including a 10-25 amino acid long amyloid-like peptide, bradykinin and somatostatin itself, which had been studied previously), probably acts through the alteration of an "open-closed" equilibrium.	exosite	9-16	kininogen 1	Homo sapiens	173-183
26671187-6	2016	Functionality of kinin-B1 and B2 receptors was evidenced by stimulation of intracellular calcium fluxes by their respective agonists, des-Arg9-bradykinin (DBK) and bradykinin (BK).	Calcium	89-96	kininogen 1	Homo sapiens	143-153
27999472-1	2016	Angioedema is a rare adverse reaction of carbamazepine, which causes localized tissue edema in submucosal and subcutaneous tissue mediated by histamine, serotonin, and kinins (bradykinin).	Carbamazepine	41-54	kininogen 1	Homo sapiens	176-186
27999472-1	2016	Angioedema is a rare adverse reaction of carbamazepine, which causes localized tissue edema in submucosal and subcutaneous tissue mediated by histamine, serotonin, and kinins (bradykinin).	Histamine	142-151	kininogen 1	Homo sapiens	176-186
27173110-0	2016	Use of deuterium labeling by high-temperature solid-state hydrogen-exchange reaction for mass spectrometric analysis of bradykinin biotransformation.	Deuterium	7-16	kininogen 1	Homo sapiens	120-130
27173110-0	2016	Use of deuterium labeling by high-temperature solid-state hydrogen-exchange reaction for mass spectrometric analysis of bradykinin biotransformation.	Hydrogen	58-66	kininogen 1	Homo sapiens	120-130
27173110-9	2016	Deuterium-labeled and unlabeled BKs were incubated with human plasma and their corresponding fragments BK(1-5) and BK(1-7), well known as the major metabolites, were detected.	Deuterium	0-9	kininogen 1	Homo sapiens	103-105
27173110-9	2016	Deuterium-labeled and unlabeled BKs were incubated with human plasma and their corresponding fragments BK(1-5) and BK(1-7), well known as the major metabolites, were detected.	Berkelium	32-35	kininogen 1	Homo sapiens	103-105
26829968-7	2016	The molecular ion yield of the bradykinin was maximized by using 30 keV Bi3 (+) primary ions in a DHB matrix but in the HCCA matrix, the maximum molecular ion yield was obtained by using 30 keV Bi7 (+) primary ions.	2,5-dihydroxybenzoic acid	98-101	kininogen 1	Homo sapiens	31-41
26914408-0	2016	Endothelin-1 shifts the mediator of bradykinin-induced relaxation from NO to H2 O2 in resistance arteries from patients with cardiovascular disease.	Hydrogen Peroxide	77-82	kininogen 1	Homo sapiens	36-46
26914408-5	2016	BK-induced relaxation was (i) abolished by L-NAME in K(+) -contracted arteries, (ii) partly inhibited by L-NAME in the presence of U46619 and (iii) not altered by indomethacin, L-NAME plus inhibitors of small and intermediate conductance calcium-activated K(+) channels, but attenuated by catalase, in ET-1-contracted arteries.	NG-Nitroarginine Methyl Ester	43-49	kininogen 1	Homo sapiens	0-2
26914408-5	2016	BK-induced relaxation was (i) abolished by L-NAME in K(+) -contracted arteries, (ii) partly inhibited by L-NAME in the presence of U46619 and (iii) not altered by indomethacin, L-NAME plus inhibitors of small and intermediate conductance calcium-activated K(+) channels, but attenuated by catalase, in ET-1-contracted arteries.	NG-Nitroarginine Methyl Ester	105-111	kininogen 1	Homo sapiens	0-2
26914408-5	2016	BK-induced relaxation was (i) abolished by L-NAME in K(+) -contracted arteries, (ii) partly inhibited by L-NAME in the presence of U46619 and (iii) not altered by indomethacin, L-NAME plus inhibitors of small and intermediate conductance calcium-activated K(+) channels, but attenuated by catalase, in ET-1-contracted arteries.	NG-Nitroarginine Methyl Ester	105-111	kininogen 1	Homo sapiens	0-2
26914408-8	2016	Catalase-sensitive staining of cellular ROS with CellROX Deep Red was significantly increased in the presence of both 1 muM BK and 2 nM ET-1 but not either peptide alone.	ros	40-43	kininogen 1	Homo sapiens	124-126
26914408-9	2016	CONCLUSIONS AND IMPLICATIONS: In resistance arteries from patients with CVD, exogenous ET-1 shifts the mediator of relaxing responses to the endothelium-dependent vasodilator BK from NO to H2 O2 and neither NADPH oxidases, xanthine oxidase nor NOS appear to be involved in this effect.	Hydrogen Peroxide	189-194	kininogen 1	Homo sapiens	175-177
26952290-0	2016	Plasma kallikrein-bradykinin pathway promotes circulatory nitric oxide metabolite availability during hypoxia.	Nitric Oxide	58-70	kininogen 1	Homo sapiens	18-28
26944020-4	2016	We found that overnight treatment of DRG cultures with a cocktail of inflammatory mediators bradykinin (BK), adenosine triphosphate (ATP), norepinephrine (NE) and prostaglandin E2 (PGE2) strongly increased the population size of the small-diameter neurons displaying low-voltage activated (LVA, T-type) Ca(2+) currents while having no effect on the peak LVA current amplitude.	Dinoprostone	163-179	kininogen 1	Homo sapiens	92-102
26944020-9	2016	Our data suggest that inflammatory mediators BK and ATP increase the abundance of LVA-positive DRG neurons in total neuronal population by stimulating the recruitment of a "reserve pool" of CaV3.2 channels, particularly in neurons that do not display measurable LVA currents under control conditions.	mevinolinic acid	82-85	kininogen 1	Homo sapiens	45-47
27328010-0	2016	Copper, differently from zinc, affects the conformation, oligomerization state and activity of bradykinin.	Copper	0-6	kininogen 1	Homo sapiens	95-105
27328010-3	2016	However, although copper and zinc dyshomeostasis has been demonstrated to be largely involved in the development of AD, a detailed study of the interaction of BK with these two metal ions has never been addressed.	Metals	177-182	kininogen 1	Homo sapiens	159-161
27328010-4	2016	In this work, we have applied mass spectrometry, circular dichroism as well as computational methods in order to assess if copper and zinc have the ability to modulate the conformation and oligomerization of BK.	Copper	123-129	kininogen 1	Homo sapiens	208-210
27328010-6	2016	The biochemical analyses on monocyte/macrophage cell culture (THP-1 Cell Line human) in line with the effect of metals on the conformation of BK showed that the presence of copper can affect the signaling cascade mediated by the BK receptors.	Copper	173-179	kininogen 1	Homo sapiens	142-144
27106139-11	2016	Functionally, BK inhibited leukocyte adhesion and PE caused an increase in SMC cGMP.	Cyclic GMP	79-83	kininogen 1	Homo sapiens	14-16
26840628-12	2016	Serum ADMA positively correlated with IR score and negatively with pD2 for bradykinin.	N,N-dimethylarginine	6-10	kininogen 1	Homo sapiens	75-85
26671187-6	2016	Functionality of kinin-B1 and B2 receptors was evidenced by stimulation of intracellular calcium fluxes by their respective agonists, des-Arg9-bradykinin (DBK) and bradykinin (BK).	-arg9	137-142	kininogen 1	Homo sapiens	143-153
26671187-6	2016	Functionality of kinin-B1 and B2 receptors was evidenced by stimulation of intracellular calcium fluxes by their respective agonists, des-Arg9-bradykinin (DBK) and bradykinin (BK).	-arg9	137-142	kininogen 1	Homo sapiens	156-158
26671187-6	2016	Functionality of kinin-B1 and B2 receptors was evidenced by stimulation of intracellular calcium fluxes by their respective agonists, des-Arg9-bradykinin (DBK) and bradykinin (BK).	Calcium	89-96	kininogen 1	Homo sapiens	164-174
26671187-6	2016	Functionality of kinin-B1 and B2 receptors was evidenced by stimulation of intracellular calcium fluxes by their respective agonists, des-Arg9-bradykinin (DBK) and bradykinin (BK).	Calcium	89-96	kininogen 1	Homo sapiens	156-158
26992459-10	2016	Omapatrilat blocked three pathways that break down bradykinin, leading to high rates of angioedema.	omapatrilat	0-11	kininogen 1	Homo sapiens	51-61
26786060-5	2016	TAFI also plays a role in inflammatory processes via the removal of C-terminal arginine or lysine residues from bradykinin, thrombin-cleaved osteopontin, C3a, C5a and chemerin.	Arginine	79-87	kininogen 1	Homo sapiens	112-122
26786060-5	2016	TAFI also plays a role in inflammatory processes via the removal of C-terminal arginine or lysine residues from bradykinin, thrombin-cleaved osteopontin, C3a, C5a and chemerin.	Lysine	91-97	kininogen 1	Homo sapiens	112-122
26721779-18	2016	Placental conditioned media impaired bradykinin-induced vasodilation; this effect was reversed by metformin.	Metformin	98-107	kininogen 1	Homo sapiens	37-47
26957155-6	2016	We further applied it to examine the design of template molecules for aromatic meta-C-H activation in solutions and investigate solution conformations of the nonapeptide Bradykinin involving slow cis-trans isomerizations of three proline residues.	Proline	230-237	kininogen 1	Homo sapiens	170-180
26660642-16	2016	At 72 h, serelaxin treatment improved bradykinin-mediated relaxation through COX2-derived PGI2 production.	serelaxin protein, human	9-18	kininogen 1	Homo sapiens	38-48
26660642-16	2016	At 72 h, serelaxin treatment improved bradykinin-mediated relaxation through COX2-derived PGI2 production.	Epoprostenol	90-94	kininogen 1	Homo sapiens	38-48
26672467-0	2016	Highly effective detection of inflamed cells using a modified bradykinin ligand labeled with FITC fluorescence.	Fluorescein-5-isothiocyanate	93-97	kininogen 1	Homo sapiens	62-72
27069632-12	2016	Both forms of aspirin decrease bradykinin-stimulated thromboxane and prostacyclin production, but some stimulated prostacyclin production remains during treatment with NHP-554C.	Aspirin	14-21	kininogen 1	Homo sapiens	31-41
27069632-12	2016	Both forms of aspirin decrease bradykinin-stimulated thromboxane and prostacyclin production, but some stimulated prostacyclin production remains during treatment with NHP-554C.	Thromboxanes	53-64	kininogen 1	Homo sapiens	31-41
27069632-12	2016	Both forms of aspirin decrease bradykinin-stimulated thromboxane and prostacyclin production, but some stimulated prostacyclin production remains during treatment with NHP-554C.	Epoprostenol	69-81	kininogen 1	Homo sapiens	31-41
26634895-9	2016	Functional expression of B2R was confirmed by a transient disruptive action of BK on fictive locomotion generated by a combination of NMDA, 5-HT and dopamine.	N-Methylaspartate	134-138	kininogen 1	Homo sapiens	79-81
26634895-9	2016	Functional expression of B2R was confirmed by a transient disruptive action of BK on fictive locomotion generated by a combination of NMDA, 5-HT and dopamine.	Serotonin	140-144	kininogen 1	Homo sapiens	79-81
26634895-9	2016	Functional expression of B2R was confirmed by a transient disruptive action of BK on fictive locomotion generated by a combination of NMDA, 5-HT and dopamine.	Dopamine	149-157	kininogen 1	Homo sapiens	79-81
26280447-1	2016	The aim of this MiniReview was to introduce the newly invented dual-acting drug valsartan/sacubitril (LCZ696), which combines an angiotensin receptor blocker (valsartan) with sacubitril, a specific inhibitor of the neutral endopeptidase (NEP) that degrades vasoactive peptides, including natriuretic peptides ANP and BNP, but also glucagon, enkephalins and bradykinin, among others.	Valsartan	80-89	kininogen 1	Homo sapiens	357-367
26280447-1	2016	The aim of this MiniReview was to introduce the newly invented dual-acting drug valsartan/sacubitril (LCZ696), which combines an angiotensin receptor blocker (valsartan) with sacubitril, a specific inhibitor of the neutral endopeptidase (NEP) that degrades vasoactive peptides, including natriuretic peptides ANP and BNP, but also glucagon, enkephalins and bradykinin, among others.	sacubitril and valsartan sodium hydrate drug combination	90-100	kininogen 1	Homo sapiens	357-367
26280447-1	2016	The aim of this MiniReview was to introduce the newly invented dual-acting drug valsartan/sacubitril (LCZ696), which combines an angiotensin receptor blocker (valsartan) with sacubitril, a specific inhibitor of the neutral endopeptidase (NEP) that degrades vasoactive peptides, including natriuretic peptides ANP and BNP, but also glucagon, enkephalins and bradykinin, among others.	sacubitril and valsartan sodium hydrate drug combination	102-108	kininogen 1	Homo sapiens	357-367
27069632-0	2016	Comparative effects of immediate-release and extended-release aspirin on basal and bradykinin-stimulated excretion of thromboxane and prostacyclin metabolites.	Aspirin	62-69	kininogen 1	Homo sapiens	83-93
27069632-0	2016	Comparative effects of immediate-release and extended-release aspirin on basal and bradykinin-stimulated excretion of thromboxane and prostacyclin metabolites.	Thromboxanes	118-129	kininogen 1	Homo sapiens	83-93
27069632-0	2016	Comparative effects of immediate-release and extended-release aspirin on basal and bradykinin-stimulated excretion of thromboxane and prostacyclin metabolites.	Epoprostenol	134-146	kininogen 1	Homo sapiens	83-93
27069632-8	2016	Both doses of ASA and NHP significantly reduced excretion of both thromboxane and prostacyclin metabolites following intravenous bradykinin.	Aspirin	14-17	kininogen 1	Homo sapiens	129-139
27069632-9	2016	During NHP-554C 162.5 mg/d, but not during ASA, bradykinin significantly increased urinary 2,3-dinor-6-keto-PGF1alpha.	2,3-dinor-6-ketoprostaglandin F1alpha	91-117	kininogen 1	Homo sapiens	48-58
27069632-10	2016	Nevertheless, 11-dehydro-thromboxane B2 and 2,3-dinor-6-keto-PGF1alpha responses to bradykinin were statistically similar during ASA and NHP-554C.	11-dehydro-thromboxane B2	14-39	kininogen 1	Homo sapiens	84-94
27069632-10	2016	Nevertheless, 11-dehydro-thromboxane B2 and 2,3-dinor-6-keto-PGF1alpha responses to bradykinin were statistically similar during ASA and NHP-554C.	2,3-dinor-6-ketoprostaglandin F1alpha	44-70	kininogen 1	Homo sapiens	84-94
26946694-2	2016	The aims of this review are to describe the clinical approach and diagnosis of non-hereditary bradykinin-mediated angioedema induced by drugs such as: angiotensin-converting inhibitor, sartan, gliptins, rapamycin or some thrombolytic reagents and renin inhibitors.	Sirolimus	203-212	kininogen 1	Homo sapiens	94-104
26842379-9	2016	In recent years, some new drugs have been introduced in the treatment of bradykinin-mediated angioedema, such as bradykinin B2-receptor antagonist, icatibant, and kallikrein inhibitor, ecallantide, which allow to improve treatment outcomes.	ecallantide	185-196	kininogen 1	Homo sapiens	73-83
26842379-9	2016	In recent years, some new drugs have been introduced in the treatment of bradykinin-mediated angioedema, such as bradykinin B2-receptor antagonist, icatibant, and kallikrein inhibitor, ecallantide, which allow to improve treatment outcomes.	ecallantide	185-196	kininogen 1	Homo sapiens	113-123
26494370-8	2015	We therefore evaluated the effect of bradykinin on ADMA production in A549 cells; a cell line that expresses BK receptors.	N,N-dimethylarginine	51-55	kininogen 1	Homo sapiens	37-47
26494370-11	2015	In vitro studies further suggest that this may occur through BK-mediated increase in ADMA production during ACE inhibition.	N,N-dimethylarginine	85-89	kininogen 1	Homo sapiens	61-63
26068400-4	2015	The Phe(5/8) and Arg(9) residues of BK generally participated in the interactions with colloidal suspended Ag surfaces.	Phenylalanine	4-7	kininogen 1	Homo sapiens	36-38
26360782-5	2015	Bradykinin (BK) treatment decreased human EPC (hEPC) senescence and intracellular oxygen radical production, resulting in reduced retinoblastoma 1 (RB) RNA expression in H2O2-induced senescent hEPCs and a reversal of the B2R downregulation that is normally observed in senescent cells.	Reactive Oxygen Species	82-96	kininogen 1	Homo sapiens	0-10
26360782-5	2015	Bradykinin (BK) treatment decreased human EPC (hEPC) senescence and intracellular oxygen radical production, resulting in reduced retinoblastoma 1 (RB) RNA expression in H2O2-induced senescent hEPCs and a reversal of the B2R downregulation that is normally observed in senescent cells.	Reactive Oxygen Species	82-96	kininogen 1	Homo sapiens	12-14
26360782-5	2015	Bradykinin (BK) treatment decreased human EPC (hEPC) senescence and intracellular oxygen radical production, resulting in reduced retinoblastoma 1 (RB) RNA expression in H2O2-induced senescent hEPCs and a reversal of the B2R downregulation that is normally observed in senescent cells.	Hydrogen Peroxide	170-174	kininogen 1	Homo sapiens	0-10
26360782-5	2015	Bradykinin (BK) treatment decreased human EPC (hEPC) senescence and intracellular oxygen radical production, resulting in reduced retinoblastoma 1 (RB) RNA expression in H2O2-induced senescent hEPCs and a reversal of the B2R downregulation that is normally observed in senescent cells.	Hydrogen Peroxide	170-174	kininogen 1	Homo sapiens	12-14
26360782-6	2015	Furthermore, BK treatment of H2O2-exposed cells leads to elevated phosphorylation of RB, AKT, and cyclin D1 compared with H2O2-treatment alone.	Hydrogen Peroxide	29-33	kininogen 1	Homo sapiens	13-15
26360782-6	2015	Furthermore, BK treatment of H2O2-exposed cells leads to elevated phosphorylation of RB, AKT, and cyclin D1 compared with H2O2-treatment alone.	Hydrogen Peroxide	122-126	kininogen 1	Homo sapiens	13-15
26235941-7	2015	BK, through activation of the kinin B2 receptor, potentiated the COX-2 mediated prostaglandin release in cytokines-primed RPE cells while new protein synthesis and prostaglandin production contribute to the potentiating effect of cytokines on BK-induced Ca(2+) response.	Prostaglandins	80-93	kininogen 1	Homo sapiens	0-2
26235941-7	2015	BK, through activation of the kinin B2 receptor, potentiated the COX-2 mediated prostaglandin release in cytokines-primed RPE cells while new protein synthesis and prostaglandin production contribute to the potentiating effect of cytokines on BK-induced Ca(2+) response.	Prostaglandins	164-177	kininogen 1	Homo sapiens	0-2
26619738-4	2015	Bradykinin-mediated angioedema, so much rare than histamine-mediated one, has to be known, because it is potentially lethal.	Histamine	50-59	kininogen 1	Homo sapiens	0-10
25872163-7	2015	In the presence of L-NAME and indomethacin, DPI and ML-171 had no effect in females, but enhanced the bradykinin-induced vasorelaxation in males.	NG-Nitroarginine Methyl Ester	19-25	kininogen 1	Homo sapiens	102-112
25872163-7	2015	In the presence of L-NAME and indomethacin, DPI and ML-171 had no effect in females, but enhanced the bradykinin-induced vasorelaxation in males.	3-aminodiphenyleneiodium	44-47	kininogen 1	Homo sapiens	102-112
26106824-0	2015	Bradykinin increased the permeability of BTB via NOS/NO/ZONAB-mediating down-regulation of claudin-5 and occludin.	btb	41-44	kininogen 1	Homo sapiens	0-10
26106824-2	2015	NOS inhibitors l-NAME and 7-NI could effectively block the effect of BK on increasing BTB permeability, decreasing the expressions of claudin-5 and occludin and promoting the translocation of ZONAB.	NG-Nitroarginine Methyl Ester	15-21	kininogen 1	Homo sapiens	69-71
26106824-2	2015	NOS inhibitors l-NAME and 7-NI could effectively block the effect of BK on increasing BTB permeability, decreasing the expressions of claudin-5 and occludin and promoting the translocation of ZONAB.	7-nitroindazole	26-30	kininogen 1	Homo sapiens	69-71
26106824-2	2015	NOS inhibitors l-NAME and 7-NI could effectively block the effect of BK on increasing BTB permeability, decreasing the expressions of claudin-5 and occludin and promoting the translocation of ZONAB.	btb	86-89	kininogen 1	Homo sapiens	69-71
26106824-3	2015	Overexpression of ZONAB could significantly enhance BK-mediating BTB permeability.	btb	65-68	kininogen 1	Homo sapiens	52-54
26106824-5	2015	This study indicated NOS/NO/ZONAB pathway might be involved in BK"s increasing the permeability of BTB.	btb	99-102	kininogen 1	Homo sapiens	63-65
26386501-4	2015	Combining NIs with ACEIs is unsafe because of an unacceptably high prevalence of angioedema, which may be mediated by elevated levels of endogenous bradykinin.	Nickel	10-13	kininogen 1	Homo sapiens	148-158
26235941-0	2015	Enhanced Ca(2+) response and stimulation of prostaglandin release by the bradykinin B2 receptor in human retinal pigment epithelial cells primed with proinflammatory cytokines.	Prostaglandins	44-57	kininogen 1	Homo sapiens	73-83
26234931-7	2015	We also found concordant findings in the serum of the participants, which include a decrease in cortisol levels and a significant increase in the active vasodilator metabolite of bradykinin (des-Arg(9)-bradykinin).	des-arg	191-198	kininogen 1	Homo sapiens	179-189
26234931-7	2015	We also found concordant findings in the serum of the participants, which include a decrease in cortisol levels and a significant increase in the active vasodilator metabolite of bradykinin (des-Arg(9)-bradykinin).	des-arg	191-198	kininogen 1	Homo sapiens	202-212
26047642-4	2015	Here we show that bradykinin (BK) stimulation of HASMC increases amphiregulin secretion in a mechanism dependent on BK-induced COX-2 expression, increased PGE2 output, and the stimulation of HASMC EP2 and EP4 receptors.	hasmc	49-54	kininogen 1	Homo sapiens	18-28
26047642-4	2015	Here we show that bradykinin (BK) stimulation of HASMC increases amphiregulin secretion in a mechanism dependent on BK-induced COX-2 expression, increased PGE2 output, and the stimulation of HASMC EP2 and EP4 receptors.	hasmc	49-54	kininogen 1	Homo sapiens	30-32
26047642-4	2015	Here we show that bradykinin (BK) stimulation of HASMC increases amphiregulin secretion in a mechanism dependent on BK-induced COX-2 expression, increased PGE2 output, and the stimulation of HASMC EP2 and EP4 receptors.	hasmc	49-54	kininogen 1	Homo sapiens	116-118
26047642-4	2015	Here we show that bradykinin (BK) stimulation of HASMC increases amphiregulin secretion in a mechanism dependent on BK-induced COX-2 expression, increased PGE2 output, and the stimulation of HASMC EP2 and EP4 receptors.	Dinoprostone	155-159	kininogen 1	Homo sapiens	18-28
26047642-4	2015	Here we show that bradykinin (BK) stimulation of HASMC increases amphiregulin secretion in a mechanism dependent on BK-induced COX-2 expression, increased PGE2 output, and the stimulation of HASMC EP2 and EP4 receptors.	Dinoprostone	155-159	kininogen 1	Homo sapiens	30-32
26047642-5	2015	Conditioned medium from BK treated HASMC induced CXCL8, VEGF, and COX-2 mRNA and protein accumulation in airway epithelial cells, which were blocked by anti-amphiregulin antibodies and amphiregulin siRNA, suggesting a paracrine effect of HASMC-derived amphiregulin on airway epithelial cells.	hasmc	35-40	kininogen 1	Homo sapiens	24-26
26047642-5	2015	Conditioned medium from BK treated HASMC induced CXCL8, VEGF, and COX-2 mRNA and protein accumulation in airway epithelial cells, which were blocked by anti-amphiregulin antibodies and amphiregulin siRNA, suggesting a paracrine effect of HASMC-derived amphiregulin on airway epithelial cells.	hasmc	238-243	kininogen 1	Homo sapiens	24-26
26106828-4	2015	RECENT FINDINGS: Increased understanding of the pathogenesis of C1-INH-HAE allowed in recent years the development of new drugs targeted to inhibit bradykinin synthesis (Ecallantide) or activity (Icatibant).	ecallantide	170-181	kininogen 1	Homo sapiens	148-158
26068400-4	2015	The Phe(5/8) and Arg(9) residues of BK generally participated in the interactions with colloidal suspended Ag surfaces.	Arginine	17-20	kininogen 1	Homo sapiens	36-38
26046576-7	2015	Compare with controls (96.03% +- 6.2%), the maximal relaxation induced by bradykinin was significantly attenuated (61.55% +- 4.8%, p&lt;0.01), and significantly restored by L-citrulline (82.67 +- 6.4%, p&lt;0.05) after 24 hours of ADMA exposure.	Citrulline	173-185	kininogen 1	Homo sapiens	74-84
26046576-7	2015	Compare with controls (96.03% +- 6.2%), the maximal relaxation induced by bradykinin was significantly attenuated (61.55% +- 4.8%, p&lt;0.01), and significantly restored by L-citrulline (82.67 +- 6.4%, p&lt;0.05) after 24 hours of ADMA exposure.	N,N-dimethylarginine	231-235	kininogen 1	Homo sapiens	74-84
23764715-0	2015	In vitro comparison of bradykinin degradation by aliskiren, a renin inhibitor, and an inhibitor of angiotensin-converting enzyme.	aliskiren	49-58	kininogen 1	Homo sapiens	23-33
23764715-3	2015	We determined whether aliskiren, a renin inhibitor, has an effect on the rate of bradykinin degradation.	aliskiren	22-31	kininogen 1	Homo sapiens	81-91
23764715-8	2015	An inhibitory effect of aliskiren on the rate of bradykinin degradation by human pulmonary endothelial cells was observed, estimated to be about 5% of that of enalapril.	aliskiren	24-33	kininogen 1	Homo sapiens	49-59
25652142-3	2015	EXPERIMENTAL APPROACH: The effect of kaempferol on the relaxation of porcine coronary arteries to endothelium-dependent (bradykinin) and -independent (sodium nitroprusside) relaxing agents was studied in an in vitro organ chamber setup.	kaempferol	37-47	kininogen 1	Homo sapiens	121-131
25652142-5	2015	KEY RESULTS: At a concentration without direct effect on vascular tone, kaempferol (3 x 10(-6) M) enhanced relaxations produced by bradykinin and sodium nitroprusside.	kaempferol	72-82	kininogen 1	Homo sapiens	131-141
25970620-12	2015	Collectively, we report here for the first time that fibroblasts, KNG/BK, and BKRs are overexpressed in CRSsNP mucosa and BK upregulates chemokine expression, proliferation, and proinflammatory molecule expression in NMDFs via B2R activation, which lead to a functional increase in monocyte-fibroblast interaction.	nmdfs	217-222	kininogen 1	Homo sapiens	78-80
25290246-8	2015	Bradykinin-stimulated calcium influx is also decreased in PAH PASMC.	Calcium	22-29	kininogen 1	Homo sapiens	0-10
25873305-0	2015	Divergence in endothelin-1- and bradykinin-activated store-operated calcium entry in afferent sensory neurons.	Calcium	68-75	kininogen 1	Homo sapiens	32-42
25775573-8	2015	Kinetic studies were carried out in fused water droplets for acid-induced unfolding of cytochrome c and hydrogen-deuterium exchange in bradykinin.	Water	42-47	kininogen 1	Homo sapiens	135-145
25620134-6	2015	2-APB (TRPC &amp; TRPM antagonist) inhibited the maximum relaxation (Rmax) of the bradykinin-induced vasorelaxation and abolished the EDH-type response in PCAs from both sexes.	2-aminoethoxydiphenyl borate	0-5	kininogen 1	Homo sapiens	82-92
25620134-6	2015	2-APB (TRPC &amp; TRPM antagonist) inhibited the maximum relaxation (Rmax) of the bradykinin-induced vasorelaxation and abolished the EDH-type response in PCAs from both sexes.	trpc	7-11	kininogen 1	Homo sapiens	82-92
25620134-6	2015	2-APB (TRPC &amp; TRPM antagonist) inhibited the maximum relaxation (Rmax) of the bradykinin-induced vasorelaxation and abolished the EDH-type response in PCAs from both sexes.	Adenosine Monophosphate	13-16	kininogen 1	Homo sapiens	82-92
25620134-7	2015	SKF96365 (TRPC antagonist) inhibited the Rmax of bradykinin-induced vasorelaxation in males, and inhibited Rmax of the EDH-type response in both sexes.	1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole	0-8	kininogen 1	Homo sapiens	49-59
25620134-8	2015	Pyr3 (TRPC3 antagonist) inhibited both the NO and EDH components of the bradykinin-induced vasorelaxation in males, but not females.	EDH	50-53	kininogen 1	Homo sapiens	72-82
25879450-7	2015	Des-Arg(1)-bradykinin was released from LK by Sap9 at a comparably high yield, but this peptide was assumed to be biologically inactive because it was unable to interact with cellular B2-type kinin receptors.	des-arg	0-7	kininogen 1	Homo sapiens	11-21
25290246-8	2015	Bradykinin-stimulated calcium influx is also decreased in PAH PASMC.	pasmc	62-67	kininogen 1	Homo sapiens	0-10
25584415-5	2015	EGF and BK solely increased Ser-727 and IFN-gamma increased Tyr-705 phosphorylation of STAT-3.	Serine	28-31	kininogen 1	Homo sapiens	8-10
25584415-6	2015	Specific inhibition of ERK-1/2 activity blocked EGF- and BK-induced STAT-3 activation and Ser-727 phosphorylation.	Serine	90-93	kininogen 1	Homo sapiens	57-59
25838788-0	2015	An IMS-IMS threshold method for semi-quantitative determination of activation barriers: Interconversion of proline cis trans forms in triply protonated bradykinin.	Proline	107-114	kininogen 1	Homo sapiens	152-162
25775573-8	2015	Kinetic studies were carried out in fused water droplets for acid-induced unfolding of cytochrome c and hydrogen-deuterium exchange in bradykinin.	Hydrogen	104-112	kininogen 1	Homo sapiens	135-145
25775573-8	2015	Kinetic studies were carried out in fused water droplets for acid-induced unfolding of cytochrome c and hydrogen-deuterium exchange in bradykinin.	Deuterium	113-122	kininogen 1	Homo sapiens	135-145
25477429-7	2015	Two of these loci replicated in an independent sample for both plasma renin and aldosterone concentrations (SNP rs5030062 in kininogen 1 [KNG1]: P=0.001 for plasma renin, P=0.024 for plasma aldosterone concentration; and rs4253311 with P&lt;0.001 for both plasma renin and aldosterone concentration).	Aldosterone	80-91	kininogen 1	Homo sapiens	138-142
25477429-7	2015	Two of these loci replicated in an independent sample for both plasma renin and aldosterone concentrations (SNP rs5030062 in kininogen 1 [KNG1]: P=0.001 for plasma renin, P=0.024 for plasma aldosterone concentration; and rs4253311 with P&lt;0.001 for both plasma renin and aldosterone concentration).	Aldosterone	80-91	kininogen 1	Homo sapiens	125-136
25650214-0	2015	Lesson of the month 2: The limitations of steroid therapy in bradykinin-mediated angioedema attacks.	Steroids	42-49	kininogen 1	Homo sapiens	61-71
25838788-3	2015	The energetic barriers between six conformations of [BK+3H]3+ range from 0.23 +-0.01 to 0.55 +-0.03 eV.	Tritium	56-58	kininogen 1	Homo sapiens	53-55
25838788-6	2015	The combination of structural assignments, experimentally determined barrier heights, onset of the quasi-equilibrium region, and dissociation threshold are used to derive a semi-quantitative potential energy surface for main features of [BK+3H]3+.	Tritium	241-243	kininogen 1	Homo sapiens	238-240
24875192-7	2015	Notably, a variety of secreted paracrine and autocrine agents such as bradykinin, ATP, endothelin, nitric oxide, and prostaglandin E2 counterbalance and limit the natriferic effects of aldosterone and the water-retaining effects of AVP.	Aldosterone	185-196	kininogen 1	Homo sapiens	70-80
25468883-9	2015	In isometric myography on porcine coronary arteries, RA-2 inhibited bradykinin-induced endothelium-derived hyperpolarization (EDH)-type relaxation in U46619-precontracted rings.	EDH	126-129	kininogen 1	Homo sapiens	68-78
24875192-7	2015	Notably, a variety of secreted paracrine and autocrine agents such as bradykinin, ATP, endothelin, nitric oxide, and prostaglandin E2 counterbalance and limit the natriferic effects of aldosterone and the water-retaining effects of AVP.	Water	205-210	kininogen 1	Homo sapiens	70-80
25874051-3	2015	Due to destructive effects of bradykinin on the nervous system in ischemic stroke, it seems reasonable that using Noscapine as a Bradykinin antagonist may improve patients" outcome after ischemic stroke.	Noscapine	114-123	kininogen 1	Homo sapiens	30-40
26517864-9	2015	Moreover, the NO synthase antagonist L-NAME and PI3K inhibitor LY294002 dramatically abolished the inhibitory effects of bradykinin on tissue factor expression.	NG-Nitroarginine Methyl Ester	37-43	kininogen 1	Homo sapiens	121-131
26517864-9	2015	Moreover, the NO synthase antagonist L-NAME and PI3K inhibitor LY294002 dramatically abolished the inhibitory effects of bradykinin on tissue factor expression.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	63-71	kininogen 1	Homo sapiens	121-131
25241342-3	2014	We have previously shown that bradykinin (BK) induces both a reversible dissipation of vinculin from FAs, by the phospholipase C (PLC)-mediated hydrolysis of PtdIns(4,5)P2, and the concomitant internalization of vinculin.	Phosphatidylinositol 4,5-Diphosphate	158-171	kininogen 1	Homo sapiens	30-40
25874051-3	2015	Due to destructive effects of bradykinin on the nervous system in ischemic stroke, it seems reasonable that using Noscapine as a Bradykinin antagonist may improve patients" outcome after ischemic stroke.	Noscapine	114-123	kininogen 1	Homo sapiens	129-139
24899570-8	2015	Both serum and synovial fluid samples showed significant decreases for a majority of inflammatory cytokines, leptin, and bradykinin in the oral hyaluronic acid preparation group.	Hyaluronic Acid	144-159	kininogen 1	Homo sapiens	121-131
24985363-0	2015	Erratum to: The effects of an oral preparation containing hyaluronic acid (Oralvisc( )) on obese knee osteoarthritis patients determined by pain, function, bradykinin, leptin, inflammatory cytokines, and heavy water analyses.	Hyaluronic Acid	58-73	kininogen 1	Homo sapiens	156-166
25817868-0	2015	Control of ENaC-mediated sodium reabsorption in the distal nephron by Bradykinin.	Sodium	25-31	kininogen 1	Homo sapiens	70-80
25817868-2	2015	Apart from being a vasodilator, BK also increases urinary sodium excretion to reduce systemic blood pressure.	Sodium	58-64	kininogen 1	Homo sapiens	32-34
25817868-3	2015	It is becoming appreciated that BK modulates function of the epithelial Na(+) channel in the distal part of the renal nephron to affect tubular sodium reabsorption.	Sodium	144-150	kininogen 1	Homo sapiens	32-34
25546407-8	2014	The maximal relaxant response to the endothelium-dependent dilators ACh and BK were lower in HD patients (P&lt;0.01-P&lt;0.0001) (worse for ACh than BK); however the endothelium-independent dilator SNP was similar in both groups.	Acetylcholine	68-71	kininogen 1	Homo sapiens	149-151
25241342-3	2014	We have previously shown that bradykinin (BK) induces both a reversible dissipation of vinculin from FAs, by the phospholipase C (PLC)-mediated hydrolysis of PtdIns(4,5)P2, and the concomitant internalization of vinculin.	Phosphatidylinositol 4,5-Diphosphate	158-171	kininogen 1	Homo sapiens	42-44
25056222-7	2014	The proliferative effects induced by the incubation of des-Arg(9)-BK and BK are likely related to the activation of PI3K/Akt and ERK 1/2 pathways.	des-arg	55-62	kininogen 1	Homo sapiens	66-68
25194042-6	2014	To test if bleb formation is related to bradykinin-promoted glioma invasion we blocked glioma migration with blebbistatin, a blocker of myosin kinase II, which is necessary for proper bleb retraction.	blebbistatin	109-121	kininogen 1	Homo sapiens	40-50
24924235-6	2014	The positive bradykinin-induced effect on the cell-cell interaction was reversed by a carboxypeptidase inhibitor (MGTA), hence we suspected a significant role of the des-Arg kinin metabolites, which acted through the kinin receptor type 1.	mgta	114-118	kininogen 1	Homo sapiens	13-23
24833299-0	2014	Bradykinin induces NO and PGF2alpha production via B2 receptor activation from cultured porcine basilar arterial endothelial cells.	Dinoprost	26-35	kininogen 1	Homo sapiens	0-10
25368550-8	2014	Vasoinhibins also prevented the BK-induced actin cytoskeleton redistribution, as did L-NAME.	NG-Nitroarginine Methyl Ester	85-91	kininogen 1	Homo sapiens	32-34
25368550-9	2014	BK transiently decreased human RPE (ARPE-19) cell monolayer resistance, and this effect was blocked by vasoinhibins, L-NAME, and NAC.	NG-Nitroarginine Methyl Ester	117-123	kininogen 1	Homo sapiens	0-2
25368550-9	2014	BK transiently decreased human RPE (ARPE-19) cell monolayer resistance, and this effect was blocked by vasoinhibins, L-NAME, and NAC.	Acetylcysteine	129-132	kininogen 1	Homo sapiens	0-2
25368550-11	2014	Similar to BK, the radical initiator Luperox induced a reduction in ARPE-19 cell monolayer resistance, which was prevented by vasoinhibins.	dicumyl peroxide	37-44	kininogen 1	Homo sapiens	11-13
25505603-6	2014	When bradykinin was used to induce endogenous PGE2 release, PGT expression similarly induced a reduction in Ca(2+) responses.	Dinoprostone	46-50	kininogen 1	Homo sapiens	5-15
25505603-8	2014	As in the EP1 experiments, expression of PGT at the plasma membrane caused a reduction in bradykinin-induced cAMP accumulation.	Cyclic AMP	109-113	kininogen 1	Homo sapiens	90-100
24960080-0	2014	Endothelium-derived nitric oxide (NO) activates the NO-epidermal growth factor receptor-mediated signaling pathway in bradykinin-stimulated angiogenesis.	Nitric Oxide	20-32	kininogen 1	Homo sapiens	118-128
24960080-2	2014	Stimulation of different endothelial cell lines with bradykinin (BK) activates the endothelial NO synthase (eNOS) and promotes EGF-R tyrosine phosphorylation.	Tyrosine	133-141	kininogen 1	Homo sapiens	53-63
24960080-2	2014	Stimulation of different endothelial cell lines with bradykinin (BK) activates the endothelial NO synthase (eNOS) and promotes EGF-R tyrosine phosphorylation.	Tyrosine	133-141	kininogen 1	Homo sapiens	65-67
24960080-10	2014	BK-induced proliferation of endothelial cells was partially inhibited by the NOS inhibitor (L-NAME) and by the MEK inhibitor (PD98059).	NG-Nitroarginine Methyl Ester	92-98	kininogen 1	Homo sapiens	0-2
24960080-10	2014	BK-induced proliferation of endothelial cells was partially inhibited by the NOS inhibitor (L-NAME) and by the MEK inhibitor (PD98059).	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	126-133	kininogen 1	Homo sapiens	0-2
24960080-14	2014	Additionally, pre-treatment of BK-stimulated HUVEC with L-NAME, PD98059, and with SU5416, a specific inhibitor of VEGFR resulted in inhibition of in vitro angiogenesis.	NG-Nitroarginine Methyl Ester	56-62	kininogen 1	Homo sapiens	31-33
24960080-14	2014	Additionally, pre-treatment of BK-stimulated HUVEC with L-NAME, PD98059, and with SU5416, a specific inhibitor of VEGFR resulted in inhibition of in vitro angiogenesis.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	64-71	kininogen 1	Homo sapiens	31-33
24960080-14	2014	Additionally, pre-treatment of BK-stimulated HUVEC with L-NAME, PD98059, and with SU5416, a specific inhibitor of VEGFR resulted in inhibition of in vitro angiogenesis.	Semaxinib	82-88	kininogen 1	Homo sapiens	31-33
24675657-7	2014	Inhibition with N(G)-monomethyl-L-arginine was greater in whites compared with blacks with bradykinin, acetylcholine, and exercise.	omega-N-Methylarginine	16-42	kininogen 1	Homo sapiens	91-101
24675657-8	2014	Inhibition with tetraethylammonium was lower in blacks with bradykinin, but greater during exercise and with acetylcholine.	Tetraethylammonium	16-34	kininogen 1	Homo sapiens	60-70
24467384-11	2014	In male PCAs, at maximum bradykinin concentration, the EDH-mediated response was reduced in the presence of apamin but not TRAM-34.	EDH	55-58	kininogen 1	Homo sapiens	25-35
25168672-7	2014	Acute focal application of M or KATP channel enhancers or a hyperpolarization-activated cyclic nucleotide-gated channel blocker to L5 DRG in vivo significantly alleviated pain induced by hind paw injection of bradykinin.	Nucleotides, Cyclic	88-105	kininogen 1	Homo sapiens	209-219
24648264-9	2014	Moreover, bradykinin and C3- and C4-derived peptides were produced promptly after blood extraction when samples were collected into conventional EDTA tubes, and the use of PI prevented their generation.	Edetic Acid	145-149	kininogen 1	Homo sapiens	10-20
24920677-6	2014	The bradykinin-mediated activation of TRPM7 also led to a greater increase in [Mg(2+)]cyt in IPAH-PASMC than in normal PASMC.	magnesium ion	79-85	kininogen 1	Homo sapiens	4-14
24920677-6	2014	The bradykinin-mediated activation of TRPM7 also led to a greater increase in [Mg(2+)]cyt in IPAH-PASMC than in normal PASMC.	ipah-pasmc	93-103	kininogen 1	Homo sapiens	4-14
24920677-6	2014	The bradykinin-mediated activation of TRPM7 also led to a greater increase in [Mg(2+)]cyt in IPAH-PASMC than in normal PASMC.	pasmc	98-103	kininogen 1	Homo sapiens	4-14
24957134-9	2014	In addition, our organ bath studies showed that Salix procyanidins reversed the abrogation of the relaxant response to bradykinin by oxidized low-density lipoproteins (oxLDL) in coronary arteries, suggesting a vasoprotective effect of willow bark against detrimental oxLDL in pathological conditions.	salix procyanidins	48-66	kininogen 1	Homo sapiens	119-129
24833299-9	2014	The cultured PBAECs produced PGD2, PGE2, and PGF2alpha spontaneously, and BK significantly enhanced the production of PGF2alpha, but not that of PGD2 and PGE2.	Dinoprost	118-127	kininogen 1	Homo sapiens	74-76
24833299-10	2014	The B2, but not B1, antagonist completely abolished the BK-enhanced production of PGF2alpha.	Dinoprost	82-91	kininogen 1	Homo sapiens	56-58
24833299-11	2014	These results suggest that BK induces production of NO and PGF2alpha simultaneously from PBAECs via B2 receptor activation.	Dinoprost	59-68	kininogen 1	Homo sapiens	27-29
24816515-2	2014	We hypothesized that melatonin supplementation in a compromised pregnancy enhances the bradykinin (BK)-induced relaxations of placental arteries thereby ensuring sufficient umbilical blood flow to the developing fetus.	Melatonin	21-30	kininogen 1	Homo sapiens	87-97
24816515-2	2014	We hypothesized that melatonin supplementation in a compromised pregnancy enhances the bradykinin (BK)-induced relaxations of placental arteries thereby ensuring sufficient umbilical blood flow to the developing fetus.	Melatonin	21-30	kininogen 1	Homo sapiens	99-101
24816515-11	2014	CONCLUSION: An increase in placental vessel sensitivity to bradykinin-induced relaxation may contribute to melatonin-induced increases in umbilical artery blood flow.	Melatonin	107-116	kininogen 1	Homo sapiens	59-69
24936247-3	2014	However, evidence suggests that adenosine, released during the initial ischemic insult, activates a variety of G protein-coupled agonists, such as opioids, bradykinin, and catecholamines, resulting in the activation of protein kinases, especially protein kinase C (PKC).	Adenosine	32-41	kininogen 1	Homo sapiens	156-166
24846348-6	2014	Highly abundant proteins such as serum albumin, serotransferrin, prothrombin, alpha-fetoprotein, and kininogen-1 were commonly found on both PVA- and dextran-coated SPIONs.	pva	141-144	kininogen 1	Homo sapiens	101-112
24846348-6	2014	Highly abundant proteins such as serum albumin, serotransferrin, prothrombin, alpha-fetoprotein, and kininogen-1 were commonly found on both PVA- and dextran-coated SPIONs.	Dextrans	150-157	kininogen 1	Homo sapiens	101-112
24886333-9	2014	Functional diversity was observed between clonal populations with 10 muM isoproterenol-induced cyclic AMP responses ranging from 1.4 - 5.4 fold cf basal and bradykinin-induced inositol phosphate from 1.8 - 5.2 fold cf basal.	Isoproterenol	73-86	kininogen 1	Homo sapiens	157-167
24886333-9	2014	Functional diversity was observed between clonal populations with 10 muM isoproterenol-induced cyclic AMP responses ranging from 1.4 - 5.4 fold cf basal and bradykinin-induced inositol phosphate from 1.8 - 5.2 fold cf basal.	Cyclic AMP	95-105	kininogen 1	Homo sapiens	157-167
24886333-9	2014	Functional diversity was observed between clonal populations with 10 muM isoproterenol-induced cyclic AMP responses ranging from 1.4 - 5.4 fold cf basal and bradykinin-induced inositol phosphate from 1.8 - 5.2 fold cf basal.	Inositol Phosphates	176-194	kininogen 1	Homo sapiens	157-167
24516103-2	2014	Dipeptidyl peptidase-4 degrades other peptides with a penultimate proline or alanine, including bradykinin and substance P, which are also substrates of angiotensin-converting enzyme (ACE).	Proline	66-73	kininogen 1	Homo sapiens	96-106
24516103-2	2014	Dipeptidyl peptidase-4 degrades other peptides with a penultimate proline or alanine, including bradykinin and substance P, which are also substrates of angiotensin-converting enzyme (ACE).	Alanine	77-84	kininogen 1	Homo sapiens	96-106
24516103-8	2014	Enalaprilat increased bradykinin-stimulated vasodilation and tissue plasminogen activator release; sitagliptin did not affect these responses to bradykinin.	Enalaprilat	0-11	kininogen 1	Homo sapiens	22-32
24390175-4	2014	Bradykinin caused concentration-dependent and endothelium-dependent relaxations that were not affected by DIZE but were potentiated to a similar extent by angiotensin-(1-7) and captopril, given alone or in combination.	Captopril	177-186	kininogen 1	Homo sapiens	0-10
24390175-5	2014	Bradykinin responses potentiated by angiotensin-(1-7) and captopril were not affected by the BK1 antagonist SSR240612 and remained augmented in the presence of either N-nitro-L-arginine methyl ester hydrochloride plus indomethacin or TRAM-34 plus UCL-1684.	Captopril	58-67	kininogen 1	Homo sapiens	0-10
24390175-5	2014	Bradykinin responses potentiated by angiotensin-(1-7) and captopril were not affected by the BK1 antagonist SSR240612 and remained augmented in the presence of either N-nitro-L-arginine methyl ester hydrochloride plus indomethacin or TRAM-34 plus UCL-1684.	L-NAME hydrochloride	167-212	kininogen 1	Homo sapiens	0-10
24390175-5	2014	Bradykinin responses potentiated by angiotensin-(1-7) and captopril were not affected by the BK1 antagonist SSR240612 and remained augmented in the presence of either N-nitro-L-arginine methyl ester hydrochloride plus indomethacin or TRAM-34 plus UCL-1684.	Indomethacin	218-230	kininogen 1	Homo sapiens	0-10
24390175-5	2014	Bradykinin responses potentiated by angiotensin-(1-7) and captopril were not affected by the BK1 antagonist SSR240612 and remained augmented in the presence of either N-nitro-L-arginine methyl ester hydrochloride plus indomethacin or TRAM-34 plus UCL-1684.	6,10-diaza-3(1,3),8(1,4)dibenzena-1,5(1,4)diquinolinacyclodecaphane	247-255	kininogen 1	Homo sapiens	0-10
24390175-7	2014	These results suggest that in coronary arteries, angiotensin-(1-7) and captopril both improves NO bioavailability and enhances endothelium-dependent hyperpolarization to bradykinin solely by ACE1 inhibition.	Captopril	71-80	kininogen 1	Homo sapiens	170-180
24639651-1	2014	While bradykinin (BK) is known to be degraded by angiotensin converting enzyme (ACE), we have recently discovered that Met-Lys-BK-Ser-Ser is paradoxically activated by ACE.	Serine	130-133	kininogen 1	Homo sapiens	6-16
24023037-1	2014	We evaluated the bradykinin generation level during leukocytapheresis (LCAP) using novel Cellsorba(TM) CS-180S, which has sodium pyrosulfite and sodium carbonate as a filling solution.	sodium metabisulfite	122-140	kininogen 1	Homo sapiens	17-27
24023037-3	2014	Regardless of the type of anticoagulant used, bradykinin levels were lower with the novel CS-180S than with the conventional CS-180S (28.7 +- 53.3 vs. 8.0 +- 2.7 as the mean +- standard deviation).	Cesium	90-92	kininogen 1	Homo sapiens	46-56
24023037-3	2014	Regardless of the type of anticoagulant used, bradykinin levels were lower with the novel CS-180S than with the conventional CS-180S (28.7 +- 53.3 vs. 8.0 +- 2.7 as the mean +- standard deviation).	Cesium	125-127	kininogen 1	Homo sapiens	46-56
24485840-8	2014	In the paper we review studies on hemodynamic effects of catecholamines, neuropeptide Y, angiotensin II, aldosterone, natriuretic peptides, endothelins, histamine and bradykinin in the context of their role in a cross-talk between peripheral and brain mechanisms involved in the regulation of arterial blood pressure.	Catecholamines	57-71	kininogen 1	Homo sapiens	167-177
24639651-1	2014	While bradykinin (BK) is known to be degraded by angiotensin converting enzyme (ACE), we have recently discovered that Met-Lys-BK-Ser-Ser is paradoxically activated by ACE.	Serine	130-133	kininogen 1	Homo sapiens	18-20
24639651-1	2014	While bradykinin (BK) is known to be degraded by angiotensin converting enzyme (ACE), we have recently discovered that Met-Lys-BK-Ser-Ser is paradoxically activated by ACE.	Serine	130-133	kininogen 1	Homo sapiens	127-129
24639651-4	2014	Of three BK sequences extended by a C-terminal dipeptide, BK-His-Leu had the most desirable profile, exhibiting little direct affinity for the receptor but a significant one for ACE (as shown by competition of [(3)H]BK binding to B2R-GFP or of [(3)H]enalaprilat to recombinant ACE, respectively).	Dipeptides	47-56	kininogen 1	Homo sapiens	58-60
24639651-4	2014	Of three BK sequences extended by a C-terminal dipeptide, BK-His-Leu had the most desirable profile, exhibiting little direct affinity for the receptor but a significant one for ACE (as shown by competition of [(3)H]BK binding to B2R-GFP or of [(3)H]enalaprilat to recombinant ACE, respectively).	Dipeptides	47-56	kininogen 1	Homo sapiens	58-60
24639651-4	2014	Of three BK sequences extended by a C-terminal dipeptide, BK-His-Leu had the most desirable profile, exhibiting little direct affinity for the receptor but a significant one for ACE (as shown by competition of [(3)H]BK binding to B2R-GFP or of [(3)H]enalaprilat to recombinant ACE, respectively).	Leucine	65-68	kininogen 1	Homo sapiens	9-11
24639651-4	2014	Of three BK sequences extended by a C-terminal dipeptide, BK-His-Leu had the most desirable profile, exhibiting little direct affinity for the receptor but a significant one for ACE (as shown by competition of [(3)H]BK binding to B2R-GFP or of [(3)H]enalaprilat to recombinant ACE, respectively).	Leucine	65-68	kininogen 1	Homo sapiens	58-60
24639651-4	2014	Of three BK sequences extended by a C-terminal dipeptide, BK-His-Leu had the most desirable profile, exhibiting little direct affinity for the receptor but a significant one for ACE (as shown by competition of [(3)H]BK binding to B2R-GFP or of [(3)H]enalaprilat to recombinant ACE, respectively).	Leucine	65-68	kininogen 1	Homo sapiens	58-60
24639651-4	2014	Of three BK sequences extended by a C-terminal dipeptide, BK-His-Leu had the most desirable profile, exhibiting little direct affinity for the receptor but a significant one for ACE (as shown by competition of [(3)H]BK binding to B2R-GFP or of [(3)H]enalaprilat to recombinant ACE, respectively).	Enalaprilat	250-261	kininogen 1	Homo sapiens	58-60
24639651-4	2014	Of three BK sequences extended by a C-terminal dipeptide, BK-His-Leu had the most desirable profile, exhibiting little direct affinity for the receptor but a significant one for ACE (as shown by competition of [(3)H]BK binding to B2R-GFP or of [(3)H]enalaprilat to recombinant ACE, respectively).	Enalaprilat	250-261	kininogen 1	Homo sapiens	58-60
24639651-5	2014	The potency of the contractile effect of this analog on the vein was reduced 18-fold by the ACE inhibitor enalaprilat, pharmacologically evidencing BK regeneration in situ.	Enalaprilat	106-117	kininogen 1	Homo sapiens	148-150
24639651-7	2014	B2R-GFP internalization in response to 100 nM of the extended peptides recapitulated these findings, as enalaprilat selectively inhibited the effect of BK-His-Leu and Plummer"s inhibitor, that of BK-Arg.	Enalaprilat	104-115	kininogen 1	Homo sapiens	152-154
24639651-9	2014	The novel C-terminally extended BKs had no or very little affinity for the kinin B1 receptor (competition of [(3)H]Lys-des-Arg(9)-BK binding).	lys-des-arg	115-126	kininogen 1	Homo sapiens	32-34
24138103-6	2014	Thiorphan, captopril, and omapatrilat all enhanced the vasodilator response to bradykinin (all P &lt; 0.01).	Thiorphan	0-9	kininogen 1	Homo sapiens	79-89
24356973-2	2014	To demonstrate application potentials, these bdk alcohols are used to chelate with various Lewis acids, including Tb (III), Eu (III), and B (III).	Alcohols	49-57	kininogen 1	Homo sapiens	45-48
24356973-2	2014	To demonstrate application potentials, these bdk alcohols are used to chelate with various Lewis acids, including Tb (III), Eu (III), and B (III).	Lewis Acids	91-102	kininogen 1	Homo sapiens	45-48
24356973-2	2014	To demonstrate application potentials, these bdk alcohols are used to chelate with various Lewis acids, including Tb (III), Eu (III), and B (III).	Terbium	114-116	kininogen 1	Homo sapiens	45-48
24839774-0	2014	Bradykinin stimulation of nitric oxide production is not sufficient for gamma-globin induction.	Nitric Oxide	26-38	kininogen 1	Homo sapiens	0-10
24584737-0	2014	Acute intravenous injection of serelaxin (recombinant human relaxin-2) causes rapid and sustained bradykinin-mediated vasorelaxation.	serelaxin protein, human	31-40	kininogen 1	Homo sapiens	98-108
24584737-6	2014	Serelaxin treatment also selectively enhanced bradykinin-mediated endothelium-dependent relaxation.	serelaxin protein, human	0-9	kininogen 1	Homo sapiens	46-56
24584737-8	2014	Serelaxin-mediated augmentation of bradykinin-evoked relaxation involved endothelium-derived hyperpolarization after 3 hours and prostacyclin-mediated relaxation after 24 hours.	serelaxin protein, human	0-9	kininogen 1	Homo sapiens	35-45
24584737-8	2014	Serelaxin-mediated augmentation of bradykinin-evoked relaxation involved endothelium-derived hyperpolarization after 3 hours and prostacyclin-mediated relaxation after 24 hours.	Epoprostenol	129-141	kininogen 1	Homo sapiens	35-45
24117346-1	2014	The efficacy of the ACE (angiotensin-converting enzyme) inhibitor perindopril in coronary artery disease [EUROPA (European trial on reduction of cardiac events with perindopril in stable coronary artery disease) study] is associated with the rs12050217 A/G single nucleotide polymorphism in the B1 receptor (bradykinin type 1 receptor) gene.	Perindopril	66-77	kininogen 1	Homo sapiens	308-318
24117346-3	2014	Vasorelaxant responses of human coronary microarteries from subjects without coronary disease to des-Arg(9)-bradykinin and to bradykinin were studied in organ bath experiments.	des-arg	97-104	kininogen 1	Homo sapiens	108-118
24117346-4	2014	Des-Arg9-bradykinin responses were endothelium-dependent and exclusively mediated by B1 receptors, whereas responses to bradykinin were induced through B2 receptors (bradykinin type 2 receptors).	des-arg9	0-8	kininogen 1	Homo sapiens	9-19
24117346-5	2014	The presence of the G allele reduced the response to 3 x 10(-8) mol/l des-Arg(9)-bradykinin by 29% [AA (n=13) compared with AG/GG (n=8); P&lt;0.03], and tended to lower concentration-related responses (P=0.065) to this agonist, whereas the responses to bradykinin were unaffected by the rs12050217 genotype.	des-arg	70-77	kininogen 1	Homo sapiens	81-91
24117346-6	2014	In freshly obtained human mononuclear cells 1 mumol/l des-Arg(9)-bradykinin increased expression of the pro-inflammatory factors CXCL5 (CXC chemokine ligand 5) and IL6 (interleukin-6).	des-arg	54-61	kininogen 1	Homo sapiens	65-75
24138103-6	2014	Thiorphan, captopril, and omapatrilat all enhanced the vasodilator response to bradykinin (all P &lt; 0.01).	Captopril	11-20	kininogen 1	Homo sapiens	79-89
24138103-6	2014	Thiorphan, captopril, and omapatrilat all enhanced the vasodilator response to bradykinin (all P &lt; 0.01).	omapatrilat	26-37	kininogen 1	Homo sapiens	79-89
24138103-9	2014	CONCLUSIONS: NEP inhibition with thiorphan modestly augmented the vasodilator action of bradykinin, but did not potentiate the response to adrenomedullin; dual ACE and NEP inhibition with omapatrilat, as expected, markedly augmented the response to bradykinin and also potentiated the effect of adrenomedullin.	Thiorphan	33-42	kininogen 1	Homo sapiens	88-98
24138103-9	2014	CONCLUSIONS: NEP inhibition with thiorphan modestly augmented the vasodilator action of bradykinin, but did not potentiate the response to adrenomedullin; dual ACE and NEP inhibition with omapatrilat, as expected, markedly augmented the response to bradykinin and also potentiated the effect of adrenomedullin.	Thiorphan	33-42	kininogen 1	Homo sapiens	249-259
24138103-9	2014	CONCLUSIONS: NEP inhibition with thiorphan modestly augmented the vasodilator action of bradykinin, but did not potentiate the response to adrenomedullin; dual ACE and NEP inhibition with omapatrilat, as expected, markedly augmented the response to bradykinin and also potentiated the effect of adrenomedullin.	omapatrilat	188-199	kininogen 1	Homo sapiens	249-259
24312564-6	2013	Bradykinin and adenosine triphosphate, ligands of phospholipase C-coupled membrane receptors, increased the content of 2-arachidonoylglycerol in dorsal root ganglia.	glyceryl 2-arachidonate	119-141	kininogen 1	Homo sapiens	0-10
24466329-4	2014	Pretreatment with the protein synthesis inhibitor cycloheximide or the protein kinase C inhibitor calphostin C prior to the addition of TNF completely abrogated the TNF-induced increment in peak bradykinin response.	Cycloheximide	50-63	kininogen 1	Homo sapiens	195-205
24466329-4	2014	Pretreatment with the protein synthesis inhibitor cycloheximide or the protein kinase C inhibitor calphostin C prior to the addition of TNF completely abrogated the TNF-induced increment in peak bradykinin response.	calphostin C	98-110	kininogen 1	Homo sapiens	195-205
24466329-6	2014	Exposing fibroblasts for 48 hours to 2 mM oleate also increased both the peak bradykinin response and the TNF-induced increment in peak response, which were significantly greater in diabetics than controls.	Oleic Acid	42-48	kininogen 1	Homo sapiens	78-88
24839598-4	2014	Others have demonstrated that bradykinin increased stretch-induced ATP release; however, we observed no change in control or stretch-induced ATP release with bradykinin.	Adenosine Triphosphate	67-70	kininogen 1	Homo sapiens	30-40
24678506-2	2014	With respect to stability of the cell membrane, it has been reported that bradykinin-induced nociceptive responses are significantly suppressed by the direct application of D-glucosamine.	Glucosamine	173-186	kininogen 1	Homo sapiens	74-84
24584737-12	2014	The prolonged bradykinin-mediated vasorelaxation is principally mediated through prostacyclin.	Epoprostenol	81-93	kininogen 1	Homo sapiens	14-24
24925394-3	2014	This occurs because ACE metabolizes bradykinin by removal of Phe-Arg from the C-terminus, which inactivates it.	phenylalanylarginine	61-68	kininogen 1	Homo sapiens	36-46
24492696-6	2014	Furthermore, the HMWK activity was also reduced in the patient"s three children, who exhibited the heterozygous "TC" insertion at c523-524 in exon 4.	Technetium	113-115	kininogen 1	Homo sapiens	17-21
24925526-2	2014	Although BK stimulates both nitric oxide and endothelium-derived hyperpolarizing factor (EDHF) release, the role of EDHF in t-PA release remains unexplored.	Nitric Oxide	28-40	kininogen 1	Homo sapiens	9-11
24925526-2	2014	Although BK stimulates both nitric oxide and endothelium-derived hyperpolarizing factor (EDHF) release, the role of EDHF in t-PA release remains unexplored.	-derived hyperpolarizing factor	56-87	kininogen 1	Homo sapiens	9-11
24925526-2	2014	Although BK stimulates both nitric oxide and endothelium-derived hyperpolarizing factor (EDHF) release, the role of EDHF in t-PA release remains unexplored.	edhf	89-93	kininogen 1	Homo sapiens	9-11
24925526-7	2014	Fluconazole attenuated both BK-mediated vasodilation (-23.3 +- 2.7% FBF, p &lt; 0.0001) and t-PA release (from 50.9 +- 9.0 to 21.3 +- 8.9 ng/min/100 ml, p = 0.02).	Fluconazole	0-11	kininogen 1	Homo sapiens	28-30
24925526-10	2014	CONCLUSION: BK-stimulated t-PA release is partly due to cytochrome P450-derived epoxides and is inhibited by K(+)Ca channel blockade.	Epoxy Compounds	80-88	kininogen 1	Homo sapiens	12-14
24925526-11	2014	Thus, BK stimulates both EDHF-dependent vasodilation and t-PA release.	edhf	25-29	kininogen 1	Homo sapiens	6-8
25130038-5	2014	Bradykinin is pharmacologically active polypeptide that can promote both cardiovascular and renal function, for example, vasodilation, natriuresis, diuresis, and release of nitric oxide (NO).	Nitric Oxide	173-185	kininogen 1	Homo sapiens	0-10
23846330-6	2013	RESULTS: Exposure to Hcy for 24 h attenuated bradykinin-induced relaxation and NO release, downregulated eNOS mRNA expression and protein expressions of eNOS and p-eNOS(Ser1177) whereas it upregulated iNOS expression.	Homocysteine	21-24	kininogen 1	Homo sapiens	45-55
23954712-7	2013	The analysis of the stability of SAPP-generated kinins in plasma suggested that they are biologically equivalent to bradykinin, the best agonist of B2 receptor subtype and can be quickly converted to des-Arg(9)-bradykinin, the agonist of inflammation-inducible B1 receptors.	des-arg	200-207	kininogen 1	Homo sapiens	116-126
24016859-2	2013	First, a peptide consisting of the antihistamine cetirizine (CTZ) condensed at the N-terminus of epsilon-aminocaproyl-bradykinin (epsilonACA-BK) was evaluated for an antihistamine activity that could be revealed by degradation of the peptide part of the molecule.	Cetirizine	49-59	kininogen 1	Homo sapiens	118-128
24016859-2	2013	First, a peptide consisting of the antihistamine cetirizine (CTZ) condensed at the N-terminus of epsilon-aminocaproyl-bradykinin (epsilonACA-BK) was evaluated for an antihistamine activity that could be revealed by degradation of the peptide part of the molecule.	Cetirizine	61-64	kininogen 1	Homo sapiens	118-128
23954712-7	2013	The analysis of the stability of SAPP-generated kinins in plasma suggested that they are biologically equivalent to bradykinin, the best agonist of B2 receptor subtype and can be quickly converted to des-Arg(9)-bradykinin, the agonist of inflammation-inducible B1 receptors.	des-arg	200-207	kininogen 1	Homo sapiens	211-221
24047499-0	2013	Bradykinin-induced Ca2+ signaling in human subcutaneous fibroblasts involves ATP release via hemichannels leading to P2Y12 receptors activation.	Adenosine Triphosphate	77-80	kininogen 1	Homo sapiens	0-10
24047499-4	2013	Here, we investigated the involvement of ATP in bradykinin-induced Ca2+ signals in human subcutaneous fibroblasts.	Adenosine Triphosphate	41-44	kininogen 1	Homo sapiens	48-58
24047499-8	2013	Human subcutaneous fibroblasts respond to bradykinin by releasing ATP via connexin and pannexin hemichannels, since blockade of connexins, with 2-octanol or carbenoxolone, and pannexin-1, with 10Panx, attenuated bradykinin-induced [Ca2+]i plateau, whereas inhibitors of vesicular exocytosis, such as brefeldin A and bafilomycin A1, were inactive.	Adenosine Triphosphate	66-69	kininogen 1	Homo sapiens	42-52
24047499-8	2013	Human subcutaneous fibroblasts respond to bradykinin by releasing ATP via connexin and pannexin hemichannels, since blockade of connexins, with 2-octanol or carbenoxolone, and pannexin-1, with 10Panx, attenuated bradykinin-induced [Ca2+]i plateau, whereas inhibitors of vesicular exocytosis, such as brefeldin A and bafilomycin A1, were inactive.	Adenosine Triphosphate	66-69	kininogen 1	Homo sapiens	212-222
24047499-8	2013	Human subcutaneous fibroblasts respond to bradykinin by releasing ATP via connexin and pannexin hemichannels, since blockade of connexins, with 2-octanol or carbenoxolone, and pannexin-1, with 10Panx, attenuated bradykinin-induced [Ca2+]i plateau, whereas inhibitors of vesicular exocytosis, such as brefeldin A and bafilomycin A1, were inactive.	pannexin hemichannels	87-108	kininogen 1	Homo sapiens	42-52
24047499-8	2013	Human subcutaneous fibroblasts respond to bradykinin by releasing ATP via connexin and pannexin hemichannels, since blockade of connexins, with 2-octanol or carbenoxolone, and pannexin-1, with 10Panx, attenuated bradykinin-induced [Ca2+]i plateau, whereas inhibitors of vesicular exocytosis, such as brefeldin A and bafilomycin A1, were inactive.	2-octanol	144-153	kininogen 1	Homo sapiens	42-52
24047499-8	2013	Human subcutaneous fibroblasts respond to bradykinin by releasing ATP via connexin and pannexin hemichannels, since blockade of connexins, with 2-octanol or carbenoxolone, and pannexin-1, with 10Panx, attenuated bradykinin-induced [Ca2+]i plateau, whereas inhibitors of vesicular exocytosis, such as brefeldin A and bafilomycin A1, were inactive.	Carbenoxolone	157-170	kininogen 1	Homo sapiens	42-52
24047499-8	2013	Human subcutaneous fibroblasts respond to bradykinin by releasing ATP via connexin and pannexin hemichannels, since blockade of connexins, with 2-octanol or carbenoxolone, and pannexin-1, with 10Panx, attenuated bradykinin-induced [Ca2+]i plateau, whereas inhibitors of vesicular exocytosis, such as brefeldin A and bafilomycin A1, were inactive.	10PANX	193-199	kininogen 1	Homo sapiens	42-52
24047499-8	2013	Human subcutaneous fibroblasts respond to bradykinin by releasing ATP via connexin and pannexin hemichannels, since blockade of connexins, with 2-octanol or carbenoxolone, and pannexin-1, with 10Panx, attenuated bradykinin-induced [Ca2+]i plateau, whereas inhibitors of vesicular exocytosis, such as brefeldin A and bafilomycin A1, were inactive.	Brefeldin A	300-311	kininogen 1	Homo sapiens	42-52
23494059-5	2013	PK is activated by coagulation factor XIIa and then cleaves HK to generate bradykinin and factor XII to generate further XIIa.A structure has been described for the activated PK protease domain in complex with the inhibitor benzamidine.	benzamidine	224-235	kininogen 1	Homo sapiens	60-62
24047499-8	2013	Human subcutaneous fibroblasts respond to bradykinin by releasing ATP via connexin and pannexin hemichannels, since blockade of connexins, with 2-octanol or carbenoxolone, and pannexin-1, with 10Panx, attenuated bradykinin-induced [Ca2+]i plateau, whereas inhibitors of vesicular exocytosis, such as brefeldin A and bafilomycin A1, were inactive.	bafilomycin A1	316-330	kininogen 1	Homo sapiens	42-52
24047499-10	2013	Inhibition of ectonucleotidase activity and, thus, ADP formation from released ATP with POM-1 or by Mg2+ removal from media reduced bradykinin-induced [Ca2+]i plateau.	Adenosine Diphosphate	51-54	kininogen 1	Homo sapiens	132-142
24047499-10	2013	Inhibition of ectonucleotidase activity and, thus, ADP formation from released ATP with POM-1 or by Mg2+ removal from media reduced bradykinin-induced [Ca2+]i plateau.	Adenosine Triphosphate	79-82	kininogen 1	Homo sapiens	132-142
24047499-10	2013	Inhibition of ectonucleotidase activity and, thus, ADP formation from released ATP with POM-1 or by Mg2+ removal from media reduced bradykinin-induced [Ca2+]i plateau.	magnesium ion	100-104	kininogen 1	Homo sapiens	132-142
24047499-13	2013	CONCLUSIONS: Bradykinin induces ATP release from human subcutaneous fibroblasts via connexin and pannexin-1-containing hemichannels leading to [Ca2+]i mobilization through the cooperation of B2 and P2Y12 receptors.	Adenosine Triphosphate	32-35	kininogen 1	Homo sapiens	13-23
24047499-13	2013	CONCLUSIONS: Bradykinin induces ATP release from human subcutaneous fibroblasts via connexin and pannexin-1-containing hemichannels leading to [Ca2+]i mobilization through the cooperation of B2 and P2Y12 receptors.	hemichannels	119-131	kininogen 1	Homo sapiens	13-23
23494059-5	2013	PK is activated by coagulation factor XIIa and then cleaves HK to generate bradykinin and factor XII to generate further XIIa.A structure has been described for the activated PK protease domain in complex with the inhibitor benzamidine.	benzamidine	224-235	kininogen 1	Homo sapiens	75-85
23672780-7	2013	RESULTS: We demonstrate that prekallikrein-HK will activate to kallikrein in phosphate-containing buffers and that the rate is further accelerated on addition of heat shock protein 90.	Phosphates	77-86	kininogen 1	Homo sapiens	43-45
23796753-6	2013	In preadipocytes, BK also induced a rapid and transient [Ca2+](i) mobilization, a rapid and sustained increase in ERK1/2 activation and enhanced forskolin-stimulated cAMP accumulation.	Colforsin	145-154	kininogen 1	Homo sapiens	18-20
23796753-6	2013	In preadipocytes, BK also induced a rapid and transient [Ca2+](i) mobilization, a rapid and sustained increase in ERK1/2 activation and enhanced forskolin-stimulated cAMP accumulation.	Cyclic AMP	166-170	kininogen 1	Homo sapiens	18-20
23796753-8	2013	The B1 receptor agonist, Lys-[des-Arg9]-BK, displayed poor activity or was without effect while overall BK effects were prevented by the selective B2 receptor antagonist, fasitibant chloride, but not by the B1 selective antagonist, Lys-[Leu8][des-Arg9]-BK.	Lysine	25-28	kininogen 1	Homo sapiens	40-42
23796753-8	2013	The B1 receptor agonist, Lys-[des-Arg9]-BK, displayed poor activity or was without effect while overall BK effects were prevented by the selective B2 receptor antagonist, fasitibant chloride, but not by the B1 selective antagonist, Lys-[Leu8][des-Arg9]-BK.	des-arg9	30-38	kininogen 1	Homo sapiens	40-42
23796753-8	2013	The B1 receptor agonist, Lys-[des-Arg9]-BK, displayed poor activity or was without effect while overall BK effects were prevented by the selective B2 receptor antagonist, fasitibant chloride, but not by the B1 selective antagonist, Lys-[Leu8][des-Arg9]-BK.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	171-190	kininogen 1	Homo sapiens	104-106
23796753-8	2013	The B1 receptor agonist, Lys-[des-Arg9]-BK, displayed poor activity or was without effect while overall BK effects were prevented by the selective B2 receptor antagonist, fasitibant chloride, but not by the B1 selective antagonist, Lys-[Leu8][des-Arg9]-BK.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	171-190	kininogen 1	Homo sapiens	104-106
23933903-2	2013	Among the ACE inhibitor class, the agent perindopril, in particular, has pleiotropic effects that are not equally shared by other ACE inhibitors, including bradykinin site selectivity and subsequent enhancement of nitric oxide and inhibition of endothelial cell apoptosis.	Perindopril	41-52	kininogen 1	Homo sapiens	156-166
23715428-1	2013	The trimer of a bradykinin derivative displayed a more than five-fold increase in binding affinity for phosphatidylserine-enriched nanovesicles as compared to its monomeric precursor.	Phosphatidylserines	103-121	kininogen 1	Homo sapiens	16-26
23735753-3	2013	Here, we report neuroprotective properties for bradykinin against organophosphate poisoning using acute hippocampal slices as an in vitro model.	Organophosphates	66-81	kininogen 1	Homo sapiens	47-57
23735753-7	2013	However, the kinin-B1 receptor (B1BKR) agonist Lys-des-Arg(9)-bradykinin, inducing the phosphorylation of mitogen-activated protein kinase (MEK/MAPK) and cell death, abolished bradykinin-mediated neuroprotection, an effect, which was reverted by the ERK inhibitor PD98059.	lys-des-arg	47-58	kininogen 1	Homo sapiens	62-72
23735753-7	2013	However, the kinin-B1 receptor (B1BKR) agonist Lys-des-Arg(9)-bradykinin, inducing the phosphorylation of mitogen-activated protein kinase (MEK/MAPK) and cell death, abolished bradykinin-mediated neuroprotection, an effect, which was reverted by the ERK inhibitor PD98059.	lys-des-arg	47-58	kininogen 1	Homo sapiens	176-186
23735753-7	2013	However, the kinin-B1 receptor (B1BKR) agonist Lys-des-Arg(9)-bradykinin, inducing the phosphorylation of mitogen-activated protein kinase (MEK/MAPK) and cell death, abolished bradykinin-mediated neuroprotection, an effect, which was reverted by the ERK inhibitor PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	264-271	kininogen 1	Homo sapiens	62-72
23735753-9	2013	On the other hand pralidoxime, an oxime, reactivating acetylcholinesterase (AChE) after organophosphate poisoning, induced population spike recovery after DFP exposure in the presence of bradykinin and Lys-des-Arg(9)-bradykinin.	pralidoxime	18-29	kininogen 1	Homo sapiens	187-197
23735753-9	2013	On the other hand pralidoxime, an oxime, reactivating acetylcholinesterase (AChE) after organophosphate poisoning, induced population spike recovery after DFP exposure in the presence of bradykinin and Lys-des-Arg(9)-bradykinin.	pralidoxime	18-29	kininogen 1	Homo sapiens	217-227
23735753-9	2013	On the other hand pralidoxime, an oxime, reactivating acetylcholinesterase (AChE) after organophosphate poisoning, induced population spike recovery after DFP exposure in the presence of bradykinin and Lys-des-Arg(9)-bradykinin.	Oximes	24-29	kininogen 1	Homo sapiens	187-197
23735753-9	2013	On the other hand pralidoxime, an oxime, reactivating acetylcholinesterase (AChE) after organophosphate poisoning, induced population spike recovery after DFP exposure in the presence of bradykinin and Lys-des-Arg(9)-bradykinin.	Oximes	24-29	kininogen 1	Homo sapiens	217-227
23826374-0	2013	Activity of Bradykinin B2 Receptor Is Regulated by Long-Chain Polyunsaturated Fatty Acids.	long-chain polyunsaturated fatty acids	51-89	kininogen 1	Homo sapiens	12-22
23588115-9	2013	In HBAFb AG1478, GM6001, the ERK1/2-inhibitor U0126 and the p38 inhibitor SB203580 suppressed bradykinin-induced cell proliferation, but only SB203580 reduced myofibroblast differentiation.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	17-23	kininogen 1	Homo sapiens	94-104
23588115-7	2013	Bradykinin increased ERK1/2 and p38 phosphorylation via bradykinin B2 receptor; EGF receptor inhibitor AG1478 and panmetalloproteinase inhibitor GM6001 blocked bradykinin-induced ERK1/2 activation but not p38 phosphorylation.	RTKI cpd	103-109	kininogen 1	Homo sapiens	0-10
23588115-7	2013	Bradykinin increased ERK1/2 and p38 phosphorylation via bradykinin B2 receptor; EGF receptor inhibitor AG1478 and panmetalloproteinase inhibitor GM6001 blocked bradykinin-induced ERK1/2 activation but not p38 phosphorylation.	RTKI cpd	103-109	kininogen 1	Homo sapiens	160-170
23588115-7	2013	Bradykinin increased ERK1/2 and p38 phosphorylation via bradykinin B2 receptor; EGF receptor inhibitor AG1478 and panmetalloproteinase inhibitor GM6001 blocked bradykinin-induced ERK1/2 activation but not p38 phosphorylation.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	145-151	kininogen 1	Homo sapiens	0-10
23588115-7	2013	Bradykinin increased ERK1/2 and p38 phosphorylation via bradykinin B2 receptor; EGF receptor inhibitor AG1478 and panmetalloproteinase inhibitor GM6001 blocked bradykinin-induced ERK1/2 activation but not p38 phosphorylation.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	145-151	kininogen 1	Homo sapiens	56-66
23588115-7	2013	Bradykinin increased ERK1/2 and p38 phosphorylation via bradykinin B2 receptor; EGF receptor inhibitor AG1478 and panmetalloproteinase inhibitor GM6001 blocked bradykinin-induced ERK1/2 activation but not p38 phosphorylation.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	145-151	kininogen 1	Homo sapiens	160-170
23588115-8	2013	Bradykinin, via bradykinin B2 receptor, induced EGF receptor phosphorylation that was suppressed by AG1478.	RTKI cpd	100-106	kininogen 1	Homo sapiens	0-10
23588115-8	2013	Bradykinin, via bradykinin B2 receptor, induced EGF receptor phosphorylation that was suppressed by AG1478.	RTKI cpd	100-106	kininogen 1	Homo sapiens	16-26
23588115-9	2013	In HBAFb AG1478, GM6001, the ERK1/2-inhibitor U0126 and the p38 inhibitor SB203580 suppressed bradykinin-induced cell proliferation, but only SB203580 reduced myofibroblast differentiation.	U 0126	46-51	kininogen 1	Homo sapiens	94-104
23588115-9	2013	In HBAFb AG1478, GM6001, the ERK1/2-inhibitor U0126 and the p38 inhibitor SB203580 suppressed bradykinin-induced cell proliferation, but only SB203580 reduced myofibroblast differentiation.	SB 203580	74-82	kininogen 1	Homo sapiens	94-104
23454145-7	2013	Cell-pre-incubation with bradykinin induced changes in ABCG expression levels after 7-ketostigmasterol-incubation; however, the energetic metabolism inhibition reduced NPC1L1 expression only in 7-ketocholesterol-incubated cells.	7-ketostigmasterol	84-102	kininogen 1	Homo sapiens	25-35
23421411-2	2013	AREAS COVERED: The TRPV1/capsaicin receptor is an integrative, chemoceptive, noxious heat-gated cation channel also gated by several endogenous ligands and sensitized by phosphorylation through intracellular cascades triggered from receptors of bradykinin, prostanoids, NGF and interactions with TRPA1.	Prostaglandins	257-268	kininogen 1	Homo sapiens	245-255
23454145-7	2013	Cell-pre-incubation with bradykinin induced changes in ABCG expression levels after 7-ketostigmasterol-incubation; however, the energetic metabolism inhibition reduced NPC1L1 expression only in 7-ketocholesterol-incubated cells.	7-ketocholesterol	194-211	kininogen 1	Homo sapiens	25-35
23307413-0	2013	Multiple factors from bradykinin-challenged astrocytes contribute to the neuronal apoptosis: involvement of astroglial ROS, MMP-9, and HO-1/CO system.	Reactive Oxygen Species	119-122	kininogen 1	Homo sapiens	22-32
23307413-1	2013	Bradykinin (BK) has been shown to induce the expression of several inflammatory mediators, including reactive oxygen species (ROS) and matrix metalloproteinases (MMPs), in brain astrocytes.	Reactive Oxygen Species	101-124	kininogen 1	Homo sapiens	0-10
23307413-1	2013	Bradykinin (BK) has been shown to induce the expression of several inflammatory mediators, including reactive oxygen species (ROS) and matrix metalloproteinases (MMPs), in brain astrocytes.	Reactive Oxygen Species	101-124	kininogen 1	Homo sapiens	12-14
23307413-1	2013	Bradykinin (BK) has been shown to induce the expression of several inflammatory mediators, including reactive oxygen species (ROS) and matrix metalloproteinases (MMPs), in brain astrocytes.	Reactive Oxygen Species	126-129	kininogen 1	Homo sapiens	0-10
23307413-1	2013	Bradykinin (BK) has been shown to induce the expression of several inflammatory mediators, including reactive oxygen species (ROS) and matrix metalloproteinases (MMPs), in brain astrocytes.	Reactive Oxygen Species	126-129	kininogen 1	Homo sapiens	12-14
23505046-6	2013	Positively selected sites are located in all protein domains with the exclusion of the bradykinin region and also involve AMP sequences (including the highly effective NAT26 peptide); positively selected sites also occur at alternative cleavage sites for neutrophil-released kinins.	Adenosine Monophosphate	122-125	kininogen 1	Homo sapiens	87-97
23307413-4	2013	Here, we found that multiple factors were released from brain astrocytes (RBA-1) exposed to BK in the conditioned culture media (BK-CM), including ROS, MMP-9, and heme oxygenase-1 (HO-1)/carbon monoxide (CO), leading to neuronal cell (SK-N-SH) death.	Reactive Oxygen Species	147-150	kininogen 1	Homo sapiens	92-94
23307413-4	2013	Here, we found that multiple factors were released from brain astrocytes (RBA-1) exposed to BK in the conditioned culture media (BK-CM), including ROS, MMP-9, and heme oxygenase-1 (HO-1)/carbon monoxide (CO), leading to neuronal cell (SK-N-SH) death.	Reactive Oxygen Species	147-150	kininogen 1	Homo sapiens	129-131
23307413-4	2013	Here, we found that multiple factors were released from brain astrocytes (RBA-1) exposed to BK in the conditioned culture media (BK-CM), including ROS, MMP-9, and heme oxygenase-1 (HO-1)/carbon monoxide (CO), leading to neuronal cell (SK-N-SH) death.	Carbon Monoxide	187-202	kininogen 1	Homo sapiens	92-94
23307413-4	2013	Here, we found that multiple factors were released from brain astrocytes (RBA-1) exposed to BK in the conditioned culture media (BK-CM), including ROS, MMP-9, and heme oxygenase-1 (HO-1)/carbon monoxide (CO), leading to neuronal cell (SK-N-SH) death.	Carbon Monoxide	187-202	kininogen 1	Homo sapiens	129-131
23307413-4	2013	Here, we found that multiple factors were released from brain astrocytes (RBA-1) exposed to BK in the conditioned culture media (BK-CM), including ROS, MMP-9, and heme oxygenase-1 (HO-1)/carbon monoxide (CO), leading to neuronal cell (SK-N-SH) death.	Carbon Monoxide	204-206	kininogen 1	Homo sapiens	92-94
23307413-4	2013	Here, we found that multiple factors were released from brain astrocytes (RBA-1) exposed to BK in the conditioned culture media (BK-CM), including ROS, MMP-9, and heme oxygenase-1 (HO-1)/carbon monoxide (CO), leading to neuronal cell (SK-N-SH) death.	Carbon Monoxide	204-206	kininogen 1	Homo sapiens	129-131
23422725-1	2013	Bradykinin (BK) is an inflammatory mediator that can evoke oedema and vasodilatation, and is a potent algogen signalling via the B1 and B2 G-protein coupled receptors.	algogen	102-109	kininogen 1	Homo sapiens	0-10
23422725-1	2013	Bradykinin (BK) is an inflammatory mediator that can evoke oedema and vasodilatation, and is a potent algogen signalling via the B1 and B2 G-protein coupled receptors.	algogen	102-109	kininogen 1	Homo sapiens	12-14
23418089-0	2013	Relationship between bradykinin-induced relaxation and endogenous epoxyeicosanoid synthesis in human bronchi.	epoxyeicosanoid	66-81	kininogen 1	Homo sapiens	21-31
23471234-4	2013	Intra-arterial bradykinin increased plasma t-PA concentrations in the chamber effluent (P&lt;0.01 for all versus saline) that was quadrupled in the presence of enalapril (P&lt;0.0001 versus placebo).	Sodium Chloride	113-119	kininogen 1	Homo sapiens	15-25
23471234-4	2013	Intra-arterial bradykinin increased plasma t-PA concentrations in the chamber effluent (P&lt;0.01 for all versus saline) that was quadrupled in the presence of enalapril (P&lt;0.0001 versus placebo).	Enalapril	160-169	kininogen 1	Homo sapiens	15-25
23459756-8	2013	In these vessels, the pre-incubation with the Mas antagonists A779 or d-Pro-angiotensin-(1-7) totally abolished the vasodilatory capacity of both angiotensin-(1-7) and bradykinin, which was nitric oxide mediated.	Nitric Oxide	190-202	kininogen 1	Homo sapiens	168-178
23459756-10	2013	Pre-incubation of human umbilical vein endothelial cells with A779 prevented bradykinin-mediated NO generation and NO synthase phosphorylation at serine 1177.	Serine	146-152	kininogen 1	Homo sapiens	77-87
23489086-4	2013	Quantitative labeling of bradykinin peptide was accomplished with a commercially available 2",2""-(10-(2-((2,5-dioxopyrrolidin-1-yl)oxy)-2-oxoethyl)-1,4,7,10-tetraazacyclododecane-1,4,7-triyl) triacetic acid (DOTA-NHS-ester) and subsequently tagged with Eu.	DOTA-NHS ester	209-223	kininogen 1	Homo sapiens	25-35
23489086-6	2013	The non-species-specific ID LC-ICPMS method was cross-validated by a species-specific ID GC/MS approach, which is based on the determination of phenylalanine in bradykinin to derive the concentration of the peptide in the sample.	Phenylalanine	144-157	kininogen 1	Homo sapiens	161-171
23418089-6	2013	One micromolar BK or 1 muM 14,15-EET induced a 45% relaxation on the tension induced by 30 nM U-46619 [a thromboxane-prostanoid (TP)-receptor agonist].	thromboxane-prostanoid	105-127	kininogen 1	Homo sapiens	15-17
23418089-9	2013	Data also indicate that 3 muM MS-PPOH reduced the hyperpolarizing effects of BK by 43%.	propenylphosphonic acid	33-37	kininogen 1	Homo sapiens	77-79
23361105-1	2013	Bradykinin increases during cardiopulmonary bypass (CPB) and stimulates the release of nitric oxide, inflammatory cytokines, and tissue-type plasminogen activator (t-PA), acting through its B2 receptor.	Nitric Oxide	87-99	kininogen 1	Homo sapiens	0-10
23376352-0	2013	Bradykinin modulates spontaneous nerve growth factor production and stretch-induced ATP release in human urothelium.	Adenosine Triphosphate	84-87	kininogen 1	Homo sapiens	0-10
23347427-6	2013	: Elucidate the effects of the endopeptidase inhibitor KC 12615 on the contraction/relaxation response of isolated human vaginal smooth muscle to Big ET-1, bradykinin, CNP, or VIP.	kc 12615	55-63	kininogen 1	Homo sapiens	156-166
23347427-15	2013	Preexposure of the tissue to KC 12615 increased the relaxation exerted by bradykinin, CNP, or VIP (to -39.2 +- 5.8%, -40.7 +- 7.3%, and -44.6 +- 19%, respectively).	kc 12615	29-37	kininogen 1	Homo sapiens	74-84
23376352-5	2013	Bradykinin concentration-dependently (pEC50=8.3, Emax 4434+-277nM) increased urothelial intracellular calcium levels and induced phosphorylation of the mitogen-activated protein kinase (MAPK) ERK1/2.	Calcium	102-109	kininogen 1	Homo sapiens	0-10
23376352-7	2013	Bradykinin-induced (100nM) B2 receptor activation markedly increased (192+-13% of control levels) stretch-induced ATP release from UROtsa in hypotonic medium, the effect being dependent on intracellular calcium elevations.	Adenosine Triphosphate	114-117	kininogen 1	Homo sapiens	0-10
23376352-7	2013	Bradykinin-induced (100nM) B2 receptor activation markedly increased (192+-13% of control levels) stretch-induced ATP release from UROtsa in hypotonic medium, the effect being dependent on intracellular calcium elevations.	Calcium	203-210	kininogen 1	Homo sapiens	0-10
23376352-11	2013	In conclusion, we show that bradykinin represents a versatile modulator of human urothelial phenotype, accelerating stretch-induced ATP release, spontaneous release of NGF, as well as expression of sensory ion channel TRPV1.	Adenosine Triphosphate	132-135	kininogen 1	Homo sapiens	28-38
26105895-12	2013	(3) The concentrations of cGMP with BK and without BK and eNOS were not reduced in PE.	Cyclic GMP	26-30	kininogen 1	Homo sapiens	36-38
23373819-0	2013	Cis-trans isomerizations of proline residues are key to bradykinin conformations.	Proline	28-35	kininogen 1	Homo sapiens	56-66
23425693-6	2013	RESULTS: Intraluminal treatment with homocysteine (1 mM, 180 minutes) significantly attenuated arteriolar dilation in response to the endothelium-dependent NO-mediated agonists bradykinin and A23187 but not in response to the endothelium-independent NO donor sodium nitroprusside.	Homocysteine	37-49	kininogen 1	Homo sapiens	177-187
23122229-7	2013	Moreover, the designed biosensor was able to monitor release of IP(3) upon induction by different inducers like Bradykinin and ATP.	Inositol 1,4,5-Trisphosphate	64-69	kininogen 1	Homo sapiens	112-122
23249676-1	2013	Endothelium-derived hyperpolarizing factors (EDHFs) regulate vascular tone by contributing to the vasorelaxations to shear stress and endothelial agonists such as bradykinin and acetylcholine.	edhfs	45-50	kininogen 1	Homo sapiens	163-173
23351078-7	2013	The burst of intracellular calcium induced by either bradykinin (B2 agonist) or des-Arg(10) -Lys-bradykinin (B1 agonist) in gingival fibroblasts pretreated with IL-1beta was impaired by IL-4.	Calcium	27-34	kininogen 1	Homo sapiens	53-63
23351078-7	2013	The burst of intracellular calcium induced by either bradykinin (B2 agonist) or des-Arg(10) -Lys-bradykinin (B1 agonist) in gingival fibroblasts pretreated with IL-1beta was impaired by IL-4.	Calcium	27-34	kininogen 1	Homo sapiens	97-107
23351078-7	2013	The burst of intracellular calcium induced by either bradykinin (B2 agonist) or des-Arg(10) -Lys-bradykinin (B1 agonist) in gingival fibroblasts pretreated with IL-1beta was impaired by IL-4.	des-arg	80-87	kininogen 1	Homo sapiens	97-107
23096780-3	2013	The formation of construct-agonist complexes was revealed by electron paramagnetic resonance spectra and fluorescence measurements of spin labeled biologically active analogs of AngII and BK (Toac(1)-AngII and Toac(0)-BK), where Toac is the amino acid-type paramagnetic and fluorescence quencher 2, 2, 6, 6-tetramethylpiperidine-1-oxyl-4-amino-4-carboxylic acid.	2,2,6,6-tetramethylpiperidine-N-oxide-4-amino-4-carboxylic acid	192-196	kininogen 1	Homo sapiens	188-190
23096780-3	2013	The formation of construct-agonist complexes was revealed by electron paramagnetic resonance spectra and fluorescence measurements of spin labeled biologically active analogs of AngII and BK (Toac(1)-AngII and Toac(0)-BK), where Toac is the amino acid-type paramagnetic and fluorescence quencher 2, 2, 6, 6-tetramethylpiperidine-1-oxyl-4-amino-4-carboxylic acid.	2, 2, 6, 6-tetramethylpiperidine-1-oxyl-4-amino-4-carboxylic acid	296-361	kininogen 1	Homo sapiens	188-190
23096780-3	2013	The formation of construct-agonist complexes was revealed by electron paramagnetic resonance spectra and fluorescence measurements of spin labeled biologically active analogs of AngII and BK (Toac(1)-AngII and Toac(0)-BK), where Toac is the amino acid-type paramagnetic and fluorescence quencher 2, 2, 6, 6-tetramethylpiperidine-1-oxyl-4-amino-4-carboxylic acid.	2, 2, 6, 6-tetramethylpiperidine-1-oxyl-4-amino-4-carboxylic acid	296-361	kininogen 1	Homo sapiens	210-220
23362191-1	2013	We recently identified a novel human B2 receptor (B2R) agonist [Hyp(3),Thi(5),(N)Chg(7),Thi(8)]-bradykinin (NG291) with greater in vitro and in vivo potency and duration of action than natural bradykinin (BK).	2-acetyl-4(5)-tetrahydroxybutylimidazole	71-74	kininogen 1	Homo sapiens	96-106
23362191-1	2013	We recently identified a novel human B2 receptor (B2R) agonist [Hyp(3),Thi(5),(N)Chg(7),Thi(8)]-bradykinin (NG291) with greater in vitro and in vivo potency and duration of action than natural bradykinin (BK).	2-acetyl-4(5)-tetrahydroxybutylimidazole	88-91	kininogen 1	Homo sapiens	96-106
23469905-4	2013	Delapril has a high lipophilicity and weak bradykinin potentiating action.	delapril	0-8	kininogen 1	Homo sapiens	43-53
23255592-7	2013	BK induced Ca(2+)-dependent eNOS phosphorylation at Ser(1177), Thr(495), and Ser(114) in cytokine-treated HLMVEC, but these modifications were not dependent on JNK1/2 activation and were not responsible for prolonged NO output.	Serine	52-55	kininogen 1	Homo sapiens	0-2
23255592-7	2013	BK induced Ca(2+)-dependent eNOS phosphorylation at Ser(1177), Thr(495), and Ser(114) in cytokine-treated HLMVEC, but these modifications were not dependent on JNK1/2 activation and were not responsible for prolonged NO output.	Threonine	63-66	kininogen 1	Homo sapiens	0-2
23255592-7	2013	BK induced Ca(2+)-dependent eNOS phosphorylation at Ser(1177), Thr(495), and Ser(114) in cytokine-treated HLMVEC, but these modifications were not dependent on JNK1/2 activation and were not responsible for prolonged NO output.	Serine	77-80	kininogen 1	Homo sapiens	0-2
23065130-8	2013	In human ASM cells, exposure to [6]-gingerol, [8]-gingerol, and [6]-shogaol, but not [10]-gingerol (100 muM), blunted subsequent Ca(2+) responses to bradykinin (10 muM) and S-(-)-Bay K 8644 (10 muM).	gingerol	32-44	kininogen 1	Homo sapiens	149-159
23065130-8	2013	In human ASM cells, exposure to [6]-gingerol, [8]-gingerol, and [6]-shogaol, but not [10]-gingerol (100 muM), blunted subsequent Ca(2+) responses to bradykinin (10 muM) and S-(-)-Bay K 8644 (10 muM).	8-gingerol	46-58	kininogen 1	Homo sapiens	149-159
23065130-8	2013	In human ASM cells, exposure to [6]-gingerol, [8]-gingerol, and [6]-shogaol, but not [10]-gingerol (100 muM), blunted subsequent Ca(2+) responses to bradykinin (10 muM) and S-(-)-Bay K 8644 (10 muM).	shogaol	64-75	kininogen 1	Homo sapiens	149-159
23373819-1	2013	A recent ion mobility-mass spectrometry (IM-MS) study of the nonapeptide bradykinin (BK, amino acid sequence Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) found evidence for 10 populations of conformations that depend upon the solution composition [J.	Arginine	109-112	kininogen 1	Homo sapiens	73-83
23373819-1	2013	A recent ion mobility-mass spectrometry (IM-MS) study of the nonapeptide bradykinin (BK, amino acid sequence Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) found evidence for 10 populations of conformations that depend upon the solution composition [J.	Proline	116-119	kininogen 1	Homo sapiens	73-83
23379308-3	2013	Here we report that the overexpression of PS1 full-length holoprotein forms, in particular familial Alzheimer"s disease-causing forms of PS1, result in significantly attenuated calcium release from thapsigargin- and bradykinin-sensitive stores.	Calcium	177-184	kininogen 1	Homo sapiens	216-226
23373819-1	2013	A recent ion mobility-mass spectrometry (IM-MS) study of the nonapeptide bradykinin (BK, amino acid sequence Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) found evidence for 10 populations of conformations that depend upon the solution composition [J.	Glycine	130-133	kininogen 1	Homo sapiens	73-83
23373819-1	2013	A recent ion mobility-mass spectrometry (IM-MS) study of the nonapeptide bradykinin (BK, amino acid sequence Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) found evidence for 10 populations of conformations that depend upon the solution composition [J.	Phenylalanine	137-140	kininogen 1	Homo sapiens	73-83
23373819-1	2013	A recent ion mobility-mass spectrometry (IM-MS) study of the nonapeptide bradykinin (BK, amino acid sequence Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) found evidence for 10 populations of conformations that depend upon the solution composition [J.	Serine	144-147	kininogen 1	Homo sapiens	73-83
23373819-1	2013	A recent ion mobility-mass spectrometry (IM-MS) study of the nonapeptide bradykinin (BK, amino acid sequence Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) found evidence for 10 populations of conformations that depend upon the solution composition [J.	Proline	123-126	kininogen 1	Homo sapiens	73-83
23373819-1	2013	A recent ion mobility-mass spectrometry (IM-MS) study of the nonapeptide bradykinin (BK, amino acid sequence Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) found evidence for 10 populations of conformations that depend upon the solution composition [J.	Phenylalanine	158-161	kininogen 1	Homo sapiens	73-83
23373819-1	2013	A recent ion mobility-mass spectrometry (IM-MS) study of the nonapeptide bradykinin (BK, amino acid sequence Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) found evidence for 10 populations of conformations that depend upon the solution composition [J.	Arginine	165-168	kininogen 1	Homo sapiens	73-83
23373819-7	2013	IM-MS distributions of the analogue peptides, when compared to the distribution for BK, indicate the multiple structures are associated with different combinations of cis and trans forms of the three proline residues.	Proline	200-207	kininogen 1	Homo sapiens	84-86
23345219-4	2013	Using simultaneous fura-2 Ca(2+) imaging and amphotericin B perforated patch-clamp electrophysiology, we find that bradykinin raises [Ca(2+)](i) and induces a biphasic voltage response.	Fura-2	19-25	kininogen 1	Homo sapiens	115-125
23345219-4	2013	Using simultaneous fura-2 Ca(2+) imaging and amphotericin B perforated patch-clamp electrophysiology, we find that bradykinin raises [Ca(2+)](i) and induces a biphasic voltage response.	Amphotericin B	45-59	kininogen 1	Homo sapiens	115-125
23358696-10	2013	Furthermore, CXB, UMC and DMC greatly reduced inflammatory pain behavior induced by bradykinin, mechanical pain behavior induced by stimulation with von Frey filaments and thermal pain behavior in the Hargreaves test.	Celecoxib	13-16	kininogen 1	Homo sapiens	84-94
23406939-4	2013	As part of preclinical investigation of ecallantide, a potent bradykinin pathway inhibitor,  we evaluated three AAE patients treated successfully with that agent.	ecallantide	40-51	kininogen 1	Homo sapiens	62-72
24324963-3	2013	Increasing tyrosine phosphorylation with the phosphatase inhibitor, sodium orthovanadate produced arterial contraction which was lower in tumoral than in control arteries, whereas it reduced the contraction to noradrenaline in tumoral but not in control arteries and reduced the relaxation to bradykinin in control but not in tumoral arteries.	Tyrosine	11-19	kininogen 1	Homo sapiens	293-303
24324963-3	2013	Increasing tyrosine phosphorylation with the phosphatase inhibitor, sodium orthovanadate produced arterial contraction which was lower in tumoral than in control arteries, whereas it reduced the contraction to noradrenaline in tumoral but not in control arteries and reduced the relaxation to bradykinin in control but not in tumoral arteries.	Sodium orthovanadate	68-88	kininogen 1	Homo sapiens	293-303
23400285-5	2013	We have examined the phase-modulation fluorescence lifetime shift using protein compensation in cells, and have measured the calcium ion concentration in cells stimulated with bradykinin.	Calcium	125-132	kininogen 1	Homo sapiens	176-186
23883876-6	2013	LA at 0.1-5 mumol/L attenuated bradykinin (BK)-induced NO and PGI2 production while suppressing the BK-induced Ca(2+) response dose-dependently.	Epoprostenol	62-66	kininogen 1	Homo sapiens	31-41
23883876-6	2013	LA at 0.1-5 mumol/L attenuated bradykinin (BK)-induced NO and PGI2 production while suppressing the BK-induced Ca(2+) response dose-dependently.	Epoprostenol	62-66	kininogen 1	Homo sapiens	43-45
23603844-7	2013	Moreover, we found that in the coronary arterioles of obese patients, BK-induced dilation was augmented by in vitro captopril administration.	Captopril	116-125	kininogen 1	Homo sapiens	70-72
24113503-13	2013	Endothelium-induced vasodilatation in response to bradykinin reached only 12.3 +- 2.5% in NaCl-group, but 19.3 +- 5.2% in blood-group (p = 0.033).	Sodium Chloride	90-94	kininogen 1	Homo sapiens	50-60
24113503-14	2013	Alike, EC50-concentration of bradykinin for half-maximal relaxation was significantly lower in blood- than in NaCl-group (log EC50 -7.08 +- 0.3 and -5.91 +- 0.4; respectively; p = 0.046).	Sodium Chloride	110-114	kininogen 1	Homo sapiens	29-39
22303912-7	2013	sEHIs promote blood vessels to release bradykinin via an EET-mediated STAT3 signaling pathway to elicit tolerance to ischemia.	sehis	0-5	kininogen 1	Homo sapiens	39-49
23358696-10	2013	Furthermore, CXB, UMC and DMC greatly reduced inflammatory pain behavior induced by bradykinin, mechanical pain behavior induced by stimulation with von Frey filaments and thermal pain behavior in the Hargreaves test.	umc	18-21	kininogen 1	Homo sapiens	84-94
23358696-10	2013	Furthermore, CXB, UMC and DMC greatly reduced inflammatory pain behavior induced by bradykinin, mechanical pain behavior induced by stimulation with von Frey filaments and thermal pain behavior in the Hargreaves test.	2,5-dimethylcelecoxib	26-29	kininogen 1	Homo sapiens	84-94
22653778-9	2013	Bradykinin-mediated chemomigration and metalloproteinase expression was attenuated by PKCdelta inhibitor (rottlerin), PKCdelta siRNA, c-Src inhibitor (PP2) and c-Src mutant.	rottlerin	106-115	kininogen 1	Homo sapiens	0-10
22559215-7	2012	Cytosolic Ca(2+) transients, induced by the hormone bradykinin, were of a higher amplitude and decayed faster in Trolox-treated cells.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	113-119	kininogen 1	Homo sapiens	52-62
23054060-3	2012	BK (100 nM) depolarized cells activating bradykinin receptor type 2 (B(2)R) and Ca(2+)-dependent Cl(-) channels inhibitable by 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB; 10 muM).	5-nitro-2-(3-phenylpropylamino)benzoic acid	127-170	kininogen 1	Homo sapiens	41-51
23054060-3	2012	BK (100 nM) depolarized cells activating bradykinin receptor type 2 (B(2)R) and Ca(2+)-dependent Cl(-) channels inhibitable by 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB; 10 muM).	5-nitro-2-(3-phenylpropylamino)benzoic acid	172-176	kininogen 1	Homo sapiens	41-51
23054060-5	2012	[Des-Arg(9)]-bradykinin, an activator of B(1)R, had no effect on intracellular Ca(2+).	des-arg	1-8	kininogen 1	Homo sapiens	13-23
23082758-6	2012	In addition, the binding of Arg-Pro-Pro, the cleavage product of bradykinin and Thr(6) - bradykinin, provides additional detail of the general peptide binding in AnCE.	arginyl-prolyl-proline	28-39	kininogen 1	Homo sapiens	65-75
23082758-6	2012	In addition, the binding of Arg-Pro-Pro, the cleavage product of bradykinin and Thr(6) - bradykinin, provides additional detail of the general peptide binding in AnCE.	arginyl-prolyl-proline	28-39	kininogen 1	Homo sapiens	89-99
23082758-6	2012	In addition, the binding of Arg-Pro-Pro, the cleavage product of bradykinin and Thr(6) - bradykinin, provides additional detail of the general peptide binding in AnCE.	Threonine	80-83	kininogen 1	Homo sapiens	89-99
22929539-1	2012	Bacterial infections are a potent mechanism for enzymatic generation of kinins such as bradykinin (BK), a universal mediator for inducing inflammatory reaction by associating with the B2 receptor and stimulating liberation of arachidonic acid and synthesis of prostaglandin E2 (PGE2).	Arachidonic Acid	226-242	kininogen 1	Homo sapiens	87-97
22929539-1	2012	Bacterial infections are a potent mechanism for enzymatic generation of kinins such as bradykinin (BK), a universal mediator for inducing inflammatory reaction by associating with the B2 receptor and stimulating liberation of arachidonic acid and synthesis of prostaglandin E2 (PGE2).	Arachidonic Acid	226-242	kininogen 1	Homo sapiens	99-101
22929539-1	2012	Bacterial infections are a potent mechanism for enzymatic generation of kinins such as bradykinin (BK), a universal mediator for inducing inflammatory reaction by associating with the B2 receptor and stimulating liberation of arachidonic acid and synthesis of prostaglandin E2 (PGE2).	Dinoprostone	260-276	kininogen 1	Homo sapiens	87-97
22929539-1	2012	Bacterial infections are a potent mechanism for enzymatic generation of kinins such as bradykinin (BK), a universal mediator for inducing inflammatory reaction by associating with the B2 receptor and stimulating liberation of arachidonic acid and synthesis of prostaglandin E2 (PGE2).	Dinoprostone	260-276	kininogen 1	Homo sapiens	99-101
22929539-1	2012	Bacterial infections are a potent mechanism for enzymatic generation of kinins such as bradykinin (BK), a universal mediator for inducing inflammatory reaction by associating with the B2 receptor and stimulating liberation of arachidonic acid and synthesis of prostaglandin E2 (PGE2).	Dinoprostone	278-282	kininogen 1	Homo sapiens	87-97
22929539-1	2012	Bacterial infections are a potent mechanism for enzymatic generation of kinins such as bradykinin (BK), a universal mediator for inducing inflammatory reaction by associating with the B2 receptor and stimulating liberation of arachidonic acid and synthesis of prostaglandin E2 (PGE2).	Dinoprostone	278-282	kininogen 1	Homo sapiens	99-101
22929539-6	2012	When HGF cells were incubated with BK resulted of an increased in cyclooxygenase-2 (COX-2) expression and prostaglandin E2 synthesis.	Dinoprostone	106-122	kininogen 1	Homo sapiens	35-37
22935637-2	2012	We studied bradykinin-induced expression of bradykinin B(2) receptor and bradykinin- and lipopolysaccharide (LPS)-induced IL-8 release, MPO (marker of neutrophil activation) and 3-nitrotyrosine (3-NT; marker of "nitrosative stress") production in human bronchial epithelial cells BEAS-2B alone or in co-culture with human neutrophils.	3-nitrotyrosine	178-193	kininogen 1	Homo sapiens	11-21
23088211-3	2012	Here, we evaluated whether a glucocorticoid, budesonide (BUD), and a long-acting beta2-agonist, formoterol (FM), either alone or in combination, modified BK-induced lung fibroblast differentiation, and affected the BK-activated intracellular signaling pathways.	Formoterol Fumarate	96-106	kininogen 1	Homo sapiens	154-156
23131076-4	2012	Histamine-mediated (allergic) angioedema occurs through a type I hypersensitivity reaction, whereas bradykinin-mediated (non-allergic) angioedema is iatrogenic or hereditary in origin.Although their clinical presentations bear similarities, the treatment algorithm for histamine-mediated angioedema differs significantly from that for bradykinin-mediated angioedema.	Histamine	0-9	kininogen 1	Homo sapiens	335-345
23131076-4	2012	Histamine-mediated (allergic) angioedema occurs through a type I hypersensitivity reaction, whereas bradykinin-mediated (non-allergic) angioedema is iatrogenic or hereditary in origin.Although their clinical presentations bear similarities, the treatment algorithm for histamine-mediated angioedema differs significantly from that for bradykinin-mediated angioedema.	Histamine	269-278	kininogen 1	Homo sapiens	100-110
22935637-2	2012	We studied bradykinin-induced expression of bradykinin B(2) receptor and bradykinin- and lipopolysaccharide (LPS)-induced IL-8 release, MPO (marker of neutrophil activation) and 3-nitrotyrosine (3-NT; marker of "nitrosative stress") production in human bronchial epithelial cells BEAS-2B alone or in co-culture with human neutrophils.	3-nitrotyrosine	195-199	kininogen 1	Homo sapiens	11-21
22935637-7	2012	In BEAS-2B cells co-cultured with human neutrophils bradykinin increased MPO release and 3-NT production compared to BEAS-2B cells with human neutrophils (P&lt;0.001), and the addition of LPS in BEAS-2B cells with human neutrophils and bradykinin induced a further dramatically increase of MPO release and 3-NT formation (P&lt;0.001).	3-nitrotyrosine	89-93	kininogen 1	Homo sapiens	52-62
22935637-7	2012	In BEAS-2B cells co-cultured with human neutrophils bradykinin increased MPO release and 3-NT production compared to BEAS-2B cells with human neutrophils (P&lt;0.001), and the addition of LPS in BEAS-2B cells with human neutrophils and bradykinin induced a further dramatically increase of MPO release and 3-NT formation (P&lt;0.001).	3-nitrotyrosine	306-310	kininogen 1	Homo sapiens	52-62
23163996-5	2012	RESULTS: In microvessels precontracted with a thromboxane analogue, the endothelium-dependent relaxations to bradykinin (10 nmol/L to 30 mumol/L) mediated by EDHF, that is, nonsensitive to COX (10 mumol/L indomethacin) and NO synthase blockade (100 mumol/L N-nitro-L-arginine methyl ester), were higher in children than in adults.	Thromboxanes	46-57	kininogen 1	Homo sapiens	109-119
23163996-5	2012	RESULTS: In microvessels precontracted with a thromboxane analogue, the endothelium-dependent relaxations to bradykinin (10 nmol/L to 30 mumol/L) mediated by EDHF, that is, nonsensitive to COX (10 mumol/L indomethacin) and NO synthase blockade (100 mumol/L N-nitro-L-arginine methyl ester), were higher in children than in adults.	edhf	158-162	kininogen 1	Homo sapiens	109-119
23163996-5	2012	RESULTS: In microvessels precontracted with a thromboxane analogue, the endothelium-dependent relaxations to bradykinin (10 nmol/L to 30 mumol/L) mediated by EDHF, that is, nonsensitive to COX (10 mumol/L indomethacin) and NO synthase blockade (100 mumol/L N-nitro-L-arginine methyl ester), were higher in children than in adults.	Indomethacin	205-217	kininogen 1	Homo sapiens	109-119
23163996-5	2012	RESULTS: In microvessels precontracted with a thromboxane analogue, the endothelium-dependent relaxations to bradykinin (10 nmol/L to 30 mumol/L) mediated by EDHF, that is, nonsensitive to COX (10 mumol/L indomethacin) and NO synthase blockade (100 mumol/L N-nitro-L-arginine methyl ester), were higher in children than in adults.	n-nitro-l-arginine methyl ester	257-288	kininogen 1	Homo sapiens	109-119
22902525-7	2012	The HNO scavenger l-cysteine blocked bradykinin-induced relaxation in PCAs, and potentiated it in PCMAs.	Cysteine	18-28	kininogen 1	Homo sapiens	37-47
22890813-7	2012	RESULTS: Exposure to ADMA significantly decreased the bradykinin-induced vasorelaxation and reduced the protein expression of p-eNOS(Ser1177) whereas increased the expression of p-eNOS(Thr495) and nitrotyrosine.	N,N-dimethylarginine	21-25	kininogen 1	Homo sapiens	54-64
22652200-8	2012	In cultured ASM cells, incubation with high glucose concentrations significantly (P &lt; 0.05) enhanced bradykinin-induced intracellular calcium flux and the levels of pMYPT1, which were inhibited by Y27632 (P &lt; 0.05).	Glucose	44-51	kininogen 1	Homo sapiens	104-114
22652200-8	2012	In cultured ASM cells, incubation with high glucose concentrations significantly (P &lt; 0.05) enhanced bradykinin-induced intracellular calcium flux and the levels of pMYPT1, which were inhibited by Y27632 (P &lt; 0.05).	Calcium	137-144	kininogen 1	Homo sapiens	104-114
22890813-8	2012	Pre-incubation with AVE3085 restored the bradykinin-induced relaxation, reversed the decrease of p-eNOS(Ser1177), and lowered the level of p-eNOS(Thr495) and nitrotyrosine.	2,2-difluorobenzo(1,3)dioxole-5-carboxylic acid indan-2-ylamide	20-27	kininogen 1	Homo sapiens	41-51
22890813-9	2012	NO release in response to bradykinin was significantly reduced by ADMA and such reduction was restored by AVE3085.	N,N-dimethylarginine	66-70	kininogen 1	Homo sapiens	26-36
22861813-4	2012	Pharmacological inhibition of CatA by the natural product ebelactone B increased renal bradykinin levels and prevented the development of salt-induced hypertension.	ebelactone B	58-70	kininogen 1	Homo sapiens	87-97
22944684-5	2012	Additionally, albeit with a lower yield, des-Arg(9)-Met-Lys-bradykinin, an effective agonist of B1-subtype receptors, was released.	des-arg	41-48	kininogen 1	Homo sapiens	60-70
22522052-3	2012	We found that replacement of the C-terminal Arg in the natural kB2R activators bradykinin (BK) or kallidin (KD) with Lys (K(9)-BK or K(10)-KD) resulted in agonists that effectively stimulate the downstream signaling of both the kB1R and kB2R as measured by increased inositol turnover, intracellular calcium, ERK1/2 phosphorylation, arachidonic acid release and NO production.	Arginine	44-47	kininogen 1	Homo sapiens	79-89
22522052-3	2012	We found that replacement of the C-terminal Arg in the natural kB2R activators bradykinin (BK) or kallidin (KD) with Lys (K(9)-BK or K(10)-KD) resulted in agonists that effectively stimulate the downstream signaling of both the kB1R and kB2R as measured by increased inositol turnover, intracellular calcium, ERK1/2 phosphorylation, arachidonic acid release and NO production.	Arginine	44-47	kininogen 1	Homo sapiens	91-93
22522052-3	2012	We found that replacement of the C-terminal Arg in the natural kB2R activators bradykinin (BK) or kallidin (KD) with Lys (K(9)-BK or K(10)-KD) resulted in agonists that effectively stimulate the downstream signaling of both the kB1R and kB2R as measured by increased inositol turnover, intracellular calcium, ERK1/2 phosphorylation, arachidonic acid release and NO production.	Inositol	267-275	kininogen 1	Homo sapiens	79-89
22522052-3	2012	We found that replacement of the C-terminal Arg in the natural kB2R activators bradykinin (BK) or kallidin (KD) with Lys (K(9)-BK or K(10)-KD) resulted in agonists that effectively stimulate the downstream signaling of both the kB1R and kB2R as measured by increased inositol turnover, intracellular calcium, ERK1/2 phosphorylation, arachidonic acid release and NO production.	Inositol	267-275	kininogen 1	Homo sapiens	91-93
22522052-3	2012	We found that replacement of the C-terminal Arg in the natural kB2R activators bradykinin (BK) or kallidin (KD) with Lys (K(9)-BK or K(10)-KD) resulted in agonists that effectively stimulate the downstream signaling of both the kB1R and kB2R as measured by increased inositol turnover, intracellular calcium, ERK1/2 phosphorylation, arachidonic acid release and NO production.	Inositol	267-275	kininogen 1	Homo sapiens	127-129
22522052-3	2012	We found that replacement of the C-terminal Arg in the natural kB2R activators bradykinin (BK) or kallidin (KD) with Lys (K(9)-BK or K(10)-KD) resulted in agonists that effectively stimulate the downstream signaling of both the kB1R and kB2R as measured by increased inositol turnover, intracellular calcium, ERK1/2 phosphorylation, arachidonic acid release and NO production.	Calcium	300-307	kininogen 1	Homo sapiens	79-89
22522052-3	2012	We found that replacement of the C-terminal Arg in the natural kB2R activators bradykinin (BK) or kallidin (KD) with Lys (K(9)-BK or K(10)-KD) resulted in agonists that effectively stimulate the downstream signaling of both the kB1R and kB2R as measured by increased inositol turnover, intracellular calcium, ERK1/2 phosphorylation, arachidonic acid release and NO production.	Calcium	300-307	kininogen 1	Homo sapiens	91-93
22522052-3	2012	We found that replacement of the C-terminal Arg in the natural kB2R activators bradykinin (BK) or kallidin (KD) with Lys (K(9)-BK or K(10)-KD) resulted in agonists that effectively stimulate the downstream signaling of both the kB1R and kB2R as measured by increased inositol turnover, intracellular calcium, ERK1/2 phosphorylation, arachidonic acid release and NO production.	Calcium	300-307	kininogen 1	Homo sapiens	127-129
22522052-3	2012	We found that replacement of the C-terminal Arg in the natural kB2R activators bradykinin (BK) or kallidin (KD) with Lys (K(9)-BK or K(10)-KD) resulted in agonists that effectively stimulate the downstream signaling of both the kB1R and kB2R as measured by increased inositol turnover, intracellular calcium, ERK1/2 phosphorylation, arachidonic acid release and NO production.	Arachidonic Acid	333-349	kininogen 1	Homo sapiens	79-89
22522052-3	2012	We found that replacement of the C-terminal Arg in the natural kB2R activators bradykinin (BK) or kallidin (KD) with Lys (K(9)-BK or K(10)-KD) resulted in agonists that effectively stimulate the downstream signaling of both the kB1R and kB2R as measured by increased inositol turnover, intracellular calcium, ERK1/2 phosphorylation, arachidonic acid release and NO production.	Arachidonic Acid	333-349	kininogen 1	Homo sapiens	91-93
22522052-3	2012	We found that replacement of the C-terminal Arg in the natural kB2R activators bradykinin (BK) or kallidin (KD) with Lys (K(9)-BK or K(10)-KD) resulted in agonists that effectively stimulate the downstream signaling of both the kB1R and kB2R as measured by increased inositol turnover, intracellular calcium, ERK1/2 phosphorylation, arachidonic acid release and NO production.	Arachidonic Acid	333-349	kininogen 1	Homo sapiens	127-129
22607268-7	2012	Treatment of SK-N-SH cells with SP600125 also triggered InsP3R-mediated Ca2+ release from the ER by addition of 500 nM bradykinin, an agonist of InsP3 receptor (InsP3R1) without changing the expression of InsP3R1.	sk-n	13-17	kininogen 1	Homo sapiens	119-129
22607268-7	2012	Treatment of SK-N-SH cells with SP600125 also triggered InsP3R-mediated Ca2+ release from the ER by addition of 500 nM bradykinin, an agonist of InsP3 receptor (InsP3R1) without changing the expression of InsP3R1.	pyrazolanthrone	32-40	kininogen 1	Homo sapiens	119-129
22855054-6	2012	Diamide pretreatment increased the sensitivity of HAECs to histamine-stimulated Ca(2+) oscillations and BAECs to bradykinin-stimulated Ca(2+) oscillations.	Diamide	0-7	kininogen 1	Homo sapiens	113-123
22638761-1	2012	This study investigates the effect of the selective and potent B(2) receptor antagonist fasitibant (MEN16132) on the proinflammatory effect of bradykinin (BK) and its interaction with interleukin 1beta (IL-1beta) in human synoviocytes.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	100-108	kininogen 1	Homo sapiens	143-153
22638761-1	2012	This study investigates the effect of the selective and potent B(2) receptor antagonist fasitibant (MEN16132) on the proinflammatory effect of bradykinin (BK) and its interaction with interleukin 1beta (IL-1beta) in human synoviocytes.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	100-108	kininogen 1	Homo sapiens	155-157
22638761-3	2012	Radioligand binding ([(3) H]BK) and BK-induced inositolphosphate experiments were performed.	Inositol Phosphates	47-64	kininogen 1	Homo sapiens	36-38
22638761-4	2012	Incubation of synoviocytes with BK induced a sustained production of PGE(2) and transient COX-2 gene expression that were prevented by pretreatment with fasitibant (1 muM, 30 min preincubation).	Prostaglandins E	69-72	kininogen 1	Homo sapiens	32-34
22638761-6	2012	The combined treatment of cells with BK and IL-1beta induced an even increase of released PGE(2) and COX-2 gene and protein expression indicating a synergistic rather than an additive effect, not related to an increase of B(2) receptors density or its coupling.	Prostaglandins E	90-93	kininogen 1	Homo sapiens	37-39
22638761-7	2012	These potentiating effects of BK on PGE(2) production and increased COX-2 expression produced by IL-1beta were B(2)-receptor-mediated as fasitibant could prevent them.	Dinoprostone	36-42	kininogen 1	Homo sapiens	30-32
22638761-10	2012	BK can potentiate the COX-2 gene expression and consequent prostanoid production induced by IL-1beta.	Prostaglandins	59-69	kininogen 1	Homo sapiens	0-2
22523335-0	2012	The interaction of blood flow, insulin, and bradykinin in regulating glucose uptake in lower-body adipose tissue in lean and obese subjects.	Glucose	69-76	kininogen 1	Homo sapiens	44-54
22523335-2	2012	Insulin and bradykinin are meal-stimulated promoters of AT blood flow and glucose metabolism.	Glucose	74-81	kininogen 1	Homo sapiens	12-22
22523335-9	2012	In the lean group, bradykinin increased insulin-mediated AT glucose uptake from 8.6 +- 1.6 to 12.3 +- 2.4 mumol/min   kg (P = 0.038).	Glucose	60-67	kininogen 1	Homo sapiens	19-29
22488046-3	2012	In this paper we report an study based on energy transfer in two bradykinin derived peptides labeled with the donor-acceptor pair Abz/Eddnp (ortho-aminobenzoic acid/N-[2,4-dinitrophenyl]-ethylenediamine).	abz/eddnp	130-139	kininogen 1	Homo sapiens	65-75
22488046-3	2012	In this paper we report an study based on energy transfer in two bradykinin derived peptides labeled with the donor-acceptor pair Abz/Eddnp (ortho-aminobenzoic acid/N-[2,4-dinitrophenyl]-ethylenediamine).	ortho-Aminobenzoates	141-164	kininogen 1	Homo sapiens	65-75
22488046-3	2012	In this paper we report an study based on energy transfer in two bradykinin derived peptides labeled with the donor-acceptor pair Abz/Eddnp (ortho-aminobenzoic acid/N-[2,4-dinitrophenyl]-ethylenediamine).	N-(2,4-dinitrophenyl)ethylenediamine	165-202	kininogen 1	Homo sapiens	65-75
22488046-7	2012	The proline residue, in position 4 of the bradykinin sequence promotes a turn in the longer peptide chain, shortening its end-to-end distance.	Proline	4-11	kininogen 1	Homo sapiens	42-52
22958486-9	2012	Here, we discuss the regulation of podocyte actin dynamics by angiotensin or bradykinin-mediated calcium influx and downstream Rho GTPase signaling pathways and how these pathways are operative in other cells including fibroblasts and cancer cells.	Calcium	97-104	kininogen 1	Homo sapiens	77-87
22472866-3	2012	Ecallantide works by binding to kallikrein, preventing the conversion of kininogen to bradykinin, which reduces vascular permeability, thus reducing the swelling associated with acute attacks of HAE.	ecallantide	0-11	kininogen 1	Homo sapiens	86-96
22301626-1	2012	This study aimed to determine whether PGI(2) would be evoked by the endogenous endothelial B(2) receptor agonist bradykinin (BK) in the porcine interlobular renal artery and, if so, to determine how it would influence the vasomotor reaction, and the specific cyclooxygenase (COX) isoform(s) involved in its synthesis.	Epoprostenol	38-44	kininogen 1	Homo sapiens	113-123
22301626-1	2012	This study aimed to determine whether PGI(2) would be evoked by the endogenous endothelial B(2) receptor agonist bradykinin (BK) in the porcine interlobular renal artery and, if so, to determine how it would influence the vasomotor reaction, and the specific cyclooxygenase (COX) isoform(s) involved in its synthesis.	Epoprostenol	38-44	kininogen 1	Homo sapiens	125-127
22301626-3	2012	Results showed that BK evoked an increase in the production of 6-keto-PGF(1alpha), which was abolished by endothelial denudation that removed COX-1 expression, or was reduced by COX-1 inhibition.	6-keto-pgf	63-73	kininogen 1	Homo sapiens	20-22
22304761-8	2012	Bradykinin and BK1 receptor agonist [Lys-des-Arg9]-BK also facilitated IBa.	indolebutyric acid	71-74	kininogen 1	Homo sapiens	15-17
22304761-9	2012	After 24 h or 7 days exposure to BK, that is, under chronic inflammatory conditions, application of 1,25(OH)2D3 inhibited IBa.	Calcitriol	100-111	kininogen 1	Homo sapiens	33-35
22304761-9	2012	After 24 h or 7 days exposure to BK, that is, under chronic inflammatory conditions, application of 1,25(OH)2D3 inhibited IBa.	indolebutyric acid	122-125	kininogen 1	Homo sapiens	33-35
22304761-0	2012	Chronic bradykinin treatment alters 1alpha,25-dihydroxyvitamin D3-induced calcium current modulation in pre-osteoblasts.	Calcitriol	36-65	kininogen 1	Homo sapiens	8-18
22304761-0	2012	Chronic bradykinin treatment alters 1alpha,25-dihydroxyvitamin D3-induced calcium current modulation in pre-osteoblasts.	Calcium	74-81	kininogen 1	Homo sapiens	8-18
22304761-8	2012	Bradykinin and BK1 receptor agonist [Lys-des-Arg9]-BK also facilitated IBa.	indolebutyric acid	71-74	kininogen 1	Homo sapiens	0-10
22349904-9	2012	The uneven surface fluorescence associated to the B(1)R agonist B-10378 (CF-epsilon-ACA-Lys-des-Arg(9)-BK) is compatible with a particular form of agonist-induced receptor translocation.	b-10378	64-71	kininogen 1	Homo sapiens	103-105
22110081-8	2012	RESULTS: Isolated retinal arterioles developed stable basal tone and the vasodilations to endothelium-dependent nitric oxide (NO)-mediated agonists bradykinin and L-lactate were significantly reduced only by 90 minutes of ischemia.	Nitric Oxide	112-124	kininogen 1	Homo sapiens	148-158
22307539-2	2012	It is observed that bradykinin contains a Ser-Pro-Phe motif near the site of hydrolysis.	Serine	42-45	kininogen 1	Homo sapiens	20-30
22307539-2	2012	It is observed that bradykinin contains a Ser-Pro-Phe motif near the site of hydrolysis.	H-Pro-Phe-OH	46-53	kininogen 1	Homo sapiens	20-30
22200082-5	2012	ACE activity was assayed by monitoring cleavage of the fluorogenic substrate Mca-RPPGFSAFK(Dnp)-OH, a derivative of bradykinin, following preincubation with metal chelate-lisinopril compounds.	2,4-Dinitrophenol	91-94	kininogen 1	Homo sapiens	116-126
22200082-5	2012	ACE activity was assayed by monitoring cleavage of the fluorogenic substrate Mca-RPPGFSAFK(Dnp)-OH, a derivative of bradykinin, following preincubation with metal chelate-lisinopril compounds.	Lisinopril	171-181	kininogen 1	Homo sapiens	116-126
21835190-0	2012	Bradykinin-potentiating peptides: beyond captopril.	Captopril	41-50	kininogen 1	Homo sapiens	0-10
21835190-2	2012	The discovery of bradykinin (1949) and the bradykinin-potentiating peptides (1965) had a pivotal influence in the field, respectively, in understanding cardiovascular pathophysiology and in the development of captopril, the first active-site directed inhibitor of angiotensin-converting enzyme, and used worldwide to treat human hypertension.	Captopril	209-218	kininogen 1	Homo sapiens	17-27
21835190-2	2012	The discovery of bradykinin (1949) and the bradykinin-potentiating peptides (1965) had a pivotal influence in the field, respectively, in understanding cardiovascular pathophysiology and in the development of captopril, the first active-site directed inhibitor of angiotensin-converting enzyme, and used worldwide to treat human hypertension.	Captopril	209-218	kininogen 1	Homo sapiens	43-53
21835190-4	2012	The aim of the present article is to reveal that the snake proline-rich oligopeptides, known as bradykinin-potentiating peptides, are still a source of surprising scientific discoveries, some of them useful not only to reveal potential new targets but also to introduce prospective lead molecules for drug development.	Proline	59-66	kininogen 1	Homo sapiens	96-106
21295430-6	2012	In this case, we believe the difluoroethane-related angioedema represents either idiopathic or bradykinin-induced angioedema.	1,1-difluoroethane	29-43	kininogen 1	Homo sapiens	95-105
22904641-8	2012	The amiloride analog 5-(N-methyl-N-isobutyl)-amiloride (MIA) blocked short-term NHE activation and inhibited ERK phosphorylation, suggesting that NHE is critical for ERK activation by BK.	Amiloride	4-13	kininogen 1	Homo sapiens	184-186
22904641-8	2012	The amiloride analog 5-(N-methyl-N-isobutyl)-amiloride (MIA) blocked short-term NHE activation and inhibited ERK phosphorylation, suggesting that NHE is critical for ERK activation by BK.	5-(N-methyl-N-isobutyl)amiloride	21-54	kininogen 1	Homo sapiens	184-186
22904641-8	2012	The amiloride analog 5-(N-methyl-N-isobutyl)-amiloride (MIA) blocked short-term NHE activation and inhibited ERK phosphorylation, suggesting that NHE is critical for ERK activation by BK.	5-(N-methyl-N-isobutyl)amiloride	56-59	kininogen 1	Homo sapiens	184-186
22904641-9	2012	BK induced an approximately 40% increase in the proliferation of A498 cells as assessed by bromodeoxyuridine uptake.	Bromodeoxyuridine	91-108	kininogen 1	Homo sapiens	0-2
22563439-4	2012	The contribution of endothelium-derived hyperpolarizing factor (EDHF) to endothelium-dependent relaxation was impaired in uremic arteries after stimulation with bradykinin, but not acetylcholine, reflecting the agonist-specific differences.	endothelium-derived hyperpolarizing factor	20-62	kininogen 1	Homo sapiens	161-171
22922353-11	2012	CONCLUSION: Patients display extensive cleavage of HK in the plasma, which supports that AO precipitated by oestrogen contraception is BK-mediated.	Berkelium	135-137	kininogen 1	Homo sapiens	51-53
22563439-4	2012	The contribution of endothelium-derived hyperpolarizing factor (EDHF) to endothelium-dependent relaxation was impaired in uremic arteries after stimulation with bradykinin, but not acetylcholine, reflecting the agonist-specific differences.	edhf	64-68	kininogen 1	Homo sapiens	161-171
21719794-6	2011	Baclofen also potentiated the bradykinin-induced synthesis of inositol phosphate and transient increases in [Ca(2+)](i), which were blocked by CGP35348 or PTX.	CGP 35348	143-151	kininogen 1	Homo sapiens	30-40
22507330-0	2012	Exhaled nitric oxide is related to bronchial eosinophilia and airway hyperresponsiveness to bradykinin in allergen-induced asthma exacerbation.	Nitric Oxide	8-20	kininogen 1	Homo sapiens	92-102
22507330-3	2012	We postulated that allergen-induced increase in FeNO could be related to heightened mucosal eosinophils and AHR to bradykinin in atopic asthma.	flubendiamide	48-52	kininogen 1	Homo sapiens	115-125
22507330-9	2012	FeNO values negatively correlated with responsiveness to bradykinin only after allergen challenge (rho = -0.675, p = 0.039).	flubendiamide	0-4	kininogen 1	Homo sapiens	57-67
21719794-6	2011	Baclofen also potentiated the bradykinin-induced synthesis of inositol phosphate and transient increases in [Ca(2+)](i), which were blocked by CGP35348 or PTX.	Baclofen	0-8	kininogen 1	Homo sapiens	30-40
21719794-6	2011	Baclofen also potentiated the bradykinin-induced synthesis of inositol phosphate and transient increases in [Ca(2+)](i), which were blocked by CGP35348 or PTX.	Inositol Phosphates	62-80	kininogen 1	Homo sapiens	30-40
21983453-6	2011	Our results demonstrate that bradykinin (BK)-simulated arteriolar dilation is mediated by nitric oxide (NO) and EDHF pathways.	Nitric Oxide	90-102	kininogen 1	Homo sapiens	29-39
21982724-2	2011	Studies have shown that BK promotes the intracellular movement of calcium in human gingival fibroblasts by binding to the B2 receptor.	Calcium	66-73	kininogen 1	Homo sapiens	24-26
21898657-2	2011	Impaired metabolism of bradykinin and des-Arg(9) -bradykinin by aminopeptidase P (APP) is a key contributor to ACEi-angioedema.	des-arg	38-45	kininogen 1	Homo sapiens	50-60
21983453-6	2011	Our results demonstrate that bradykinin (BK)-simulated arteriolar dilation is mediated by nitric oxide (NO) and EDHF pathways.	edhf	112-116	kininogen 1	Homo sapiens	41-43
21697218-7	2011	Computer modelling highlighted the important role of kininogen-1 as an anchor for mediated interactions with other identified proteins including ferritin light chain and ceruloplasmin, hepatocyte growth factor-like protein, as well as complement C3 and gelsolin, thus linking various biological processes including inflammation and angiogenesis, iron transport and storage, blood coagulation, innate immunity, cell adhesion and actin filament polymerization.	Iron	346-350	kininogen 1	Homo sapiens	53-64
21864683-4	2011	Its affinity for recombinant B1 and B2 receptors is very low, as assessed by the binding competition of [3H]Lys-des-Arg9-BK and [3H]BK, respectively, but Met-Lys-BK-Ser-Ser effectively displaced a fraction of [3H]enalaprilat binding to recombinant ACE.	Tritium	129-131	kininogen 1	Homo sapiens	132-134
21864683-4	2011	Its affinity for recombinant B1 and B2 receptors is very low, as assessed by the binding competition of [3H]Lys-des-Arg9-BK and [3H]BK, respectively, but Met-Lys-BK-Ser-Ser effectively displaced a fraction of [3H]enalaprilat binding to recombinant ACE.	Tritium	129-131	kininogen 1	Homo sapiens	132-134
21864683-4	2011	Its affinity for recombinant B1 and B2 receptors is very low, as assessed by the binding competition of [3H]Lys-des-Arg9-BK and [3H]BK, respectively, but Met-Lys-BK-Ser-Ser effectively displaced a fraction of [3H]enalaprilat binding to recombinant ACE.	Tritium	129-131	kininogen 1	Homo sapiens	132-134
21864683-5	2011	Mutant recombinant ACE constructions revealed that affinity gap between BK and Met-Lys-BK-Ser-Ser is larger for the N-terminal catalytic site than for the C-terminal one, based on competition for the substrate Abz-Phe-Arg-Lys(Dnp)-Pro-OH in an enzymatic assay.	Serine	90-93	kininogen 1	Homo sapiens	72-74
21864683-5	2011	Mutant recombinant ACE constructions revealed that affinity gap between BK and Met-Lys-BK-Ser-Ser is larger for the N-terminal catalytic site than for the C-terminal one, based on competition for the substrate Abz-Phe-Arg-Lys(Dnp)-Pro-OH in an enzymatic assay.	Serine	90-93	kininogen 1	Homo sapiens	87-89
21864683-5	2011	Mutant recombinant ACE constructions revealed that affinity gap between BK and Met-Lys-BK-Ser-Ser is larger for the N-terminal catalytic site than for the C-terminal one, based on competition for the substrate Abz-Phe-Arg-Lys(Dnp)-Pro-OH in an enzymatic assay.	Serine	94-97	kininogen 1	Homo sapiens	72-74
21864683-5	2011	Mutant recombinant ACE constructions revealed that affinity gap between BK and Met-Lys-BK-Ser-Ser is larger for the N-terminal catalytic site than for the C-terminal one, based on competition for the substrate Abz-Phe-Arg-Lys(Dnp)-Pro-OH in an enzymatic assay.	Serine	94-97	kininogen 1	Homo sapiens	87-89
21864683-5	2011	Mutant recombinant ACE constructions revealed that affinity gap between BK and Met-Lys-BK-Ser-Ser is larger for the N-terminal catalytic site than for the C-terminal one, based on competition for the substrate Abz-Phe-Arg-Lys(Dnp)-Pro-OH in an enzymatic assay.	abz-phe-arg-lys	210-225	kininogen 1	Homo sapiens	72-74
21864683-5	2011	Mutant recombinant ACE constructions revealed that affinity gap between BK and Met-Lys-BK-Ser-Ser is larger for the N-terminal catalytic site than for the C-terminal one, based on competition for the substrate Abz-Phe-Arg-Lys(Dnp)-Pro-OH in an enzymatic assay.	abz-phe-arg-lys	210-225	kininogen 1	Homo sapiens	87-89
21864683-5	2011	Mutant recombinant ACE constructions revealed that affinity gap between BK and Met-Lys-BK-Ser-Ser is larger for the N-terminal catalytic site than for the C-terminal one, based on competition for the substrate Abz-Phe-Arg-Lys(Dnp)-Pro-OH in an enzymatic assay.	2,4-Dinitrophenol	226-229	kininogen 1	Homo sapiens	72-74
21864683-5	2011	Mutant recombinant ACE constructions revealed that affinity gap between BK and Met-Lys-BK-Ser-Ser is larger for the N-terminal catalytic site than for the C-terminal one, based on competition for the substrate Abz-Phe-Arg-Lys(Dnp)-Pro-OH in an enzymatic assay.	2,4-Dinitrophenol	226-229	kininogen 1	Homo sapiens	87-89
21864683-5	2011	Mutant recombinant ACE constructions revealed that affinity gap between BK and Met-Lys-BK-Ser-Ser is larger for the N-terminal catalytic site than for the C-terminal one, based on competition for the substrate Abz-Phe-Arg-Lys(Dnp)-Pro-OH in an enzymatic assay.	isoleucyl-prolyl-proline	231-237	kininogen 1	Homo sapiens	72-74
21864683-5	2011	Mutant recombinant ACE constructions revealed that affinity gap between BK and Met-Lys-BK-Ser-Ser is larger for the N-terminal catalytic site than for the C-terminal one, based on competition for the substrate Abz-Phe-Arg-Lys(Dnp)-Pro-OH in an enzymatic assay.	isoleucyl-prolyl-proline	231-237	kininogen 1	Homo sapiens	87-89
21864683-6	2011	Met-Lys-BK-Ser-Ser is a low potency stimulant of the rabbit aorta (bioassay for B1 receptors), but the human isolated umbilical vein, a contractile bioassay for the B2 receptors, responded to Met-Lys-BK-Ser-Ser more than expected from the radioligand binding assay, this agonist being ~30-fold less potent than BK in the vein.	Serine	11-14	kininogen 1	Homo sapiens	8-10
21864683-6	2011	Met-Lys-BK-Ser-Ser is a low potency stimulant of the rabbit aorta (bioassay for B1 receptors), but the human isolated umbilical vein, a contractile bioassay for the B2 receptors, responded to Met-Lys-BK-Ser-Ser more than expected from the radioligand binding assay, this agonist being ~30-fold less potent than BK in the vein.	Serine	11-14	kininogen 1	Homo sapiens	200-202
21864683-7	2011	Venous tissue treatment with the ACE inhibitor enalaprilat reduced the apparent potency of Met-Lys-BK-Ser-Ser by 15-fold, while not affecting that of BK.	Enalaprilat	47-58	kininogen 1	Homo sapiens	99-101
21864683-7	2011	Venous tissue treatment with the ACE inhibitor enalaprilat reduced the apparent potency of Met-Lys-BK-Ser-Ser by 15-fold, while not affecting that of BK.	Serine	102-105	kininogen 1	Homo sapiens	99-101
21864683-7	2011	Venous tissue treatment with the ACE inhibitor enalaprilat reduced the apparent potency of Met-Lys-BK-Ser-Ser by 15-fold, while not affecting that of BK.	Serine	106-109	kininogen 1	Homo sapiens	99-101
21864683-9	2011	In vascular tissue, ACE assumes a paradoxical activating role for Met-Lys-BK-Ser-Ser.	Serine	77-80	kininogen 1	Homo sapiens	74-76
21864683-9	2011	In vascular tissue, ACE assumes a paradoxical activating role for Met-Lys-BK-Ser-Ser.	Serine	81-84	kininogen 1	Homo sapiens	74-76
21803870-10	2011	In fura 2-loaded ASM cells, [Ca(2+)](i) responses to 1 muM ACh, 10 muM histamine, or 10 nM bradykinin were all exaggerated by TNF-alpha as well as IL-13 exposure.	Fura-2	3-9	kininogen 1	Homo sapiens	91-101
21756898-5	2011	Anti-myc antibodies, conjugated or not with secondary antibodies optionally coupled to Qdot nanomaterials, were transported into early endosome autoantigen 1-, and beta-arrestin-positive vesicles in bradykinin-stimulated intact cells expressing receptors encoded by myc-B(2)R. Antibody-conjugated cargoes progressed into late-endosomes-lysosomes within 3h without evidence of autophagy.	Tritium	353-355	kininogen 1	Homo sapiens	199-209
21864683-0	2011	Met-Lys-bradykinin-Ser-Ser, a peptide produced by the neutrophil from kininogen, is metabolically activated by angiotensin converting enzyme in vascular tissue.	Serine	19-22	kininogen 1	Homo sapiens	8-18
21864683-0	2011	Met-Lys-bradykinin-Ser-Ser, a peptide produced by the neutrophil from kininogen, is metabolically activated by angiotensin converting enzyme in vascular tissue.	Serine	23-26	kininogen 1	Homo sapiens	8-18
21864683-2	2011	It has been reported that the PR3 protease from human neutrophil releases an alternate peptide of 13 amino acids, Met-Lys-BK-Ser-Ser, from high molecular weight kininogen.	Serine	125-128	kininogen 1	Homo sapiens	122-124
21864683-4	2011	Its affinity for recombinant B1 and B2 receptors is very low, as assessed by the binding competition of [3H]Lys-des-Arg9-BK and [3H]BK, respectively, but Met-Lys-BK-Ser-Ser effectively displaced a fraction of [3H]enalaprilat binding to recombinant ACE.	Tritium	105-107	kininogen 1	Homo sapiens	121-123
21864683-4	2011	Its affinity for recombinant B1 and B2 receptors is very low, as assessed by the binding competition of [3H]Lys-des-Arg9-BK and [3H]BK, respectively, but Met-Lys-BK-Ser-Ser effectively displaced a fraction of [3H]enalaprilat binding to recombinant ACE.	Tritium	129-131	kininogen 1	Homo sapiens	132-134
21871968-4	2011	LNO(2) did not directly induce Ca(2+) influx in cultured lung epithelial cells, but inhibited bradykinin-induced Ca(2+) influx in a cGMP-independent manner.	Cyclic GMP	132-136	kininogen 1	Homo sapiens	94-104
21762687-0	2011	Gap junctions and hydrogen peroxide are involved in endothelium-derived hyperpolarising responses to bradykinin in omental arteries and veins isolated from pregnant women.	Hydrogen Peroxide	18-35	kininogen 1	Homo sapiens	101-111
21762687-5	2011	In pressurised vessels, the effects of proposed inhibitors of EDH production/function were examined on responses to bradykinin.	EDH	62-65	kininogen 1	Homo sapiens	116-126
21762687-8	2011	In both vessels, responses to bradykinin were partially blocked in the presence of the gap junction uncoupler, carbenoxolone, and reduced further with the addition of catalase, which acts to degrade H(2)O(2).	Carbenoxolone	111-124	kininogen 1	Homo sapiens	30-40
21762687-11	2011	These data show that, in human omental vessels, an EDH mechanism is produced in response to bradykinin that involves gap junction communication and the production of H(2)O(2).	Hydrogen Peroxide	166-174	kininogen 1	Homo sapiens	92-102
21651905-6	2011	Application of captopril 1 muM (angiotensin-converting enzyme inhibitor) or phosphoramidon 10 muM (neutral endopeptidase inhibitor) induced a leftward shift of bradykinin-elicited responses in human umbilical vein with endothelium while no effect was observed in tissues denuded of endothelium under the same treatment.	Captopril	15-24	kininogen 1	Homo sapiens	160-170
21651905-6	2011	Application of captopril 1 muM (angiotensin-converting enzyme inhibitor) or phosphoramidon 10 muM (neutral endopeptidase inhibitor) induced a leftward shift of bradykinin-elicited responses in human umbilical vein with endothelium while no effect was observed in tissues denuded of endothelium under the same treatment.	phosphoramidon	76-90	kininogen 1	Homo sapiens	160-170
21867693-3	2011	Exposure of the human colonic myofibroblast cell line 18Co to TNF-alpha and bradykinin induced synergistic MMP-3 mRNA and protein expression, which were blocked by the preferential PKC inhibitors GF109203X and Go6983 and by the MEK inhibitor U0126.	bisindolylmaleimide I	196-205	kininogen 1	Homo sapiens	76-86
21867693-3	2011	Exposure of the human colonic myofibroblast cell line 18Co to TNF-alpha and bradykinin induced synergistic MMP-3 mRNA and protein expression, which were blocked by the preferential PKC inhibitors GF109203X and Go6983 and by the MEK inhibitor U0126.	2-(1-(3-dimethylaminopropyl)-5-methoxyindol-3-yl)-3-(1H-indol-3-yl)maleimide	210-216	kininogen 1	Homo sapiens	76-86
21867693-3	2011	Exposure of the human colonic myofibroblast cell line 18Co to TNF-alpha and bradykinin induced synergistic MMP-3 mRNA and protein expression, which were blocked by the preferential PKC inhibitors GF109203X and Go6983 and by the MEK inhibitor U0126.	U 0126	242-247	kininogen 1	Homo sapiens	76-86
21830821-2	2011	Over the range of solution compositions studied, from 0:100 to 100:0 methanol:water and 0:100 to 90:10 dioxane:water, evidence for 10 independent populations of bradykinin structures in solution is found.	Methanol	69-77	kininogen 1	Homo sapiens	161-171
21830821-2	2011	Over the range of solution compositions studied, from 0:100 to 100:0 methanol:water and 0:100 to 90:10 dioxane:water, evidence for 10 independent populations of bradykinin structures in solution is found.	Water	78-83	kininogen 1	Homo sapiens	161-171
21830821-2	2011	Over the range of solution compositions studied, from 0:100 to 100:0 methanol:water and 0:100 to 90:10 dioxane:water, evidence for 10 independent populations of bradykinin structures in solution is found.	1,4-dioxane	103-110	kininogen 1	Homo sapiens	161-171
21830821-2	2011	Over the range of solution compositions studied, from 0:100 to 100:0 methanol:water and 0:100 to 90:10 dioxane:water, evidence for 10 independent populations of bradykinin structures in solution is found.	Water	111-116	kininogen 1	Homo sapiens	161-171
21177981-0	2011	Lys-des[Arg9]-bradykinin alters migration and production of interleukin-12 in monocyte-derived dendritic cells.	Diethylstilbestrol	3-7	kininogen 1	Homo sapiens	14-24
21177981-2	2011	Inflammation is accompanied by an increased maturation of DCs and the generation of kinins, particularly Lys-des[Arg(9)]-bradykinin (Lda-BK).	lys-des	105-112	kininogen 1	Homo sapiens	121-131
21177981-2	2011	Inflammation is accompanied by an increased maturation of DCs and the generation of kinins, particularly Lys-des[Arg(9)]-bradykinin (Lda-BK).	Arginine	113-116	kininogen 1	Homo sapiens	121-131
21924126-3	2011	The first objective of our study was to measure and to characterize the kinetic profile of bradykinin release in human plasma incubated with OSCS and contaminated heparin.	Heparin	163-170	kininogen 1	Homo sapiens	91-101
21983453-6	2011	Our results demonstrate that bradykinin (BK)-simulated arteriolar dilation is mediated by nitric oxide (NO) and EDHF pathways.	Nitric Oxide	90-102	kininogen 1	Homo sapiens	41-43
21983453-6	2011	Our results demonstrate that bradykinin (BK)-simulated arteriolar dilation is mediated by nitric oxide (NO) and EDHF pathways.	edhf	112-116	kininogen 1	Homo sapiens	29-39
21493700-4	2011	Pre-treatment with SKF96365 (an inhibitor of TRPCs) or the selective TRPC3 inhibitor Pyr3 significantly decreased bradykinin-induced vasorelaxation.	1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole	19-27	kininogen 1	Homo sapiens	114-124
21654699-5	2011	Bradykinin-triggered [Ca(2+)](i) oscillations were inhibited by interfering with connexin channels, making use of carbenoxolone, Gap27, a peptide blocker of connexin channels, and Cx37/43 knockdown.	Carbenoxolone	114-127	kininogen 1	Homo sapiens	0-10
21654699-6	2011	Gap27 inhibition of the oscillations was rapid (within minutes) and work with connexin hemichannel-permeable dyes indicated hemichannel opening and purinergic signaling in response to stimulation with BK.	hemichannel	87-98	kininogen 1	Homo sapiens	201-203
21729302-3	2011	Incubation with BK (10.0 microMol/L) for 18 hours increased the migration index 3-fold in comparison to controls or to cells preincubated with the B2R antagonist HOE-140.	4-hydroxy-2-octenal	162-165	kininogen 1	Homo sapiens	16-18
21629912-4	2011	The natural substrates of ACE, i.e., angiotensin II and bradykinin, contain a Pro-Phe motif near the site of hydrolysis.	H-Pro-Phe-OH	78-85	kininogen 1	Homo sapiens	56-66
21663732-2	2011	We have previously reported that BK increased the synthesis of interleukin-6 and prostaglandin E(2) via phosphorylation of ERK1/2 in human osteoblasts, SaM-1.	Dinoprostone	81-99	kininogen 1	Homo sapiens	33-35
21663732-6	2011	Additionally, thapsigargin, endoplasmic reticulum Ca(2+) pump inhibitor, completely inhibited BK-induced increase of intracellular Ca(2+).	Thapsigargin	14-26	kininogen 1	Homo sapiens	94-96
21371443-4	2011	KNG-I-322, a desmosdumotin B derivative, displayed a direct interaction with P-gp and demonstrated selective anti-proliferative and apoptotic activities in P-gp overexpressed Hep3B/VIN other than P-gp-deficient Hep3B cells.	desmosdumotin b	13-28	kininogen 1	Homo sapiens	0-3
21627535-5	2011	It was demonstrated, using a range of primary and transformed mesothelial and mesothelioma cell lines, that cells assembled high molecular weight kininogen and plasma prekallikrein to liberate bradykinin, a process inhibited by novobiocin, a heat shock protein 90 (HSP90) inhibitor, cysteine, bradykinin and protamine sulphate.	Novobiocin	228-238	kininogen 1	Homo sapiens	193-203
21627535-5	2011	It was demonstrated, using a range of primary and transformed mesothelial and mesothelioma cell lines, that cells assembled high molecular weight kininogen and plasma prekallikrein to liberate bradykinin, a process inhibited by novobiocin, a heat shock protein 90 (HSP90) inhibitor, cysteine, bradykinin and protamine sulphate.	Novobiocin	228-238	kininogen 1	Homo sapiens	293-303
21627535-5	2011	It was demonstrated, using a range of primary and transformed mesothelial and mesothelioma cell lines, that cells assembled high molecular weight kininogen and plasma prekallikrein to liberate bradykinin, a process inhibited by novobiocin, a heat shock protein 90 (HSP90) inhibitor, cysteine, bradykinin and protamine sulphate.	Cysteine	283-291	kininogen 1	Homo sapiens	193-203
21627535-7	2011	Calcium mobilisation was induced in some mesothelium-derived cell lines by bradykinin.	Calcium	0-7	kininogen 1	Homo sapiens	75-85
21509932-9	2011	Interestingly, Factor H and Factor I, antithrombin, prothrombin, high molecular weight kininogen (HMWK), and IgG were present in eluates from OH, COOH, and NH2 SAM surfaces and in eluates from TCPS but not in eluates from CH3 SAM surfaces, following exposure to filtered h.i.	Carbonic Acid	146-150	kininogen 1	Homo sapiens	98-102
21481442-2	2011	Ecallantide, a novel plasma kallikrein inhibitor, inhibits production of bradykinin, the key mediator of these angioedema attacks.	ecallantide	0-11	kininogen 1	Homo sapiens	73-83
21538706-4	2011	When comparing the effect of silver ions on the conformation of bradykinin a similar tendency was found.	Silver	29-35	kininogen 1	Homo sapiens	64-74
21426904-8	2011	Inhibition of MAP kinase kinase (MEK) with U0126 also blocked bradykinin-induced ERK1/2 phosphorylation.	U 0126	43-48	kininogen 1	Homo sapiens	62-72
21654087-6	2011	It was also observed that all the peptides related to buPRL could antagonize the vascular endothelial growth factor (VEGF) and bradykinin (BK)- dependent production of endothelial nitric oxide (NO), which is a pre-requisite for endothelial tube formation.	Nitric Oxide	180-192	kininogen 1	Homo sapiens	127-137
21654087-6	2011	It was also observed that all the peptides related to buPRL could antagonize the vascular endothelial growth factor (VEGF) and bradykinin (BK)- dependent production of endothelial nitric oxide (NO), which is a pre-requisite for endothelial tube formation.	Nitric Oxide	180-192	kininogen 1	Homo sapiens	139-141
21454694-5	2011	An additional mutation that reduced the affinity of CPM for C-terminal Arg and increased the affinity for C-terminal Lys inhibited the B1R response to bradykinin (with C-terminal Arg) but generated a response to Lys(9)-bradykinin.	Lysine	117-120	kininogen 1	Homo sapiens	151-161
21371443-7	2011	Notably, the P-gp inhibitor, verapamil, also directly interacted with P-gp but significantly diminished KNG-I-322-induced anti-proliferative activity.	Verapamil	29-38	kininogen 1	Homo sapiens	104-107
21371443-8	2011	After the mechanism study, the data showed that KNG-I-322 induced a dramatic down-regulation of GRP78 expression, which was significantly inhibited by verapamil and completely diminished by the knockdown of P-gp.	Verapamil	151-160	kininogen 1	Homo sapiens	48-51
21355573-3	2011	Whereas BK exhibits a stronger interaction with the membrane and prefers to stay on the interface, des-Arg9-BK, with the loss of C-terminal Arg, penetrates further.	Arginine	103-106	kininogen 1	Homo sapiens	108-110
21555712-8	2011	Both L-NMMA and TEA attenuated bradykinin-mediated vasodilation in healthy and hypercholesterolemic subjects (P&lt;0.001).	omega-N-Methylarginine	5-11	kininogen 1	Homo sapiens	31-41
21555712-8	2011	Both L-NMMA and TEA attenuated bradykinin-mediated vasodilation in healthy and hypercholesterolemic subjects (P&lt;0.001).	Tetraethylammonium	16-19	kininogen 1	Homo sapiens	31-41
21555712-13	2011	Third, bradykinin, but not acetylcholine, stimulates K(+)(Ca) channel-mediated vasodilation in healthy subjects, whereas in hypercholesterolemia, K(+)(Ca) channel-mediated vasodilation compensates for the reduced nitric oxide activity.	Nitric Oxide	213-225	kininogen 1	Homo sapiens	7-17
21355573-7	2011	Simulations with different starting orientations of the peptides with respect to the bilayer surface lead to the same observations, namely, the relative positioning of the peptides on the membrane surface, deeper penetration of the des-Arg9-BK, and the formation of turn structures.	Diethylstilbestrol	61-64	kininogen 1	Homo sapiens	241-243
21179101-10	2011	These results indicate that in normoweight hypertensive patients, despite similar BP reduction, imidapril but not candesartan improved the fibrinolytic balance, suggesting that mechanisms other than Ang II inhibition, possibly including bradykinin-mediated effects on insulin sensitivity and endothelial function, may be responsible for these different effects.	imidapril	96-105	kininogen 1	Homo sapiens	237-247
21252071-0	2011	Cleaved high-molecular-weight kininogen accelerates the onset of endothelial progenitor cell senescence by induction of reactive oxygen species.	Reactive Oxygen Species	120-143	kininogen 1	Homo sapiens	8-39
21209365-6	2011	Results demonstrate that both EPI and BK induce increases in intracellular calcium and NO levels.	Calcium	75-82	kininogen 1	Homo sapiens	38-40
21305271-1	2011	PURPOSE: The antihypertensive effects of angiotensin-converting enzyme inhibitors (ACEi) are explained, at least in part, by enhanced bradykinin-dependent nitric oxide (NO) formation and decreased angiotensin II-induced oxidative stress and vasoconstriction.	Nitric Oxide	155-167	kininogen 1	Homo sapiens	134-144
21205920-2	2011	We took advantage of this by generating two fluorescent bradykinin analogs containing 5(6)-carboxyfluorescein (CF) optionally used with the epsilon-aminocaproyl spacer condensed at the N terminus of the agonist.	6-carboxyfluorescein	86-109	kininogen 1	Homo sapiens	56-66
21281309-7	2011	Bursting activity, spontaneous calcium transients and activity of TRPM4 and ATP-sensitive K(+) channels were potentiated after brief exposures to bradykinin and incubation with wortmannin produced opposite effects that can be explained by changes in phosphatidylinositol 4,5-bisphosphate levels.	Calcium	31-38	kininogen 1	Homo sapiens	146-156
21281309-7	2011	Bursting activity, spontaneous calcium transients and activity of TRPM4 and ATP-sensitive K(+) channels were potentiated after brief exposures to bradykinin and incubation with wortmannin produced opposite effects that can be explained by changes in phosphatidylinositol 4,5-bisphosphate levels.	Wortmannin	177-187	kininogen 1	Homo sapiens	146-156
21281309-7	2011	Bursting activity, spontaneous calcium transients and activity of TRPM4 and ATP-sensitive K(+) channels were potentiated after brief exposures to bradykinin and incubation with wortmannin produced opposite effects that can be explained by changes in phosphatidylinositol 4,5-bisphosphate levels.	Phosphatidylinositol 4,5-Diphosphate	250-287	kininogen 1	Homo sapiens	146-156
21278382-3	2011	Here we provide evidence that prolonged exposure of cultured human airway smooth muscle (HuASM) cells to beta(2)-agonists directly augments procontractile signaling pathways elicited by several compounds including thrombin, bradykinin, and histamine.	beta(2)	105-112	kininogen 1	Homo sapiens	224-234
21098312-5	2011	In white Americans, Lys55Arg genotype was associated with vasodilator response to bradykinin, such that forearm blood flow was significantly lower (P = 0.043) and forearm vascular resistance was significantly higher (P = 0.013) in Arg55 variant allele carriers compared to wild-type individuals.	lys55arg	20-28	kininogen 1	Homo sapiens	82-92
21172909-6	2011	In vessel segments at 80 mm Hg, the intermediate (I)K(Ca) blocker 1-[(2-chlorophenyl)diphenyl-methyl]-1H-pyrazole (TRAM-34; 1 muM) inhibited bradykinin (0.1 nM-3 muM)-induced vasodilation, whereas the small (S) K(Ca) blocker apamin (50 and 100 nM) had no effect.	[(2-chlorophenyl)diphenyl-methyl]-1h-pyrazole	68-113	kininogen 1	Homo sapiens	141-151
21172909-8	2011	Bradykinin-mediated vasodilation was attenuated by putative gap junction block with carbenoxolone (100 muM), with remaining dilation blocked by N-nitro l-arginine methyl ester (100 muM) and [1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one] (10 muM), NO synthase and soluble guanylate cyclase blockers, respectively.	Carbenoxolone	84-97	kininogen 1	Homo sapiens	0-10
21172909-8	2011	Bradykinin-mediated vasodilation was attenuated by putative gap junction block with carbenoxolone (100 muM), with remaining dilation blocked by N-nitro l-arginine methyl ester (100 muM) and [1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one] (10 muM), NO synthase and soluble guanylate cyclase blockers, respectively.	1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one	190-235	kininogen 1	Homo sapiens	0-10
20946124-9	2011	BK-induced release of IL-6, but not of IL-8, was partially inhibited by indomethacin (10 microM) and nordihydroguaiaretic acid (10 microM).	Indomethacin	72-84	kininogen 1	Homo sapiens	0-2
20946124-9	2011	BK-induced release of IL-6, but not of IL-8, was partially inhibited by indomethacin (10 microM) and nordihydroguaiaretic acid (10 microM).	Masoprocol	101-126	kininogen 1	Homo sapiens	0-2
21076023-10	2011	Ouabain abolished the dilation in endothelium-denuded vessels to a same extent to that with the combination of ouabain and Ba(2+) in endothelium-intact vessels, whereas neither ouabain nor ouabain plus Ba(2+) reduced EDHF-mediated dilations to bradykinin and ADP.	Ouabain	0-7	kininogen 1	Homo sapiens	244-254
21322579-4	2011	The capability of the SERS-active monolith for label-free detection of biomolecules was demonstrated by measurements of bradykinin and cytochrome c.	sers	22-26	kininogen 1	Homo sapiens	120-130
21186397-2	2011	ACE also cleaves the terminal dipeptide of vasodilating hormone bradykinin (a nonapeptide) to inactivate this hormone.	Dipeptides	30-39	kininogen 1	Homo sapiens	64-74
21108627-7	2011	KEY RESULTS: Recovery of BK-induced responses was slower in cells pretreated with MEN16132 than in those treated with icatibant.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	82-90	kininogen 1	Homo sapiens	25-27
21295852-3	2011	In addition, both bradykinin and vascular endothelial growth factor (VEGF) stimulate nitric oxide (NO), and the VEGF and bradykinin receptors have multiple interactions that converge in the endothelial NO synthase (eNOS)-NO pathway.	Nitric Oxide	85-97	kininogen 1	Homo sapiens	18-28
20946124-5	2011	KEY RESULTS: Density of [3H]-BK binding sites was higher (13-30-fold) and BK evoked a greater (48-fold) IP production, in human than in rat chondrocytes.	Tritium	25-27	kininogen 1	Homo sapiens	29-31
20946124-5	2011	KEY RESULTS: Density of [3H]-BK binding sites was higher (13-30-fold) and BK evoked a greater (48-fold) IP production, in human than in rat chondrocytes.	Inositol Phosphates	104-106	kininogen 1	Homo sapiens	29-31
20946124-8	2011	In human chondrocytes, BK increased release (over 24 h) of IL-6 and IL-8, effects blocked by MEN16132 but not by the B1 receptor antagonist Lys-[Leu8][desArg9]BK.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	93-101	kininogen 1	Homo sapiens	23-25
21695090-7	2011	Ecallantide is a small recombinant protein acting as a potent, specific and reversible inhibitor of plasma kallikrein which binds to plasma kallikrein blocking its binding site, directly inhibiting the conversion of high molecular weight kininogen to bradykinin.	ecallantide	0-11	kininogen 1	Homo sapiens	251-261
20733093-8	2010	Coronary microvascular function studies after 8 days of sunitinib administration showed decreased responses to bradykinin, angiotensin II, and sodium nitroprusside, all normalizing after sunitinib withdrawal.	Sunitinib	56-65	kininogen 1	Homo sapiens	111-121
20584115-12	2011	The relaxing effects of VIP and BK were paralleled by a 4.8-fold and fivefold increase in cAMP, while the production of cGMP was stimulated 38-fold and 119-fold in the presence of CNP or BK, respectively.	Cyclic AMP	90-94	kininogen 1	Homo sapiens	32-34
20584115-12	2011	The relaxing effects of VIP and BK were paralleled by a 4.8-fold and fivefold increase in cAMP, while the production of cGMP was stimulated 38-fold and 119-fold in the presence of CNP or BK, respectively.	Cyclic GMP	120-124	kininogen 1	Homo sapiens	187-189
22073309-10	2011	In human mesenteric microvessels pre-contracted with 35 mmol/L potassium chloride, the endothelium-dependent vasodilation to bradykinin (1 nmol/L to 3 micromol/L) was equally impaired by visfatin and restored upon co-incubation with APO866.	Potassium Chloride	63-81	kininogen 1	Homo sapiens	125-135
20868656-5	2010	We also verified whether the activation of P2X3 and P2X2/3 receptors by endogenous ATP contributes to bradykinin-induced mechanical hyperalgesia via neutrophil migration and/or cytokine release.	Adenosine Triphosphate	83-86	kininogen 1	Homo sapiens	102-112
20868656-7	2010	These findings demonstrate that the activation of P2X3 and P2X2/3 receptors by endogenous ATP mediates bradykinin-induced mechanical hyperalgesia by a mechanism that does not depend on neutrophil migration or cytokines release.	Adenosine Triphosphate	90-93	kininogen 1	Homo sapiens	103-113
20971001-1	2010	A new class of indazole-derived bradykinin B(1) antagonists and their structure-activity relationships (SAR) is reported.	Indazoles	15-23	kininogen 1	Homo sapiens	32-42
21078129-0	2010	Strong cytotoxic effect of the bradykinin antagonist BKM-570 in ovarian cancer cells--analysis of the molecular mechanisms of its antiproliferative action.	BKM-570	53-60	kininogen 1	Homo sapiens	31-41
21078129-3	2010	Recently, the nonpeptide bradykinin (BK) antagonist 2,3,4,5,6-pentafluorocinnamoyl-(o-2,6-dichlorobenzyl)-l-tyrosine-N-(4-amino-2,2,6,6-tetramethyl-piperidyl) amide (BKM-570) was shown to cause impressive growth inhibition of lung and prostate tumors, displaying superior in vivo inhibitory effects than convential chemotherapeutic drugs.	BKM-570	166-173	kininogen 1	Homo sapiens	25-35
21078129-3	2010	Recently, the nonpeptide bradykinin (BK) antagonist 2,3,4,5,6-pentafluorocinnamoyl-(o-2,6-dichlorobenzyl)-l-tyrosine-N-(4-amino-2,2,6,6-tetramethyl-piperidyl) amide (BKM-570) was shown to cause impressive growth inhibition of lung and prostate tumors, displaying superior in vivo inhibitory effects than convential chemotherapeutic drugs.	BKM-570	166-173	kininogen 1	Homo sapiens	37-39
20937084-4	2010	Exposure of BV2 and N9, as well as primary microglial cells to BK or SST increased Abeta uptake in a concentration-dependent manner, whereas endothelin decreased Abeta uptake.	UNII-042A8N37WH	83-88	kininogen 1	Homo sapiens	63-65
21448379-11	2011	The mechanism could be either that Enalapril limits the angiotensin IIinduced production of superoxide radicals which would normally inactivate nitric oxide, or that it may increase bradykinin-mediated nitric oxide release.	Enalapril	35-44	kininogen 1	Homo sapiens	182-192
21448379-11	2011	The mechanism could be either that Enalapril limits the angiotensin IIinduced production of superoxide radicals which would normally inactivate nitric oxide, or that it may increase bradykinin-mediated nitric oxide release.	Nitric Oxide	202-214	kininogen 1	Homo sapiens	182-192
20923691-3	2011	For example, the (Val(1), Thr(6))-bradykinin, present in the defensive skin secretions of many ranids and phyllomedusines, can be generated from plasma kininogens in colubrid snakes-common predators of these frogs.	Threonine	26-29	kininogen 1	Homo sapiens	34-44
20923691-4	2011	Here, we report the presence of (Arg(0), Trp(5), Leu(8))-bradykinin in the skin secretion of the European edible frog, Pelophylax kl.	Arginine	33-36	kininogen 1	Homo sapiens	57-67
20923691-4	2011	Here, we report the presence of (Arg(0), Trp(5), Leu(8))-bradykinin in the skin secretion of the European edible frog, Pelophylax kl.	Tryptophan	41-44	kininogen 1	Homo sapiens	57-67
20923691-4	2011	Here, we report the presence of (Arg(0), Trp(5), Leu(8))-bradykinin in the skin secretion of the European edible frog, Pelophylax kl.	Leucine	49-52	kininogen 1	Homo sapiens	57-67
20923691-10	2011	Synthetic (Arg(0), Trp(5), Leu(8))-bradykinin was previously reported as having multiphasic effects on arterial blood pressure in conscious trout and here we have demonstrated that it can antagonize the relaxation in rat arterial smooth muscle induced by canonical mammalian bradykinin.	Arginine	11-14	kininogen 1	Homo sapiens	35-45
20923691-10	2011	Synthetic (Arg(0), Trp(5), Leu(8))-bradykinin was previously reported as having multiphasic effects on arterial blood pressure in conscious trout and here we have demonstrated that it can antagonize the relaxation in rat arterial smooth muscle induced by canonical mammalian bradykinin.	Arginine	11-14	kininogen 1	Homo sapiens	275-285
20923691-10	2011	Synthetic (Arg(0), Trp(5), Leu(8))-bradykinin was previously reported as having multiphasic effects on arterial blood pressure in conscious trout and here we have demonstrated that it can antagonize the relaxation in rat arterial smooth muscle induced by canonical mammalian bradykinin.	Tryptophan	19-22	kininogen 1	Homo sapiens	35-45
20923691-10	2011	Synthetic (Arg(0), Trp(5), Leu(8))-bradykinin was previously reported as having multiphasic effects on arterial blood pressure in conscious trout and here we have demonstrated that it can antagonize the relaxation in rat arterial smooth muscle induced by canonical mammalian bradykinin.	Tryptophan	19-22	kininogen 1	Homo sapiens	275-285
20923691-10	2011	Synthetic (Arg(0), Trp(5), Leu(8))-bradykinin was previously reported as having multiphasic effects on arterial blood pressure in conscious trout and here we have demonstrated that it can antagonize the relaxation in rat arterial smooth muscle induced by canonical mammalian bradykinin.	Leucine	27-30	kininogen 1	Homo sapiens	35-45
20923691-11	2011	The discovery of (Arg(0), Trp(5), Leu(8))-bradykinin in the defensive skin secretion of this amphibian completes the spectrum of vertebrate taxon-specific BRPs identified from this source.	Arginine	18-21	kininogen 1	Homo sapiens	42-52
20923691-11	2011	The discovery of (Arg(0), Trp(5), Leu(8))-bradykinin in the defensive skin secretion of this amphibian completes the spectrum of vertebrate taxon-specific BRPs identified from this source.	Tryptophan	26-29	kininogen 1	Homo sapiens	42-52
20923691-11	2011	The discovery of (Arg(0), Trp(5), Leu(8))-bradykinin in the defensive skin secretion of this amphibian completes the spectrum of vertebrate taxon-specific BRPs identified from this source.	Leucine	34-37	kininogen 1	Homo sapiens	42-52
20610807-3	2010	Bradykinin-induced dilatation was assessed in the presence and/or absence of pharmacological inhibitors to determine the contribution of nitric oxide and endothelium-derived hyperpolarizing factor (EDHF), as well as that of EDHF-mediated pathways such as myoendothelial gap junctions (MEGJs) and products of arachidonic acid, H(2)O(2) and cytochrome P450 2C9 (CYP2C9).	Arachidonic Acid	308-324	kininogen 1	Homo sapiens	0-10
20610807-3	2010	Bradykinin-induced dilatation was assessed in the presence and/or absence of pharmacological inhibitors to determine the contribution of nitric oxide and endothelium-derived hyperpolarizing factor (EDHF), as well as that of EDHF-mediated pathways such as myoendothelial gap junctions (MEGJs) and products of arachidonic acid, H(2)O(2) and cytochrome P450 2C9 (CYP2C9).	Water	326-331	kininogen 1	Homo sapiens	0-10
20610807-6	2010	In preeclampsia, bradykinin-induced relaxation was reduced via compromised EDHF-type responses, in which the contribution of MEGJs became negligible.	edhf	75-79	kininogen 1	Homo sapiens	17-27
20647494-0	2010	17beta-estradiol rapidly enhances bradykinin signaling in primary sensory neurons in vitro and in vivo.	Estradiol	0-16	kininogen 1	Homo sapiens	34-44
20647494-5	2010	The aim of this study was to characterize the effect of 17beta-estradiol (17beta-E(2)) on signaling of the inflammatory mediator bradykinin (BK) in primary cultures of rat sensory neurons and a behavioral model of thermal allodynia in rats.	Estradiol	56-72	kininogen 1	Homo sapiens	129-139
20647494-5	2010	The aim of this study was to characterize the effect of 17beta-estradiol (17beta-E(2)) on signaling of the inflammatory mediator bradykinin (BK) in primary cultures of rat sensory neurons and a behavioral model of thermal allodynia in rats.	17beta-e(2)	74-85	kininogen 1	Homo sapiens	129-139
20647494-7	2010	The 17beta-E(2)-mediated enhancement of BK signaling was not blocked by the transcription inhibitor anisomycin and was mediated by a membrane-associated ER.	17beta-e(2)	4-15	kininogen 1	Homo sapiens	40-42
20647494-7	2010	The 17beta-E(2)-mediated enhancement of BK signaling was not blocked by the transcription inhibitor anisomycin and was mediated by a membrane-associated ER.	Anisomycin	100-110	kininogen 1	Homo sapiens	40-42
20875097-7	2010	However exposure to bradykinin increased the Ca2+ response to a second application of ATP, consistent with increased resensitization.	Adenosine Triphosphate	86-89	kininogen 1	Homo sapiens	20-30
20875097-8	2010	The bradykinin effect on resensitization was similar in the absence of extracellular Ca2+ or in the presence of the PKC activator PMA, but was inhibited by the protein phosphatase inhibitor okadaic acid and the PI3K inhibitor LY294002.	Tetradecanoylphorbol Acetate	130-133	kininogen 1	Homo sapiens	4-14
20875097-8	2010	The bradykinin effect on resensitization was similar in the absence of extracellular Ca2+ or in the presence of the PKC activator PMA, but was inhibited by the protein phosphatase inhibitor okadaic acid and the PI3K inhibitor LY294002.	Okadaic Acid	190-202	kininogen 1	Homo sapiens	4-14
20875097-8	2010	The bradykinin effect on resensitization was similar in the absence of extracellular Ca2+ or in the presence of the PKC activator PMA, but was inhibited by the protein phosphatase inhibitor okadaic acid and the PI3K inhibitor LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	226-234	kininogen 1	Homo sapiens	4-14
20731384-3	2010	Porous silicon prepared in this way proved to be an excellent substrate for desorption/ionization on silicon (DIOS) mass spectrometry (MS) using adenosine, Pro-Leu-Gly tripeptide, and [Des-Arg(9)]-bradykinin as the model compounds.	Silicon	7-14	kininogen 1	Homo sapiens	197-207
20511415-10	2010	Acetylcholine and bradykinin relaxed norepinephrine preconstrictions by approximately 20% and approximately 40%, respectively.	Norepinephrine	37-51	kininogen 1	Homo sapiens	18-28
20536386-5	2010	A549 cells bound FITC-labelled HK, which was only partially inhibited by a combination of antibodies to the HK binding proteins.	Fluorescein-5-isothiocyanate	17-21	kininogen 1	Homo sapiens	31-33
20536386-5	2010	A549 cells bound FITC-labelled HK, which was only partially inhibited by a combination of antibodies to the HK binding proteins.	Fluorescein-5-isothiocyanate	17-21	kininogen 1	Homo sapiens	108-110
20536386-7	2010	HK-PPK activation was inhibited by cysteine, BK and protamine, and by novobiocin, a heat shock protein 90 (HSP90) inhibitor.	Cysteine	35-43	kininogen 1	Homo sapiens	0-2
20536386-7	2010	HK-PPK activation was inhibited by cysteine, BK and protamine, and by novobiocin, a heat shock protein 90 (HSP90) inhibitor.	Novobiocin	70-80	kininogen 1	Homo sapiens	0-2
20580570-6	2010	With these precautions, levels of carbamino group formation of angiotensin II and bradykinin determined from mass spectra agree with those expected to be in solution, calculated from literature equilibrium constants.	carbamino	34-43	kininogen 1	Homo sapiens	82-92
20504911-0	2010	Contribution of bradykinin B2 receptors to the inhibition by valsartan of systemic and renal effects of exogenous angiotensin II in salt-repleted humans.	Valsartan	61-70	kininogen 1	Homo sapiens	16-26
20469905-0	2010	Evidence for a quasi-equilibrium distribution of states for bradykinin [M + 3H]3+ ions in the gas phase.	Tritium	76-78	kininogen 1	Homo sapiens	60-70
20557135-5	2010	Both ITIH4 ([666-687]) and des-Arg(9)-bradykinin showed statistically significantly higher median concentrations in breast cancer samples than in matched control samples.	des-arg	27-34	kininogen 1	Homo sapiens	38-48
20557135-8	2010	In this study, we confirmed that the exoprotease breakdown peptides, ITIH4 (666-687]) and des-Arg(9)-bradykinin, differed between breast cancer cases and controls, supporting the potential of degradome markers for the diagnosis of breast cancer.	des-arg	90-97	kininogen 1	Homo sapiens	101-111
20427081-0	2010	Bradykinin forming capacity of oversulfated chondroitin sulfate contaminated heparin in vitro.	Chondroitin Sulfates	44-63	kininogen 1	Homo sapiens	0-10
20427081-0	2010	Bradykinin forming capacity of oversulfated chondroitin sulfate contaminated heparin in vitro.	Heparin	77-84	kininogen 1	Homo sapiens	0-10
20427081-6	2010	We demonstrate a highly significant correlation between the concentration of OSCS present in the contaminated heparin and BK released concentration.	Heparin	110-117	kininogen 1	Homo sapiens	122-124
20427081-7	2010	In conclusion, for the first time, we show that OSCS contaminated heparin incubated with human plasma has the capacity to liberate BK at a concentration that could explain the role of this inflammatory peptide in the pathophysiology of AR associated with OSCS contaminated heparin.	Heparin	66-73	kininogen 1	Homo sapiens	131-133
20427081-7	2010	In conclusion, for the first time, we show that OSCS contaminated heparin incubated with human plasma has the capacity to liberate BK at a concentration that could explain the role of this inflammatory peptide in the pathophysiology of AR associated with OSCS contaminated heparin.	Heparin	273-280	kininogen 1	Homo sapiens	131-133
20552714-7	2010	In an O-trap installed in a 5 T desk-top cryogen-free superconducting magnet, the resolving power of R = 80,000 was achieved for bradykinin [M + 2H](2+) (m/z 531; equivalent to 100,000 when recalculated for m/z 400) in 0.2 s analysis time (transient length), and R = 300,000 at m/z 531 for a 1 s transient.	Deuterium	145-147	kininogen 1	Homo sapiens	129-139
20580091-7	2010	However degradation of bradykinin by carboxypeptidase N (in plasma) or carboxypeptidase M (on endothelial cells) yields des-arg-9 (Kerbiriou and Griffin, 1979) bradykinin which interacts with B-1 receptors.	des-arg	120-127	kininogen 1	Homo sapiens	23-33
20580091-7	2010	However degradation of bradykinin by carboxypeptidase N (in plasma) or carboxypeptidase M (on endothelial cells) yields des-arg-9 (Kerbiriou and Griffin, 1979) bradykinin which interacts with B-1 receptors.	des-arg	120-127	kininogen 1	Homo sapiens	160-170
20670410-0	2010	Bradykinin and adenosine receptors mediate desflurane induced postconditioning in human myocardium: role of reactive oxygen species.	Desflurane	43-53	kininogen 1	Homo sapiens	0-10
20670410-0	2010	Bradykinin and adenosine receptors mediate desflurane induced postconditioning in human myocardium: role of reactive oxygen species.	Reactive Oxygen Species	108-131	kininogen 1	Homo sapiens	0-10
20670410-11	2010	Adenosine (80 +/- 9% of baseline) and bradykinin (83 +/- 4% of baseline) induced postconditioning (P &lt; 0.0001 vs control), N-mercaptopropionylglycine abolished the beneficial effects of adenosine and bradykinin (54 +/- 8 and 58 +/- 5% of baseline, respectively).	Adenosine	0-9	kininogen 1	Homo sapiens	203-213
20670410-11	2010	Adenosine (80 +/- 9% of baseline) and bradykinin (83 +/- 4% of baseline) induced postconditioning (P &lt; 0.0001 vs control), N-mercaptopropionylglycine abolished the beneficial effects of adenosine and bradykinin (54 +/- 8 and 58 +/- 5% of baseline, respectively).	n-mercaptopropionylglycine	126-152	kininogen 1	Homo sapiens	38-48
20670410-11	2010	Adenosine (80 +/- 9% of baseline) and bradykinin (83 +/- 4% of baseline) induced postconditioning (P &lt; 0.0001 vs control), N-mercaptopropionylglycine abolished the beneficial effects of adenosine and bradykinin (54 +/- 8 and 58 +/- 5% of baseline, respectively).	n-mercaptopropionylglycine	126-152	kininogen 1	Homo sapiens	203-213
20670410-11	2010	Adenosine (80 +/- 9% of baseline) and bradykinin (83 +/- 4% of baseline) induced postconditioning (P &lt; 0.0001 vs control), N-mercaptopropionylglycine abolished the beneficial effects of adenosine and bradykinin (54 +/- 8 and 58 +/- 5% of baseline, respectively).	Adenosine	189-198	kininogen 1	Homo sapiens	38-48
20670410-12	2010	CONCLUSIONS: In vitro, desflurane-induced postconditioning depends on reactive oxygen species production, activation of adenosine and bradykinin B2 receptors.	Desflurane	23-33	kininogen 1	Homo sapiens	134-144
20670410-13	2010	And, the cardioprotective effect of adenosine and bradykinin administered at the beginning of reoxygenation, was mediated, at least in part, through ROS production.	Reactive Oxygen Species	149-152	kininogen 1	Homo sapiens	50-60
20423727-1	2010	Bradykinin, a potent vasodilator, stimulates the formation of reactive oxygen species and F(2)-isoprostanes in vitro.	Reactive Oxygen Species	62-85	kininogen 1	Homo sapiens	0-10
20423727-1	2010	Bradykinin, a potent vasodilator, stimulates the formation of reactive oxygen species and F(2)-isoprostanes in vitro.	F2-Isoprostanes	90-107	kininogen 1	Homo sapiens	0-10
20423727-3	2010	This study tested the hypothesis that bradykinin induces oxidative stress through a nitric oxide (NO)-dependent mechanism in the human vasculature.	Nitric Oxide	84-96	kininogen 1	Homo sapiens	38-48
20423727-6	2010	Bradykinin caused a significant increase in FBF and net F(2)-isoprostane release in both normotensive and hypertensive subjects.	F2-Isoprostanes	56-72	kininogen 1	Homo sapiens	0-10
20423727-7	2010	During NO synthase inhibition, bradykinin significantly increased net F(2)-isoprostane release in both groups (P=0.001) and there was no effect of L-NMMA on bradykinin-stimulated F(2)-isoprostane release (P=0.46).	F2-Isoprostanes	70-86	kininogen 1	Homo sapiens	31-41
20590639-7	2010	Bradykinin, but not NS309 or CyPPA increased endothelial cell calcium.	Calcium	62-69	kininogen 1	Homo sapiens	0-10
20590639-8	2010	Pre-incubation with NS309 or CyPPA enhanced bradykinin relaxation without changing endothelial cell calcium.	6,7-dichloro-1H-indole-2,3-dione 3-oxime	20-25	kininogen 1	Homo sapiens	44-54
20590639-12	2010	CONCLUSIONS AND IMPLICATIONS: In porcine retinal arterioles, bradykinin increases endothelial cell calcium leading to activation of SK(Ca) and IK(Ca) channels.	Calcium	99-106	kininogen 1	Homo sapiens	61-71
21054968-11	2010	The ELISA outcomes documented that kininogen-1 concentration in vitreous were significantly higher in severe PVR patients than those in mild PVR (281.0 +- 63.0 &amp; 237.5 +- 32.1) microg/L (t = 5.44, P &lt; 0.05).	Adenosine Monophosphate	161-164	kininogen 1	Homo sapiens	35-46
20469905-1	2010	Multidimensional ion mobility spectrometry coupled with mass spectrometry (IMS-IMS-MS) techniques are used to select and activate six different gas-phase conformations of bradykinin [M + 3H](3+) ions.	Tritium	187-189	kininogen 1	Homo sapiens	171-181
19886924-0	2010	Efficacy of tranexamic acid in sporadic idiopathic bradykinin angioedema.	Tranexamic Acid	12-27	kininogen 1	Homo sapiens	51-61
20568386-2	2010	Ecallantide is a novel potent inhibitor of human plasma kallikrein, a key mediator of the excessive formation of bradykinin associated with the signs and symptoms of an HAE attack.	ecallantide	0-11	kininogen 1	Homo sapiens	113-123
20299424-2	2010	In the current study, we examined the regulation of hOAT3 by peptide hormone bradykinin (BK) in COS-7 cells.	carbonyl sulfide	96-99	kininogen 1	Homo sapiens	77-87
20299424-5	2010	BK-induced stimulation of hOAT3 activity could be prevented by treating hOAT3-expressing cells with staurosporine, a general inhibitor for protein kinase C (PKC).	Staurosporine	100-113	kininogen 1	Homo sapiens	0-2
19923143-2	2010	METHODS AND RESULTS: High-glucose (HG) super-induced interleukin (IL)-6, CCL-2, transforming growth factor (TGF)-beta, vascular endothelial growth factor (VEGF) and B(2)K receptor (B(2)KR) mRNA in cultured proximal tubular epithelial cells (PTEC), whereas bradykinin (BK) upregulated IL-6, CCL-2 and TGF-beta mRNA.	Glucose	26-33	kininogen 1	Homo sapiens	256-266
20567501-8	2010	High glucose disturbed BK-induced NO generation by MNC-derived cultured angiogenic cells.	Glucose	5-12	kininogen 1	Homo sapiens	23-25
20411591-6	2010	Bradykinin-mediated migration was attenuated by the selective COX-2 inhibitor NS-398.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	78-84	kininogen 1	Homo sapiens	0-10
20411591-8	2010	Bradykinin-mediated migration was attenuated by phosphoinositide 3-kinase (PI-3 kinase)/AKT inhibitors LY 294002 and wortmannin.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	103-112	kininogen 1	Homo sapiens	0-10
20411591-8	2010	Bradykinin-mediated migration was attenuated by phosphoinositide 3-kinase (PI-3 kinase)/AKT inhibitors LY 294002 and wortmannin.	Wortmannin	117-127	kininogen 1	Homo sapiens	0-10
20411591-9	2010	Bradykinin stimulation also increased the phosphorylation of the p85 subunit of PI-3 kinase and serine 473 of AKT.	Serine	96-102	kininogen 1	Homo sapiens	0-10
20411591-10	2010	Treatment of bradykinin with AP-1 inhibitors Tanshinone IIA and curcumin also reduced COX-2 expression and glioma cell migration.	tanshinone	45-59	kininogen 1	Homo sapiens	13-23
20411591-10	2010	Treatment of bradykinin with AP-1 inhibitors Tanshinone IIA and curcumin also reduced COX-2 expression and glioma cell migration.	Curcumin	64-72	kininogen 1	Homo sapiens	13-23
20411591-12	2010	AP-1 promoter analysis in the luciferase reporter construct showed that bradykinin increased AP-1 transcription activity and was inhibited by LY 294002 and wortmannin.	Wortmannin	156-166	kininogen 1	Homo sapiens	72-82
20375905-3	2010	RESULTS: IL-6 inhibited the phosphorylation of eNOS at Ser1177 and the bradykinin-stimulated nitric oxide production; however, eNOS protein expression was not changed.	Nitric Oxide	93-105	kininogen 1	Homo sapiens	71-81
20375905-4	2010	In addition, IL-6 inhibited bradykinin-stimulated Akt phosphorylation at Ser473 and Thr 308 without affecting the Akt protein expression.	Threonine	84-87	kininogen 1	Homo sapiens	28-38
20224870-1	2010	Epoxyeicosatrienoic acids (EETs) are cytochrome P450 metabolites of arachidonic acid that are produced by the vascular endothelium in response to agonists such as bradykinin and acetylcholine or physical stimuli such as shear stress or cyclic stretch.	epoxyeicosatrienoic acids	0-25	kininogen 1	Homo sapiens	163-173
20224870-1	2010	Epoxyeicosatrienoic acids (EETs) are cytochrome P450 metabolites of arachidonic acid that are produced by the vascular endothelium in response to agonists such as bradykinin and acetylcholine or physical stimuli such as shear stress or cyclic stretch.	eets	27-31	kininogen 1	Homo sapiens	163-173
20224870-1	2010	Epoxyeicosatrienoic acids (EETs) are cytochrome P450 metabolites of arachidonic acid that are produced by the vascular endothelium in response to agonists such as bradykinin and acetylcholine or physical stimuli such as shear stress or cyclic stretch.	Arachidonic Acid	68-84	kininogen 1	Homo sapiens	163-173
20631409-12	2010	The thrombolytic actions of lipophilic ACE-Is (e.g., quinapril and perindopril) were prevented by pretreatment with either bradykinin B(2) receptor antagonists (e.g., icatibant) or with endothelial COX-2 inhibitors (e.g., rofecoxib, celecoxib and high dose aspirin).	Quinapril	53-62	kininogen 1	Homo sapiens	123-133
20631409-12	2010	The thrombolytic actions of lipophilic ACE-Is (e.g., quinapril and perindopril) were prevented by pretreatment with either bradykinin B(2) receptor antagonists (e.g., icatibant) or with endothelial COX-2 inhibitors (e.g., rofecoxib, celecoxib and high dose aspirin).	Perindopril	67-78	kininogen 1	Homo sapiens	123-133
20631409-12	2010	The thrombolytic actions of lipophilic ACE-Is (e.g., quinapril and perindopril) were prevented by pretreatment with either bradykinin B(2) receptor antagonists (e.g., icatibant) or with endothelial COX-2 inhibitors (e.g., rofecoxib, celecoxib and high dose aspirin).	rofecoxib	222-231	kininogen 1	Homo sapiens	123-133
20631409-12	2010	The thrombolytic actions of lipophilic ACE-Is (e.g., quinapril and perindopril) were prevented by pretreatment with either bradykinin B(2) receptor antagonists (e.g., icatibant) or with endothelial COX-2 inhibitors (e.g., rofecoxib, celecoxib and high dose aspirin).	Celecoxib	233-242	kininogen 1	Homo sapiens	123-133
20631409-12	2010	The thrombolytic actions of lipophilic ACE-Is (e.g., quinapril and perindopril) were prevented by pretreatment with either bradykinin B(2) receptor antagonists (e.g., icatibant) or with endothelial COX-2 inhibitors (e.g., rofecoxib, celecoxib and high dose aspirin).	Aspirin	257-264	kininogen 1	Homo sapiens	123-133
20309548-6	2010	RESULTS: Exposure to ST solution with H-R at both 37 and 4 degrees C markedly reduced bradykinin-induced relaxation in coronary small arteries.	h-r	38-41	kininogen 1	Homo sapiens	86-96
20309548-7	2010	Addition of AVE3085 in ST solution at 37 degrees C preserved the vasorelaxant response to bradykinin (95.7 +/- 2.1% vs. 69.2 +/- 6.6%, p &lt; 0.01), with the protective effect comparable to that of L-arginine (96.1 +/- 3.3% vs. 70.6 +/- 8.7%, p &lt; 0.05).	2,2-difluorobenzo(1,3)dioxole-5-carboxylic acid indan-2-ylamide	12-19	kininogen 1	Homo sapiens	90-100
20174953-10	2010	Bradykinin, an inducer of nitric oxide, prompted two folds higher nitric oxide production along with simulated microgravity in a synergistic manner.	Nitric Oxide	26-38	kininogen 1	Homo sapiens	0-10
20174953-10	2010	Bradykinin, an inducer of nitric oxide, prompted two folds higher nitric oxide production along with simulated microgravity in a synergistic manner.	Nitric Oxide	66-78	kininogen 1	Homo sapiens	0-10
20152898-4	2010	In this report, we present the role of ASB in the regulation of the kininogen-bradykinin axis owing to its effect on chondroitin-4-sulfation and the interaction of C4S with kininogen.	chondroitin-4	117-130	kininogen 1	Homo sapiens	78-88
20152898-9	2010	Because ASB activity is influenced by several ions, including chloride and phosphate, ASB activity may provide a link between salt responsiveness and the bradykinin-associated mechanism of blood pressure regulation.	Chlorides	62-70	kininogen 1	Homo sapiens	154-164
20152898-9	2010	Because ASB activity is influenced by several ions, including chloride and phosphate, ASB activity may provide a link between salt responsiveness and the bradykinin-associated mechanism of blood pressure regulation.	Phosphates	75-84	kininogen 1	Homo sapiens	154-164
20152898-9	2010	Because ASB activity is influenced by several ions, including chloride and phosphate, ASB activity may provide a link between salt responsiveness and the bradykinin-associated mechanism of blood pressure regulation.	Salts	126-130	kininogen 1	Homo sapiens	154-164
20082561-0	2010	Evidence for prostacyclin and cAMP upregulation by bradykinin and insulin-like growth factor 1 in vascular smooth muscle cells.	Epoprostenol	13-25	kininogen 1	Homo sapiens	51-61
20082561-0	2010	Evidence for prostacyclin and cAMP upregulation by bradykinin and insulin-like growth factor 1 in vascular smooth muscle cells.	Cyclic AMP	30-34	kininogen 1	Homo sapiens	51-61
20082561-3	2010	Activation of BK or IGF-1 receptors stimulated the synthesis and release of prostacyclin (PGI(2)) leading to increased production of cAMP in VSMC.	Epoprostenol	76-88	kininogen 1	Homo sapiens	14-16
20082561-3	2010	Activation of BK or IGF-1 receptors stimulated the synthesis and release of prostacyclin (PGI(2)) leading to increased production of cAMP in VSMC.	Epoprostenol	90-96	kininogen 1	Homo sapiens	14-16
20082561-3	2010	Activation of BK or IGF-1 receptors stimulated the synthesis and release of prostacyclin (PGI(2)) leading to increased production of cAMP in VSMC.	Cyclic AMP	133-137	kininogen 1	Homo sapiens	14-16
20082561-3	2010	Activation of BK or IGF-1 receptors stimulated the synthesis and release of prostacyclin (PGI(2)) leading to increased production of cAMP in VSMC.	vsmc	141-145	kininogen 1	Homo sapiens	14-16
20082561-4	2010	Inhibition of p42/p44(mapk) or src kinases prevented the increase in PGI(2) and cAMP observed in response to BK or IGF-1, indicating a role for these kinases in the regulation of cPLA(2) activity in the VSMC.	Prostaglandins I	69-72	kininogen 1	Homo sapiens	109-111
20082561-4	2010	Inhibition of p42/p44(mapk) or src kinases prevented the increase in PGI(2) and cAMP observed in response to BK or IGF-1, indicating a role for these kinases in the regulation of cPLA(2) activity in the VSMC.	Cyclic AMP	80-84	kininogen 1	Homo sapiens	109-111
20135098-0	2010	MRP transporters as membrane machinery in the bradykinin-inducible export of ATP.	Adenosine Triphosphate	77-80	kininogen 1	Homo sapiens	46-56
20135098-3	2010	Activation of B2-receptor with bradykinin-induced massive release of ATP from cultured taenia coli smooth muscle cells.	Adenosine Triphosphate	69-72	kininogen 1	Homo sapiens	31-41
19897331-1	2010	Compound CU201 [SUIM-(d-Arg-Arg-Pro-Hyp-Gly-Igl-Ser-d-Igl-Oic-Arg)(2), where SUIM=suberimidyl; Hyp=trans-4-hydroxyproline; Igl=alpha-(2-indanyl)-glycine; Oic=octahydroindole-2-carboxylic acid], is a dimeric analog of the potent bradykinin antagonist peptide B9430.	CU201	9-14	kininogen 1	Homo sapiens	228-238
19850828-8	2010	Nitric oxide (NO) synthase inhibitor L-NAME nearly abolished dilations to bradykinin and flow and attenuated the adenosine-induced dilation without altering the response to nitroprusside.	Nitric Oxide	0-12	kininogen 1	Homo sapiens	74-84
19850828-8	2010	Nitric oxide (NO) synthase inhibitor L-NAME nearly abolished dilations to bradykinin and flow and attenuated the adenosine-induced dilation without altering the response to nitroprusside.	NG-Nitroarginine Methyl Ester	37-43	kininogen 1	Homo sapiens	74-84
19923143-2	2010	METHODS AND RESULTS: High-glucose (HG) super-induced interleukin (IL)-6, CCL-2, transforming growth factor (TGF)-beta, vascular endothelial growth factor (VEGF) and B(2)K receptor (B(2)KR) mRNA in cultured proximal tubular epithelial cells (PTEC), whereas bradykinin (BK) upregulated IL-6, CCL-2 and TGF-beta mRNA.	Glucose	26-33	kininogen 1	Homo sapiens	268-270
19923143-5	2010	Inhibition of MAPK p42/p44 by PD98059 partially reduced HG and BK induction of IL-6, CCL-2 and TGF-beta, whereas inhibition of PKC by staurosporine partially reduced HG- but not BK-induced overexpression of these cytokines and that of VEGF.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	30-37	kininogen 1	Homo sapiens	63-65
20007914-7	2010	In LS heart tissues, lucigenin chemiluminescence was increased 2.3-fold to angiotensin II (10(-8) mol/L), and bradykinin (10(-4) mol/L) induced reduction of myocardial oxygen consumption in vitro was decreased (40 + or - 1.3% to 16 + or - 6.3%) and completely restored by coincubation with tiron, tempol or apocynin.	10,10'-dimethyl-9,9'-biacridinium	21-30	kininogen 1	Homo sapiens	110-120
20007914-7	2010	In LS heart tissues, lucigenin chemiluminescence was increased 2.3-fold to angiotensin II (10(-8) mol/L), and bradykinin (10(-4) mol/L) induced reduction of myocardial oxygen consumption in vitro was decreased (40 + or - 1.3% to 16 + or - 6.3%) and completely restored by coincubation with tiron, tempol or apocynin.	Oxygen	168-174	kininogen 1	Homo sapiens	110-120
20007914-7	2010	In LS heart tissues, lucigenin chemiluminescence was increased 2.3-fold to angiotensin II (10(-8) mol/L), and bradykinin (10(-4) mol/L) induced reduction of myocardial oxygen consumption in vitro was decreased (40 + or - 1.3% to 16 + or - 6.3%) and completely restored by coincubation with tiron, tempol or apocynin.	1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt	290-295	kininogen 1	Homo sapiens	110-120
20007914-7	2010	In LS heart tissues, lucigenin chemiluminescence was increased 2.3-fold to angiotensin II (10(-8) mol/L), and bradykinin (10(-4) mol/L) induced reduction of myocardial oxygen consumption in vitro was decreased (40 + or - 1.3% to 16 + or - 6.3%) and completely restored by coincubation with tiron, tempol or apocynin.	tempol	297-303	kininogen 1	Homo sapiens	110-120
20007914-7	2010	In LS heart tissues, lucigenin chemiluminescence was increased 2.3-fold to angiotensin II (10(-8) mol/L), and bradykinin (10(-4) mol/L) induced reduction of myocardial oxygen consumption in vitro was decreased (40 + or - 1.3% to 16 + or - 6.3%) and completely restored by coincubation with tiron, tempol or apocynin.	acetovanillone	307-315	kininogen 1	Homo sapiens	110-120
20128797-4	2010	KEY RESULTS: Exposure to high glucose concentrations strongly inhibited eNOS phosphorylation at Ser-1177 and dephosphorylation at Thr-495 in bradykinin (BK)-stimulated cells.	Glucose	30-37	kininogen 1	Homo sapiens	141-151
20128797-4	2010	KEY RESULTS: Exposure to high glucose concentrations strongly inhibited eNOS phosphorylation at Ser-1177 and dephosphorylation at Thr-495 in bradykinin (BK)-stimulated cells.	Glucose	30-37	kininogen 1	Homo sapiens	153-155
20128797-8	2010	The phosphatidylinositol 3-kinase inhibitor wortmannin blocked the reversal by oligonol of phosphorylation at Ser-1177, but not dephosphorylation at Thr-495, in BK-stimulated cells exposed to high glucose.	Wortmannin	44-54	kininogen 1	Homo sapiens	161-163
20128797-4	2010	KEY RESULTS: Exposure to high glucose concentrations strongly inhibited eNOS phosphorylation at Ser-1177 and dephosphorylation at Thr-495 in bradykinin (BK)-stimulated cells.	Threonine	130-133	kininogen 1	Homo sapiens	141-151
20128797-4	2010	KEY RESULTS: Exposure to high glucose concentrations strongly inhibited eNOS phosphorylation at Ser-1177 and dephosphorylation at Thr-495 in bradykinin (BK)-stimulated cells.	Threonine	130-133	kininogen 1	Homo sapiens	153-155
20128797-8	2010	The phosphatidylinositol 3-kinase inhibitor wortmannin blocked the reversal by oligonol of phosphorylation at Ser-1177, but not dephosphorylation at Thr-495, in BK-stimulated cells exposed to high glucose.	oligonol	79-87	kininogen 1	Homo sapiens	161-163
20065150-3	2010	They can indirectly potentiate the actions of bradykinin (BK) and ACE-resistant BK analogs on B2Rs to elevate arachidonic acid and NO release in laboratory experiments.	Arachidonic Acid	110-126	kininogen 1	Homo sapiens	46-56
20128797-8	2010	The phosphatidylinositol 3-kinase inhibitor wortmannin blocked the reversal by oligonol of phosphorylation at Ser-1177, but not dephosphorylation at Thr-495, in BK-stimulated cells exposed to high glucose.	Serine	110-113	kininogen 1	Homo sapiens	161-163
20128797-9	2010	The effect of oligonol on BK dephosphorylation under high glucose was mimicked by protein kinase C (PKC) epsilon-neutralizing peptides.	oligonol	14-22	kininogen 1	Homo sapiens	26-28
20128797-9	2010	The effect of oligonol on BK dephosphorylation under high glucose was mimicked by protein kinase C (PKC) epsilon-neutralizing peptides.	Glucose	58-65	kininogen 1	Homo sapiens	26-28
20128797-11	2010	Oligonol also prevented high glucose-induced attenuation of BK-stimulated NO production.	oligonol	0-8	kininogen 1	Homo sapiens	60-62
20128797-11	2010	Oligonol also prevented high glucose-induced attenuation of BK-stimulated NO production.	Glucose	29-36	kininogen 1	Homo sapiens	60-62
20065150-3	2010	They can indirectly potentiate the actions of bradykinin (BK) and ACE-resistant BK analogs on B2Rs to elevate arachidonic acid and NO release in laboratory experiments.	Arachidonic Acid	110-126	kininogen 1	Homo sapiens	58-60
22466497-6	2010	It has been postulated that angiotensin II receptor activates the bradykinin-prostaglandin-nitric oxide cascade, resulting in bradykinin-mediated side effects of ARBs such as angioedema, but the true mechanism remains largely unknown.	Prostaglandins	77-90	kininogen 1	Homo sapiens	66-76
20065150-3	2010	They can indirectly potentiate the actions of bradykinin (BK) and ACE-resistant BK analogs on B2Rs to elevate arachidonic acid and NO release in laboratory experiments.	Arachidonic Acid	110-126	kininogen 1	Homo sapiens	80-82
22466497-6	2010	It has been postulated that angiotensin II receptor activates the bradykinin-prostaglandin-nitric oxide cascade, resulting in bradykinin-mediated side effects of ARBs such as angioedema, but the true mechanism remains largely unknown.	Prostaglandins	77-90	kininogen 1	Homo sapiens	126-136
21081214-1	2010	Epoxyeicosatrienoic acids (EETs) are cytochrome P450 metabolites of arachidonic acid that are produced by the vascular endothelium in responses to various stimuli such as the agonists acetylcholine (ACH) or bradykinin or by shear stress which activates phospholipase A(2) to release arachidonic acid.	epoxyeicosatrienoic acids	0-25	kininogen 1	Homo sapiens	207-217
22466497-6	2010	It has been postulated that angiotensin II receptor activates the bradykinin-prostaglandin-nitric oxide cascade, resulting in bradykinin-mediated side effects of ARBs such as angioedema, but the true mechanism remains largely unknown.	Nitric Oxide	91-103	kininogen 1	Homo sapiens	66-76
22466497-6	2010	It has been postulated that angiotensin II receptor activates the bradykinin-prostaglandin-nitric oxide cascade, resulting in bradykinin-mediated side effects of ARBs such as angioedema, but the true mechanism remains largely unknown.	Nitric Oxide	91-103	kininogen 1	Homo sapiens	126-136
20184800-9	2010	Moreover, AG-1478 (2 microM), reduced BK-induced IL-6 secretion by 28% and abrogated the synergic induction of IL-6 induced by BK plus EGF (from 8312 +/- 1267 to 3229 +/- 597 pg/ml, n = 5, p &lt; 0.05).	RTKI cpd	10-17	kininogen 1	Homo sapiens	38-40
20184800-9	2010	Moreover, AG-1478 (2 microM), reduced BK-induced IL-6 secretion by 28% and abrogated the synergic induction of IL-6 induced by BK plus EGF (from 8312 +/- 1267 to 3229 +/- 597 pg/ml, n = 5, p &lt; 0.05).	RTKI cpd	10-17	kininogen 1	Homo sapiens	127-129
20184800-10	2010	AG-1478 dual effects on IL-6 secretion induced by BK alone or BK plus EGF were also observed in cells treated with genistein, a tyrosine kinase inhibitor, and AG-825, an ErbB-2 inhibitor.	RTKI cpd	0-7	kininogen 1	Homo sapiens	50-52
20184800-10	2010	AG-1478 dual effects on IL-6 secretion induced by BK alone or BK plus EGF were also observed in cells treated with genistein, a tyrosine kinase inhibitor, and AG-825, an ErbB-2 inhibitor.	RTKI cpd	0-7	kininogen 1	Homo sapiens	62-64
20184800-10	2010	AG-1478 dual effects on IL-6 secretion induced by BK alone or BK plus EGF were also observed in cells treated with genistein, a tyrosine kinase inhibitor, and AG-825, an ErbB-2 inhibitor.	Genistein	115-124	kininogen 1	Homo sapiens	62-64
20184800-10	2010	AG-1478 dual effects on IL-6 secretion induced by BK alone or BK plus EGF were also observed in cells treated with genistein, a tyrosine kinase inhibitor, and AG-825, an ErbB-2 inhibitor.	tyrphostin AG825	159-165	kininogen 1	Homo sapiens	62-64
19861349-9	2010	Signalling pathways induced by the stimulation of the AT(2) receptor are poorly understood, but three main mechanisms have been described: (a) activation of protein phosphatases causing protein dephosphorylation; (b) activation of bradykinin/nitric oxide/cyclic guanosine 3",5"-monophosphate pathway; and (c) stimulation of phospholipase A(2) and release of arachidonic acid.	Cyclic GMP	255-291	kininogen 1	Homo sapiens	231-241
19861349-9	2010	Signalling pathways induced by the stimulation of the AT(2) receptor are poorly understood, but three main mechanisms have been described: (a) activation of protein phosphatases causing protein dephosphorylation; (b) activation of bradykinin/nitric oxide/cyclic guanosine 3",5"-monophosphate pathway; and (c) stimulation of phospholipase A(2) and release of arachidonic acid.	Arachidonic Acid	358-374	kininogen 1	Homo sapiens	231-241
19562481-3	2010	The enzyme directly transferred Galbeta1-3GalNAc to serine or threonine residues of bioactive peptides such as PAMP-12, bradykinin, peptide-T and MUC1a when Galbeta1-3GalNAcalpha1-pNP was used as a donor substrate.	Serine	52-58	kininogen 1	Homo sapiens	120-130
19562481-3	2010	The enzyme directly transferred Galbeta1-3GalNAc to serine or threonine residues of bioactive peptides such as PAMP-12, bradykinin, peptide-T and MUC1a when Galbeta1-3GalNAcalpha1-pNP was used as a donor substrate.	Threonine	62-71	kininogen 1	Homo sapiens	120-130
21081214-1	2010	Epoxyeicosatrienoic acids (EETs) are cytochrome P450 metabolites of arachidonic acid that are produced by the vascular endothelium in responses to various stimuli such as the agonists acetylcholine (ACH) or bradykinin or by shear stress which activates phospholipase A(2) to release arachidonic acid.	eets	27-31	kininogen 1	Homo sapiens	207-217
21081214-1	2010	Epoxyeicosatrienoic acids (EETs) are cytochrome P450 metabolites of arachidonic acid that are produced by the vascular endothelium in responses to various stimuli such as the agonists acetylcholine (ACH) or bradykinin or by shear stress which activates phospholipase A(2) to release arachidonic acid.	Arachidonic Acid	68-84	kininogen 1	Homo sapiens	207-217
21081214-1	2010	Epoxyeicosatrienoic acids (EETs) are cytochrome P450 metabolites of arachidonic acid that are produced by the vascular endothelium in responses to various stimuli such as the agonists acetylcholine (ACH) or bradykinin or by shear stress which activates phospholipase A(2) to release arachidonic acid.	Acetylcholine	184-197	kininogen 1	Homo sapiens	207-217
19854233-11	2010	In contrast to the result in human glioma cells, bradykinin inhibits the zymosan-induced expression of TNF-alpha and IL-1beta in rat astrocytes, which shows a species-dependent manner.	Zymosan	73-80	kininogen 1	Homo sapiens	49-59
19945846-9	2010	Propofol, but not Intralipid, reduced the vasoconstrictor effects of BK, KCl and PGF(2alpha), while the effect of Ang II was not changed.	Propofol	0-8	kininogen 1	Homo sapiens	69-71
20039100-3	2010	Inhibition studies revealed that known ACE inhibitors (captopril and bradykinin potentiating peptide; BPP1) were weak inhibitors for LdDCP as compared to human testicular ACE (htACE) with Ki values of 35.8 nM and 3.9 microM, respectively.	lddcp	133-138	kininogen 1	Homo sapiens	69-79
19841473-9	2010	L-NMMA blunted bradykinin-stimulated vasodilation (P &lt; 0.001 for FBF and FVR).	omega-N-Methylarginine	0-6	kininogen 1	Homo sapiens	15-25
19841473-10	2010	Bradykinin increased net glucose extraction (from -80 +/- 23 to -320 +/- 97 microg/min/100 ml at 200 ng/min bradykinin, P = 0.02), and L-NMMA (-143 +/- 50 microg/min/100 ml at 200 ng/min, P = 0.045) attenuated this effect.	Glucose	25-32	kininogen 1	Homo sapiens	0-10
19841473-10	2010	Bradykinin increased net glucose extraction (from -80 +/- 23 to -320 +/- 97 microg/min/100 ml at 200 ng/min bradykinin, P = 0.02), and L-NMMA (-143 +/- 50 microg/min/100 ml at 200 ng/min, P = 0.045) attenuated this effect.	omega-N-Methylarginine	135-141	kininogen 1	Homo sapiens	0-10
19841473-11	2010	In contrast, L-NMMA enhanced bradykinin-stimulated t-PA release (39.9 +/- 7.0 ng/min/100 ml versus 30.0 +/- 4.2 ng/min/100 ml at 200 ng/min, P = 0.04 for L-NMMA).	omega-N-Methylarginine	13-19	kininogen 1	Homo sapiens	29-39
19841473-11	2010	In contrast, L-NMMA enhanced bradykinin-stimulated t-PA release (39.9 +/- 7.0 ng/min/100 ml versus 30.0 +/- 4.2 ng/min/100 ml at 200 ng/min, P = 0.04 for L-NMMA).	omega-N-Methylarginine	154-160	kininogen 1	Homo sapiens	29-39
19841473-12	2010	In gender-stratified analyses, L-NMMA significantly increased bradykinin-stimulated t-PA release in women (F = 6.7, P = 0.02) but not in men.	omega-N-Methylarginine	31-37	kininogen 1	Homo sapiens	62-72
19854233-4	2010	Here, we report the functional expression of the bradykinin B(2) receptor and its modulation of zymosan-induced cytokine expression in human astrocytoma 1321N1 cells.	Zymosan	96-103	kininogen 1	Homo sapiens	49-59
19854233-9	2010	Bradykinin increased the zymosan-induced expression of TNF-alpha, and interleukin 1beta (IL-1beta) but did not affect the expression of interleukin 6 (IL-6) or interleukin 10 (IL-10).	Zymosan	25-32	kininogen 1	Homo sapiens	0-10
19841473-0	2010	Endogenous nitric oxide contributes to bradykinin-stimulated glucose uptake but attenuates vascular tissue-type plasminogen activator release.	Nitric Oxide	11-23	kininogen 1	Homo sapiens	39-49
19841473-0	2010	Endogenous nitric oxide contributes to bradykinin-stimulated glucose uptake but attenuates vascular tissue-type plasminogen activator release.	Glucose	61-68	kininogen 1	Homo sapiens	39-49
19841473-1	2010	Bradykinin causes vasodilation, stimulates tissue-type plasminogen activator (t-PA) release and, in rodents, increases muscle glucose uptake.	Glucose	126-133	kininogen 1	Homo sapiens	0-10
19929018-10	2009	For normal incidence, we find an average percentage energy transfer to gly(8)-H(+) which is in excellent agreement with the experimentally measured value 10.1 +/- 0.8% for the octapeptide des-Arg(1)-bradykinin [J. Chem.	Glycine	71-74	kininogen 1	Homo sapiens	199-209
19794144-3	2009	Here we show that treatment of 18Co cells, a model of human colonic myofibroblasts, with BK and TNF-alpha induced striking synergistic COX-2 protein expression that was paralleled by increases in the levels of transcripts encoding COX-2 and microsomal prostaglandin E synthase 1 (mPGES-1) and by the production of PGE(2).	Prostaglandins E	281-284	kininogen 1	Homo sapiens	89-91
19794144-4	2009	COX-2 expression in 18Co cells treated with BK and TNF-alpha was prevented by the B(2) BK receptor antagonist HOE-140, the preferential protein kinase C (PKC) inhibitors Ro31-8220 and GF-109203X, and Go-6976, an inhibitor of conventional PKCs and protein kinase D (PKD).	109203x	187-194	kininogen 1	Homo sapiens	44-46
19794144-4	2009	COX-2 expression in 18Co cells treated with BK and TNF-alpha was prevented by the B(2) BK receptor antagonist HOE-140, the preferential protein kinase C (PKC) inhibitors Ro31-8220 and GF-109203X, and Go-6976, an inhibitor of conventional PKCs and protein kinase D (PKD).	Go 6976	200-207	kininogen 1	Homo sapiens	44-46
19794144-5	2009	In a parallel fashion, TNF-alpha, while having no detectable effect on the activation of PKD when added alone, augmented PKD activation induced by BK, as measured by PKD phosphorylation at its activation loop (Ser(744)) and autophosphorylation site (Ser(916)).	Serine	210-213	kininogen 1	Homo sapiens	147-149
19794144-5	2009	In a parallel fashion, TNF-alpha, while having no detectable effect on the activation of PKD when added alone, augmented PKD activation induced by BK, as measured by PKD phosphorylation at its activation loop (Ser(744)) and autophosphorylation site (Ser(916)).	Serine	250-253	kininogen 1	Homo sapiens	147-149
19171191-6	2009	Upon stimulation with bradykinin (Bk), the peak increases in [Ca(2+)](c), mitochondrial Ca(2+) concentration ([Ca(2+)](m)), [ATP](c) and [ATP](m) were reduced in patient cells.	Adenosine Triphosphate	125-128	kininogen 1	Homo sapiens	22-32
19171191-6	2009	Upon stimulation with bradykinin (Bk), the peak increases in [Ca(2+)](c), mitochondrial Ca(2+) concentration ([Ca(2+)](m)), [ATP](c) and [ATP](m) were reduced in patient cells.	Adenosine Triphosphate	125-128	kininogen 1	Homo sapiens	34-36
19171191-6	2009	Upon stimulation with bradykinin (Bk), the peak increases in [Ca(2+)](c), mitochondrial Ca(2+) concentration ([Ca(2+)](m)), [ATP](c) and [ATP](m) were reduced in patient cells.	Adenosine Triphosphate	138-141	kininogen 1	Homo sapiens	22-32
19171191-6	2009	Upon stimulation with bradykinin (Bk), the peak increases in [Ca(2+)](c), mitochondrial Ca(2+) concentration ([Ca(2+)](m)), [ATP](c) and [ATP](m) were reduced in patient cells.	Adenosine Triphosphate	138-141	kininogen 1	Homo sapiens	34-36
20050188-4	2009	KEY RESULTS: [3H]-BK saturation studies indicated receptor density (Bmax) and K(d) values of 121,550 sites per cell and 1.14 nM respectively.	Tritium	14-16	kininogen 1	Homo sapiens	18-20
20050188-8	2009	Both MEN16132 (IL-6: pIC50 8.1; IL-8: pIC50 8.4) and icatibant (IL-6: pIC50 6.6; IL-8: pIC50 6.7) completely prevented this BK-induced release.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	5-13	kininogen 1	Homo sapiens	124-126
20050188-10	2009	BK-induced IL-8 release was attenuated by inhibitors of phospholipase C (U73122), p38 (SB203580), JNK (SP600125), ERK 1/2 (PD98059) MAPKs, phosphoinositide 3-kinase (LY294002), NF-kappaB (BAY-117085) and by the glucocorticoid dexamethasone.	SB 203580	87-95	kininogen 1	Homo sapiens	0-2
20050188-10	2009	BK-induced IL-8 release was attenuated by inhibitors of phospholipase C (U73122), p38 (SB203580), JNK (SP600125), ERK 1/2 (PD98059) MAPKs, phosphoinositide 3-kinase (LY294002), NF-kappaB (BAY-117085) and by the glucocorticoid dexamethasone.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	166-174	kininogen 1	Homo sapiens	0-2
20050188-10	2009	BK-induced IL-8 release was attenuated by inhibitors of phospholipase C (U73122), p38 (SB203580), JNK (SP600125), ERK 1/2 (PD98059) MAPKs, phosphoinositide 3-kinase (LY294002), NF-kappaB (BAY-117085) and by the glucocorticoid dexamethasone.	Dexamethasone	226-239	kininogen 1	Homo sapiens	0-2
20050188-12	2009	MEN16132 is a highly potent B2 receptor antagonist capable of blocking pro-inflammatory responses to BK evoked in human synoviocytes.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	0-8	kininogen 1	Homo sapiens	101-103
19944371-11	2009	The reduction in BKN-dependent relaxation was prevented by treatment for 1 month with the antioxidant N-acetylcysteine (1 g.kg.day), or losartan, an Ang II type 1 receptor blocker (10 mg.kg.day).	Acetylcysteine	102-118	kininogen 1	Homo sapiens	17-20
19944371-11	2009	The reduction in BKN-dependent relaxation was prevented by treatment for 1 month with the antioxidant N-acetylcysteine (1 g.kg.day), or losartan, an Ang II type 1 receptor blocker (10 mg.kg.day).	Losartan	136-144	kininogen 1	Homo sapiens	17-20
19944371-13	2009	The BKN-induced relaxation occurred through an L-NAME-sensitive pathway that was impaired with age.	NG-Nitroarginine Methyl Ester	47-53	kininogen 1	Homo sapiens	4-7
19474062-3	2009	Moreover, bradykinin induces anion secretion across 1 degrees PVD monolayers that is indomethacin sensitive, and both PTGS2 and PTGS1 are expressed in this model system.	Indomethacin	85-97	kininogen 1	Homo sapiens	10-20
19759271-0	2009	Bradykinin induces formation of vesicle-like structures containing vinculin and PtdIns(4,5)P2 in renal papillary collecting duct cells.	Phosphatidylinositol 4,5-Diphosphate	80-93	kininogen 1	Homo sapiens	0-10
19759271-5	2009	Regarding the reassembly of vinculin-stained FAs, we found that BK induces the formation of phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2]-enriched vinculin-containing vesicles, which, by following a polarized exocytic route, transport vinculin to the site of FA assembly, an action that depends on actin filaments.	Phosphatidylinositol 4,5-Diphosphate	92-129	kininogen 1	Homo sapiens	64-66
19759271-5	2009	Regarding the reassembly of vinculin-stained FAs, we found that BK induces the formation of phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2]-enriched vinculin-containing vesicles, which, by following a polarized exocytic route, transport vinculin to the site of FA assembly, an action that depends on actin filaments.	Phosphatidylinositol 4,5-Diphosphate	131-144	kininogen 1	Homo sapiens	64-66
19759271-6	2009	The present study, which was carried out with cells that were not genetically manipulated, shows for the first time that BK induces the formation of vesicle-like structures containing vinculin and PtdIns(4,5)P2, which transport vinculin to the site of FA assembly.	Phosphatidylinositol 4,5-Diphosphate	197-210	kininogen 1	Homo sapiens	121-123
19661060-4	2009	TRPV4 channel activation and serine phosphorylation were enhanced by exposure to the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate or by application of bradykinin, which activates PKC via a G-protein-coupled mechanism.	Serine	29-35	kininogen 1	Homo sapiens	171-181
19474062-7	2009	Testosterone upregulated basal and bradykinin-induced short-circuit current across 1 degrees PVD monolayers, indicative of anion secretion.	Testosterone	0-12	kininogen 1	Homo sapiens	35-45
19474062-10	2009	In addition, testosterone induced greater basal and bradykinin-induced anion secretion across vas deferens epithelial cells isolated from the distal segment of the duct.	Testosterone	13-25	kininogen 1	Homo sapiens	52-62
19559627-3	2009	Des-arg(9)-bradykinin signal intensity was used to evaluate the sample plates.	des-arg	0-7	kininogen 1	Homo sapiens	11-21
19745647-10	2009	One dopamine agonist (amantadine) and 1 bradykinin antagonist (CP-0127 [Bradycor]) produced marked treatment benefits (d &gt; or = 0.8) for a single measure of arousal (Glasgow Coma Scale).	deltibant	63-70	kininogen 1	Homo sapiens	40-50
19745647-10	2009	One dopamine agonist (amantadine) and 1 bradykinin antagonist (CP-0127 [Bradycor]) produced marked treatment benefits (d &gt; or = 0.8) for a single measure of arousal (Glasgow Coma Scale).	d &gt	119-124	kininogen 1	Homo sapiens	40-50
19714708-7	2009	It was also found that red phosphorus is a suitable MALDI matrix for peptides and proteins, illustrated by the examples of a Calmix mixture of bradykinin, angiotensin, renin, adrenocorticotropic hormone ACTH fragment 18-359 and insulin, and of insulin alone.	Phosphorus	23-37	kininogen 1	Homo sapiens	143-153
19886189-3	2009	It has been shown that adenosine, bradykinin, opioid peptides, calcitonin gene-related peptide and also signaling cascade involved nitric oxide, free radicals, protein kinases, mitochondrial ATP-sensitive K+ -channel, mitochondrial permeability transition pore play an important role in the mechanism of cardioprotective action of remote preconditioning.	Nitric Oxide	131-143	kininogen 1	Homo sapiens	34-44
19788733-3	2009	Here we study the role of the cyclic AMP (cAMP) effectors protein kinase A (PKA) and exchange proteins directly activated by cAMP (Epac1 and Epac2) in the bradykinin-induced IL-8 release from a human airway smooth muscle cell line and the underlying molecular mechanisms of this response.	Cyclic AMP	30-40	kininogen 1	Homo sapiens	155-165
19788733-3	2009	Here we study the role of the cyclic AMP (cAMP) effectors protein kinase A (PKA) and exchange proteins directly activated by cAMP (Epac1 and Epac2) in the bradykinin-induced IL-8 release from a human airway smooth muscle cell line and the underlying molecular mechanisms of this response.	Cyclic AMP	42-46	kininogen 1	Homo sapiens	155-165
19788733-3	2009	Here we study the role of the cyclic AMP (cAMP) effectors protein kinase A (PKA) and exchange proteins directly activated by cAMP (Epac1 and Epac2) in the bradykinin-induced IL-8 release from a human airway smooth muscle cell line and the underlying molecular mechanisms of this response.	Cyclic AMP	125-129	kininogen 1	Homo sapiens	155-165
19788733-11	2009	RESULTS: The beta2-agonist fenoterol augmented release of IL-8 by bradykinin.	Fenoterol	27-36	kininogen 1	Homo sapiens	66-76
19788733-12	2009	The PKA activator 6-Bnz-cAMP and the Epac activator 8-pCPT-2"-O-Me-cAMP significantly increased bradykinin-induced IL-8 release.	Bz-Camp	18-28	kininogen 1	Homo sapiens	96-106
19788733-12	2009	The PKA activator 6-Bnz-cAMP and the Epac activator 8-pCPT-2"-O-Me-cAMP significantly increased bradykinin-induced IL-8 release.	8-pcpt-2"-o-me	52-66	kininogen 1	Homo sapiens	96-106
19788733-12	2009	The PKA activator 6-Bnz-cAMP and the Epac activator 8-pCPT-2"-O-Me-cAMP significantly increased bradykinin-induced IL-8 release.	Cyclic AMP	24-28	kininogen 1	Homo sapiens	96-106
19788733-16	2009	Treatment of the cells with toxin B-1470 and U0126 significantly reduced bradykinin-induced IL-8 release alone or in combination with the activators of PKA and Epac.	Boron	34-35	kininogen 1	Homo sapiens	73-83
19788733-16	2009	Treatment of the cells with toxin B-1470 and U0126 significantly reduced bradykinin-induced IL-8 release alone or in combination with the activators of PKA and Epac.	U 0126	45-50	kininogen 1	Homo sapiens	73-83
19584173-0	2009	Kininogen gene (KNG) variation has a consistent effect on aldosterone response to antihypertensive drug therapy: the GERA study.	Aldosterone	58-69	kininogen 1	Homo sapiens	16-19
19584173-6	2009	The results indicated the existence of one or more variants in the kininogen gene (KNG) that influence interindividual variation in aldosterone response.	Aldosterone	132-143	kininogen 1	Homo sapiens	83-86
19525377-1	2009	Stimulation of vascular endothelial cells with agonists such as acetylcholine (ACh) or bradykinin or with shear stress activates phospholipases and releases arachidonic acid (AA).	Arachidonic Acid	157-173	kininogen 1	Homo sapiens	87-97
19389385-6	2009	In contrast to heparin, oversulfated chondroitin sulfate tightly binds factor XIIa suggesting a biochemical mechanism for the factor XIIa-based enhancement of vasoactive bradykinin production.	Chondroitin Sulfates	37-56	kininogen 1	Homo sapiens	170-180
19767824-0	2009	Cadmium attenuates bradykinin-driven nitric oxide production by interplaying with the localization pattern of endothelial nitric oxide synthase.	Cadmium	0-7	kininogen 1	Homo sapiens	19-29
19767824-0	2009	Cadmium attenuates bradykinin-driven nitric oxide production by interplaying with the localization pattern of endothelial nitric oxide synthase.	Nitric Oxide	37-49	kininogen 1	Homo sapiens	19-29
19767824-2	2009	Bradykinin is a Ca-mobilizing soluble peptide that acts via nitric oxide to promote vasodilation and capillary permeability.	Nitric Oxide	60-72	kininogen 1	Homo sapiens	0-10
19767824-3	2009	The objective of the present study was to explore the Cd implications in bradykinin-dependent endothelial functions.	Cadmium	54-56	kininogen 1	Homo sapiens	73-83
19767824-4	2009	An egg yolk angiogenesis model was employed to evaluate the effect of Cd on bradykinin-induced angiogenesis.	Cadmium	70-72	kininogen 1	Homo sapiens	76-86
19767824-5	2009	The results demonstrate that 100 nmol/L Cd attenuated bradykinin-dependent angiogenesis.	Cadmium	40-42	kininogen 1	Homo sapiens	54-64
19767824-6	2009	The results of the in vitro wound healing and tube formation assays by using EAhy 926, a transformed endothelial cell line, suggest that Cd blocked bradykinin-mediated endothelial migration and tube formation by 38% and 67%, respectively, while nitric oxide supplementation could reverse the effect of Cd on bradykinin-induced endothelial migration by 94%.	Cadmium	137-139	kininogen 1	Homo sapiens	148-158
19767824-6	2009	The results of the in vitro wound healing and tube formation assays by using EAhy 926, a transformed endothelial cell line, suggest that Cd blocked bradykinin-mediated endothelial migration and tube formation by 38% and 67%, respectively, while nitric oxide supplementation could reverse the effect of Cd on bradykinin-induced endothelial migration by 94%.	Cadmium	137-139	kininogen 1	Homo sapiens	308-318
19767824-6	2009	The results of the in vitro wound healing and tube formation assays by using EAhy 926, a transformed endothelial cell line, suggest that Cd blocked bradykinin-mediated endothelial migration and tube formation by 38% and 67%, respectively, while nitric oxide supplementation could reverse the effect of Cd on bradykinin-induced endothelial migration by 94%.	Nitric Oxide	245-257	kininogen 1	Homo sapiens	148-158
19767824-6	2009	The results of the in vitro wound healing and tube formation assays by using EAhy 926, a transformed endothelial cell line, suggest that Cd blocked bradykinin-mediated endothelial migration and tube formation by 38% and 67%, respectively, while nitric oxide supplementation could reverse the effect of Cd on bradykinin-induced endothelial migration by 94%.	Cadmium	302-304	kininogen 1	Homo sapiens	148-158
19767824-7	2009	The detection of nitric oxide by using a DAF-2DA fluorescent probe, Griess assay, and ultrasensitive electrode suggests that Cd blocked bradykinin-induced nitric oxide production.	Nitric Oxide	17-29	kininogen 1	Homo sapiens	136-146
19767824-7	2009	The detection of nitric oxide by using a DAF-2DA fluorescent probe, Griess assay, and ultrasensitive electrode suggests that Cd blocked bradykinin-induced nitric oxide production.	Cadmium	125-127	kininogen 1	Homo sapiens	136-146
19767824-7	2009	The detection of nitric oxide by using a DAF-2DA fluorescent probe, Griess assay, and ultrasensitive electrode suggests that Cd blocked bradykinin-induced nitric oxide production.	Nitric Oxide	155-167	kininogen 1	Homo sapiens	136-146
19767824-8	2009	Fluorescence imaging of eNOS-GFP transfected endothelial cells, immunofluorescence, and Western blot studies of Cd and bradykinin-treated cells show that Cd interfered with the localization pattern of eNOS, which possibly attenuates nitric oxide production in part.	Cadmium	154-156	kininogen 1	Homo sapiens	119-129
19767824-8	2009	Fluorescence imaging of eNOS-GFP transfected endothelial cells, immunofluorescence, and Western blot studies of Cd and bradykinin-treated cells show that Cd interfered with the localization pattern of eNOS, which possibly attenuates nitric oxide production in part.	Nitric Oxide	233-245	kininogen 1	Homo sapiens	119-129
19767824-9	2009	Additionally, Ca imaging of Cd- and bradykinin-treated cells suggests that Cd blocked bradykinin-dependent Ca influx into the cells, thus partially blocking Ca-dependent nitric oxide production in endothelial cells.	Cadmium	75-77	kininogen 1	Homo sapiens	36-46
19767824-9	2009	Additionally, Ca imaging of Cd- and bradykinin-treated cells suggests that Cd blocked bradykinin-dependent Ca influx into the cells, thus partially blocking Ca-dependent nitric oxide production in endothelial cells.	Cadmium	75-77	kininogen 1	Homo sapiens	86-96
19767824-9	2009	Additionally, Ca imaging of Cd- and bradykinin-treated cells suggests that Cd blocked bradykinin-dependent Ca influx into the cells, thus partially blocking Ca-dependent nitric oxide production in endothelial cells.	Nitric Oxide	170-182	kininogen 1	Homo sapiens	86-96
19767824-10	2009	The results of this study conclude that Cd blunted the effect of bradykinin by interfering with the Ca-associated NOS activity specifically by impeding subcellular trafficking of eNOS.	Cadmium	40-42	kininogen 1	Homo sapiens	65-75
19815945-0	2009	Bradykinin receptor antagonists and cyclooxygenase inhibitors in vincristine- and streptozotocin-induced hyperalgesia.	Vincristine	65-76	kininogen 1	Homo sapiens	0-10
19466707-5	2009	Helium metastable atoms generated more fragment ions than argon metastable atoms for both substance P and bradykinin regardless of the precursor ion charge state.	Helium	0-6	kininogen 1	Homo sapiens	106-116
19332384-4	2009	The results obtained demonstrate that EC(2) seeded on NaOH-treated PCL films enhance the basal NO levels and show a faster, more intense response to physiological stimuli such as VEGF, bradykinin and thrombin than vein endothelial cells (ECv).	Sodium Hydroxide	54-58	kininogen 1	Homo sapiens	185-195
19248760-6	2009	Several metabolites, including acetylcholine, bradykinin, opioids and phenylephrine, trigger preconditioning-like protection via a mitochondrial K(ATP)-ROS-dependent mechanism.	Adenosine Triphosphate	147-150	kininogen 1	Homo sapiens	46-56
19248760-6	2009	Several metabolites, including acetylcholine, bradykinin, opioids and phenylephrine, trigger preconditioning-like protection via a mitochondrial K(ATP)-ROS-dependent mechanism.	Reactive Oxygen Species	152-155	kininogen 1	Homo sapiens	46-56
19569122-0	2009	Assay of bradykinin metabolites in human body fluids by CE-LIF coupled with transient ITP preconcentration.	Inosine Triphosphate	86-89	kininogen 1	Homo sapiens	9-19
19569122-2	2009	BK fragments were derivatized with 5-(4, 6-dichloro-s-triazin-2-ylamino) fluorescein before CE-LIF analysis.	5-(4,6-dichloro-s-triazin-2-ylamino) fluorescein	35-84	kininogen 1	Homo sapiens	0-2
19456859-0	2009	Alanine screening of the intracellular loops of the human bradykinin B receptor--effects on receptor maintenance, G protein activation and internalization.	Alanine	0-7	kininogen 1	Homo sapiens	58-68
19761683-6	2009	Thiopental induced statistically significant increases in EDR at concentrations of 10(-6) - 10(-5) M bradykinin.	Thiopental	0-10	kininogen 1	Homo sapiens	101-111
19761683-7	2009	Following nitric oxide production block, thiopental significantly reduced the relaxation response at concentrations of 10(-8) - 10(-5) M bradykinin.	Thiopental	41-51	kininogen 1	Homo sapiens	137-147
19421072-2	2009	S-Nitrosothiols may also serve as endothelium-derived hyperpolarizing factors, mediating the relaxant response of porcine coronary arteries (PCAs) to bradykinin.	S-Nitrosothiols	0-15	kininogen 1	Homo sapiens	150-160
19421072-10	2009	The nitric oxide scavenger hydroxocobalamin and the Na+-K+ ATPase inhibitor ouabain abolished the responses to bradykinin and light.	Nitric Oxide	4-16	kininogen 1	Homo sapiens	111-121
19421072-10	2009	The nitric oxide scavenger hydroxocobalamin and the Na+-K+ ATPase inhibitor ouabain abolished the responses to bradykinin and light.	Hydroxocobalamin	27-43	kininogen 1	Homo sapiens	111-121
19421072-12	2009	On top of L-NAME, intermediate and small conductance Ca2+-dependent K+ channel (IKCa/SKCa) blockade further reduced the response to bradykinin and enhanced photorelaxation.	NG-Nitroarginine Methyl Ester	10-16	kininogen 1	Homo sapiens	132-142
19815945-0	2009	Bradykinin receptor antagonists and cyclooxygenase inhibitors in vincristine- and streptozotocin-induced hyperalgesia.	Streptozocin	82-96	kininogen 1	Homo sapiens	0-10
19456171-0	2009	Practical synthesis of a potent bradykinin B(1) antagonist via enantioselective hydrogenation of a pyridyl N-acyl enamide.	pyridyl n-acyl enamide	99-121	kininogen 1	Homo sapiens	32-42
19684887-9	2009	When bradykinin (BK), a potent stimulant of InsP(3)R-mediated calcium release from ER, was applied to these cells, wild-type (WT) neurons exhibited a steep rise in [Ca(2+)](i) but this was not observed in either Abeta transgenic type.	Calcium	62-69	kininogen 1	Homo sapiens	5-15
19494315-5	2009	PR3 incubated with HK, or a synthetic peptide derived from HK, induced breakdown and release of a novel tridecapeptide termed PR3-kinin, NH(2)-MKRPPGFSPFRSS-COOH, consisting of bradykinin with two additional amino acids on each terminus.	Carbonic Acid	157-161	kininogen 1	Homo sapiens	177-187
19684887-9	2009	When bradykinin (BK), a potent stimulant of InsP(3)R-mediated calcium release from ER, was applied to these cells, wild-type (WT) neurons exhibited a steep rise in [Ca(2+)](i) but this was not observed in either Abeta transgenic type.	Calcium	62-69	kininogen 1	Homo sapiens	17-19
19115248-0	2009	Effect of tamoxifen and retinoic acid on bradykinin induced proliferation in MCF-7 cells.	Tamoxifen	10-19	kininogen 1	Homo sapiens	41-51
19245678-5	2009	In microvessels from subjects aged less than 60 years, most of the bradykinin-induced relaxation was due to nitric oxide release while the rest was sensitive to cyclooxygenase (COX) blockade.	Nitric Oxide	108-120	kininogen 1	Homo sapiens	67-77
19442326-2	2009	The bradykinin system is involved in the mediation and modulation of the vasoconstrictor renin-angiotensin system and the vasodilators prostaglandin, prostacyclin, and nitric oxide in regulating sodium water balance, renal and cardiac hemodynamics, and blood pressure.	Prostaglandins	135-148	kininogen 1	Homo sapiens	4-14
19442326-2	2009	The bradykinin system is involved in the mediation and modulation of the vasoconstrictor renin-angiotensin system and the vasodilators prostaglandin, prostacyclin, and nitric oxide in regulating sodium water balance, renal and cardiac hemodynamics, and blood pressure.	Epoprostenol	150-162	kininogen 1	Homo sapiens	4-14
19442326-2	2009	The bradykinin system is involved in the mediation and modulation of the vasoconstrictor renin-angiotensin system and the vasodilators prostaglandin, prostacyclin, and nitric oxide in regulating sodium water balance, renal and cardiac hemodynamics, and blood pressure.	Nitric Oxide	168-180	kininogen 1	Homo sapiens	4-14
19442326-2	2009	The bradykinin system is involved in the mediation and modulation of the vasoconstrictor renin-angiotensin system and the vasodilators prostaglandin, prostacyclin, and nitric oxide in regulating sodium water balance, renal and cardiac hemodynamics, and blood pressure.	sodium water	195-207	kininogen 1	Homo sapiens	4-14
19396590-5	2009	Finally, prostaglandins sensitize bradykinin-induced excitation in normal tissues by restoring desensitized responses due to the inhibition of protein kinase A.	Prostaglandins	9-23	kininogen 1	Homo sapiens	34-44
19439100-10	2009	Metabolically stable bradykinin B2 agonists, methionine-lysine-bradykinin and labradimil, had differential effects on the transvascular flow rate of Gd-DTPA across the blood-brain tumor barrier.	gd-dtpa	149-156	kininogen 1	Homo sapiens	21-31
19439100-10	2009	Metabolically stable bradykinin B2 agonists, methionine-lysine-bradykinin and labradimil, had differential effects on the transvascular flow rate of Gd-DTPA across the blood-brain tumor barrier.	gd-dtpa	149-156	kininogen 1	Homo sapiens	63-73
19439100-11	2009	Both methionine-lysine-bradykinin and labradimil increased the blood half-life of Gd-DTPA sufficiently enough to increase significantly the tumor tissue Gd-DTPA area under the time-concentration curve.	Methionine	5-15	kininogen 1	Homo sapiens	23-33
19439100-11	2009	Both methionine-lysine-bradykinin and labradimil increased the blood half-life of Gd-DTPA sufficiently enough to increase significantly the tumor tissue Gd-DTPA area under the time-concentration curve.	Lysine	16-22	kininogen 1	Homo sapiens	23-33
19439100-11	2009	Both methionine-lysine-bradykinin and labradimil increased the blood half-life of Gd-DTPA sufficiently enough to increase significantly the tumor tissue Gd-DTPA area under the time-concentration curve.	gd-dtpa	82-89	kininogen 1	Homo sapiens	23-33
19439100-11	2009	Both methionine-lysine-bradykinin and labradimil increased the blood half-life of Gd-DTPA sufficiently enough to increase significantly the tumor tissue Gd-DTPA area under the time-concentration curve.	gd-dtpa	153-160	kininogen 1	Homo sapiens	23-33
19213944-0	2009	Bradykinin-induced dilation of human coronary arterioles requires NADPH oxidase-derived reactive oxygen species.	Reactive Oxygen Species	88-111	kininogen 1	Homo sapiens	0-10
19213944-2	2009	H2O2 mediates bradykinin (BK)-induced vasodilation and reduces bioavailability of epoxyeicosatrienoic acids (EETs); however, the cellular and enzymatic source of H2O2 is unknown.	Hydrogen Peroxide	0-4	kininogen 1	Homo sapiens	14-24
19213944-2	2009	H2O2 mediates bradykinin (BK)-induced vasodilation and reduces bioavailability of epoxyeicosatrienoic acids (EETs); however, the cellular and enzymatic source of H2O2 is unknown.	Hydrogen Peroxide	0-4	kininogen 1	Homo sapiens	26-28
19213944-2	2009	H2O2 mediates bradykinin (BK)-induced vasodilation and reduces bioavailability of epoxyeicosatrienoic acids (EETs); however, the cellular and enzymatic source of H2O2 is unknown.	Hydrogen Peroxide	162-166	kininogen 1	Homo sapiens	14-24
19213944-2	2009	H2O2 mediates bradykinin (BK)-induced vasodilation and reduces bioavailability of epoxyeicosatrienoic acids (EETs); however, the cellular and enzymatic source of H2O2 is unknown.	Hydrogen Peroxide	162-166	kininogen 1	Homo sapiens	26-28
19213944-8	2009	In HCAs or HCAECs incubated with dihydroethidium and dichlorodihydrofluorescein, BK induced superoxide and H2O2 formation, which was inhibited by gp91ds-tat or apocynin but not by gp91scram-tat or rotenone.	dihydroethidium	33-48	kininogen 1	Homo sapiens	81-83
19213944-8	2009	In HCAs or HCAECs incubated with dihydroethidium and dichlorodihydrofluorescein, BK induced superoxide and H2O2 formation, which was inhibited by gp91ds-tat or apocynin but not by gp91scram-tat or rotenone.	dichlorodihydrofluorescein	53-79	kininogen 1	Homo sapiens	81-83
19213944-8	2009	In HCAs or HCAECs incubated with dihydroethidium and dichlorodihydrofluorescein, BK induced superoxide and H2O2 formation, which was inhibited by gp91ds-tat or apocynin but not by gp91scram-tat or rotenone.	Superoxides	92-102	kininogen 1	Homo sapiens	81-83
19213944-8	2009	In HCAs or HCAECs incubated with dihydroethidium and dichlorodihydrofluorescein, BK induced superoxide and H2O2 formation, which was inhibited by gp91ds-tat or apocynin but not by gp91scram-tat or rotenone.	Hydrogen Peroxide	107-111	kininogen 1	Homo sapiens	81-83
19213944-8	2009	In HCAs or HCAECs incubated with dihydroethidium and dichlorodihydrofluorescein, BK induced superoxide and H2O2 formation, which was inhibited by gp91ds-tat or apocynin but not by gp91scram-tat or rotenone.	acetovanillone	160-168	kininogen 1	Homo sapiens	81-83
19213944-8	2009	In HCAs or HCAECs incubated with dihydroethidium and dichlorodihydrofluorescein, BK induced superoxide and H2O2 formation, which was inhibited by gp91ds-tat or apocynin but not by gp91scram-tat or rotenone.	gp91scram-tat	180-193	kininogen 1	Homo sapiens	81-83
19213944-8	2009	In HCAs or HCAECs incubated with dihydroethidium and dichlorodihydrofluorescein, BK induced superoxide and H2O2 formation, which was inhibited by gp91ds-tat or apocynin but not by gp91scram-tat or rotenone.	Rotenone	197-205	kininogen 1	Homo sapiens	81-83
19213944-9	2009	HPLC analysis confirmed that BK specifically induced superoxide production.	Superoxides	53-63	kininogen 1	Homo sapiens	29-31
19297385-8	2009	High serum ADMA levels were associated with decreased vasorelaxation of SV to ACh (P &lt; 0.05) and Bk (P &lt; 0.05).	N,N-dimethylarginine	11-15	kininogen 1	Homo sapiens	100-102
19297385-12	2009	Asymmetrical dimethylarginine was also independently associated with maximum vasorelaxation in response to both ACh [beta (SE): 14.252 (3.976), P = 0.001] and Bk [beta (SE): 9.564 (3.762), P = 0.013].	dimethylarginine	13-29	kininogen 1	Homo sapiens	159-161
19136639-4	2009	B-10376 has a K(i) of 10 to 20 nM to displace [(3)H]Lys-des-Arg(9)-bradykinin from rabbit or human recombinant B(1) receptors expressed in human embryonic kidney (HEK) 293 cells and is a surmountable antagonist in the rabbit aorta contractility assay (pA(2), 7.49).	lys-des-arg	52-63	kininogen 1	Homo sapiens	67-77
19150636-3	2009	In the present study, we used solid-phase methodology to synthesize a series of novel peptide analogues based on the sequence of Sar[dPhe(8)]desArg(9)-bradykinin, a relatively stable peptide agonist with moderate affinity for the human B1R.	D-phenylalanine	133-137	kininogen 1	Homo sapiens	151-161
19289643-7	2009	Sulfaphenazole (P&lt;0.01) blunted bradykinin-induced but not acetylcholine-induced tPA release in both groups.	Sulfaphenazole	0-14	kininogen 1	Homo sapiens	35-45
19289643-7	2009	Sulfaphenazole (P&lt;0.01) blunted bradykinin-induced but not acetylcholine-induced tPA release in both groups.	Phosphorus	16-17	kininogen 1	Homo sapiens	35-45
19289643-7	2009	Sulfaphenazole (P&lt;0.01) blunted bradykinin-induced but not acetylcholine-induced tPA release in both groups.	Leu-Thr	18-20	kininogen 1	Homo sapiens	35-45
19289643-9	2009	When L-NMMA was coinfused with sulfaphenazole, tPA release induced by bradykinin, but not by acetylcholine, was further reduced (P&lt;0.01).	omega-N-Methylarginine	5-11	kininogen 1	Homo sapiens	70-80
19289643-9	2009	When L-NMMA was coinfused with sulfaphenazole, tPA release induced by bradykinin, but not by acetylcholine, was further reduced (P&lt;0.01).	Sulfaphenazole	31-45	kininogen 1	Homo sapiens	70-80
19289643-10	2009	In patients with essential hypertension, tPA release by both agonists was unaffected by L-NMMA, but only bradykinin-induced tPA release was blunted by sulfaphenazole, alone or with L-NMMA (P&lt;001).	Sulfaphenazole	151-165	kininogen 1	Homo sapiens	105-115
19289643-10	2009	In patients with essential hypertension, tPA release by both agonists was unaffected by L-NMMA, but only bradykinin-induced tPA release was blunted by sulfaphenazole, alone or with L-NMMA (P&lt;001).	omega-N-Methylarginine	181-187	kininogen 1	Homo sapiens	105-115
19289643-11	2009	CONCLUSIONS: Sulfaphenazole inhibits bradykinin-induced tPA release, which suggests a modulatory role of CYP 2C9-derived endothelium-derived hyperpolarizing factors in tPA release in humans.	Sulfaphenazole	13-27	kininogen 1	Homo sapiens	37-47
19233276-7	2009	This Biomarker, based on bradykinin-induced differential phosphorylation of Erk1 and Erk2, has been used here to test the therapeutic efficacy both for bryostatin and picolog.	Bryostatins	152-162	kininogen 1	Homo sapiens	25-35
19233276-7	2009	This Biomarker, based on bradykinin-induced differential phosphorylation of Erk1 and Erk2, has been used here to test the therapeutic efficacy both for bryostatin and picolog.	picolog	167-174	kininogen 1	Homo sapiens	25-35
20161284-7	2009	Finally, the nebulizer chip was used to perform DESI-MS for analyzing peptides (BSA and bradykinin) and reserpine on the nanoporous alumina surface.	Aluminum Oxide	132-139	kininogen 1	Homo sapiens	88-98
19176602-8	2009	Moreover, when stimulated by bradykinin, the calcium response was reduced while its decay was slowed down.	Calcium	45-52	kininogen 1	Homo sapiens	29-39
19379059-2	2009	ACE inhibition by perindopril has two main effects: it inhibits the angiotensin II formation and potentiates bradykinin.	Perindopril	18-29	kininogen 1	Homo sapiens	109-119
19218343-3	2009	Endothelium-dependent vasorelaxation in response to bradykinin was reduced significantly by the ritonavir in a concentration-dependent manner.	Ritonavir	96-105	kininogen 1	Homo sapiens	52-62
19218343-4	2009	Five other HAART drugs (indinavir, lamivudine, abacavir, AZT, and ddI) and the 3-plex significantly also impaired endothelium-dependent vasorelaxation in response to bradykinin.	Lamivudine	35-45	kininogen 1	Homo sapiens	166-176
19218343-4	2009	Five other HAART drugs (indinavir, lamivudine, abacavir, AZT, and ddI) and the 3-plex significantly also impaired endothelium-dependent vasorelaxation in response to bradykinin.	abacavir	47-55	kininogen 1	Homo sapiens	166-176
19218343-4	2009	Five other HAART drugs (indinavir, lamivudine, abacavir, AZT, and ddI) and the 3-plex significantly also impaired endothelium-dependent vasorelaxation in response to bradykinin.	Zidovudine	57-60	kininogen 1	Homo sapiens	166-176
19218343-4	2009	Five other HAART drugs (indinavir, lamivudine, abacavir, AZT, and ddI) and the 3-plex significantly also impaired endothelium-dependent vasorelaxation in response to bradykinin.	Didanosine	66-69	kininogen 1	Homo sapiens	166-176
19272336-1	2009	The conformation of bradykinin (BK), Arg1-Pro2-Pro3-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9, was investigated by Nuclear Magnetic Resonance (NMR) spectroscopy and Monte Carlo simulation in two different media, i.e. in pure aqueous solution and in the presence of phospholipid vesicles.	gly4-phe5	52-61	kininogen 1	Homo sapiens	20-30
19272336-1	2009	The conformation of bradykinin (BK), Arg1-Pro2-Pro3-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9, was investigated by Nuclear Magnetic Resonance (NMR) spectroscopy and Monte Carlo simulation in two different media, i.e. in pure aqueous solution and in the presence of phospholipid vesicles.	gly4-phe5	52-61	kininogen 1	Homo sapiens	32-34
19272336-1	2009	The conformation of bradykinin (BK), Arg1-Pro2-Pro3-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9, was investigated by Nuclear Magnetic Resonance (NMR) spectroscopy and Monte Carlo simulation in two different media, i.e. in pure aqueous solution and in the presence of phospholipid vesicles.	Phospholipids	253-265	kininogen 1	Homo sapiens	20-30
19272336-1	2009	The conformation of bradykinin (BK), Arg1-Pro2-Pro3-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9, was investigated by Nuclear Magnetic Resonance (NMR) spectroscopy and Monte Carlo simulation in two different media, i.e. in pure aqueous solution and in the presence of phospholipid vesicles.	Phospholipids	253-265	kininogen 1	Homo sapiens	32-34
19220277-10	2009	Microemulsion propofol and 8% PEG660 HS enhanced plasma bradykinin generation, whereas lipid emulsion propofol and lipid solvent did not.	Propofol	14-22	kininogen 1	Homo sapiens	56-66
19220277-10	2009	Microemulsion propofol and 8% PEG660 HS enhanced plasma bradykinin generation, whereas lipid emulsion propofol and lipid solvent did not.	peg660	30-36	kininogen 1	Homo sapiens	56-66
19309242-7	2009	In contrast, heparin-induced anaphylaxis is caused by activation of the contact system, with formation of vasoactive kinins (bradykinin, des-arg(9)-bradykinin).	Heparin	13-20	kininogen 1	Homo sapiens	125-135
19309242-7	2009	In contrast, heparin-induced anaphylaxis is caused by activation of the contact system, with formation of vasoactive kinins (bradykinin, des-arg(9)-bradykinin).	Heparin	13-20	kininogen 1	Homo sapiens	148-158
19309242-7	2009	In contrast, heparin-induced anaphylaxis is caused by activation of the contact system, with formation of vasoactive kinins (bradykinin, des-arg(9)-bradykinin).	des-arg	137-144	kininogen 1	Homo sapiens	148-158
19190685-0	2009	Initial bradykinin triggers calcium-induced calcium release in C6 glioma cells and its significance.	Calcium	28-35	kininogen 1	Homo sapiens	8-18
19190685-0	2009	Initial bradykinin triggers calcium-induced calcium release in C6 glioma cells and its significance.	Calcium	44-51	kininogen 1	Homo sapiens	8-18
19190685-1	2009	OBJECTIVE: To investigate the underlying mechanism for the selective modulation of the permeability of blood-tumor barrier (BTB) by small dose of bradykinin (BK).	btb	124-127	kininogen 1	Homo sapiens	146-156
19190685-1	2009	OBJECTIVE: To investigate the underlying mechanism for the selective modulation of the permeability of blood-tumor barrier (BTB) by small dose of bradykinin (BK).	btb	124-127	kininogen 1	Homo sapiens	158-160
19190685-3	2009	RESULTS: The initial application of BK easily triggered extracellular calcium influx, which resulted in intracellular calcium store release in C6 glioma cells.	Calcium	70-77	kininogen 1	Homo sapiens	36-38
19190685-3	2009	RESULTS: The initial application of BK easily triggered extracellular calcium influx, which resulted in intracellular calcium store release in C6 glioma cells.	Calcium	118-125	kininogen 1	Homo sapiens	36-38
19190685-6	2009	Further study showed that ryanodine mediated CICR contributed greatly to the secondary NO elevation induced by BK treatment.	Ryanodine	26-35	kininogen 1	Homo sapiens	111-113
19190685-6	2009	Further study showed that ryanodine mediated CICR contributed greatly to the secondary NO elevation induced by BK treatment.	cicr	45-49	kininogen 1	Homo sapiens	111-113
19190685-7	2009	CONCLUSION: These results suggested that BK triggered CICR in C6 glioma cells and the associated NO generation might be the underlying mechanism for the selective modulation of BTB permeability by BK.	cicr	54-58	kininogen 1	Homo sapiens	41-43
19190685-7	2009	CONCLUSION: These results suggested that BK triggered CICR in C6 glioma cells and the associated NO generation might be the underlying mechanism for the selective modulation of BTB permeability by BK.	btb	177-180	kininogen 1	Homo sapiens	41-43
19190685-7	2009	CONCLUSION: These results suggested that BK triggered CICR in C6 glioma cells and the associated NO generation might be the underlying mechanism for the selective modulation of BTB permeability by BK.	btb	177-180	kininogen 1	Homo sapiens	197-199
19171072-2	2009	PRCP regulates angiotensin 1-7 (Ang 1-7) - and bradykinin (BK) - stimulated nitric oxide production in endothelial cells.	Nitric Oxide	76-88	kininogen 1	Homo sapiens	47-57
19171072-2	2009	PRCP regulates angiotensin 1-7 (Ang 1-7) - and bradykinin (BK) - stimulated nitric oxide production in endothelial cells.	Nitric Oxide	76-88	kininogen 1	Homo sapiens	59-61
19027830-5	2009	This protective effect of BK was inhibited by the B2R antagonist, HOE140, and the ERK1/2 antagonist, PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	101-108	kininogen 1	Homo sapiens	26-28
19115248-5	2009	The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid.	Tamoxifen	49-58	kininogen 1	Homo sapiens	21-31
19115248-5	2009	The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid.	Tamoxifen	49-58	kininogen 1	Homo sapiens	157-167
19115248-5	2009	The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid.	retinoic	69-77	kininogen 1	Homo sapiens	21-31
19115248-5	2009	The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid.	retinoic	69-77	kininogen 1	Homo sapiens	157-167
19115248-5	2009	The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid.	Tamoxifen	246-255	kininogen 1	Homo sapiens	21-31
19115248-5	2009	The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid.	Tretinoin	69-82	kininogen 1	Homo sapiens	21-31
19115248-5	2009	The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid.	Tretinoin	69-82	kininogen 1	Homo sapiens	157-167
19115248-6	2009	We showed that the anti-tumoral effect of tamoxifen/all-trans retinoic acid is beneficial in MCF-7 breast cancer cells grown in a bradykinin-pro-mitogenic environment, an effect that might be, at least in part, through the MAPK pathway and B2-bradykinin receptor inhibition.	Tamoxifen	42-51	kininogen 1	Homo sapiens	130-140
19115248-6	2009	We showed that the anti-tumoral effect of tamoxifen/all-trans retinoic acid is beneficial in MCF-7 breast cancer cells grown in a bradykinin-pro-mitogenic environment, an effect that might be, at least in part, through the MAPK pathway and B2-bradykinin receptor inhibition.	Tretinoin	62-75	kininogen 1	Homo sapiens	130-140
19123797-2	2009	Fractionation of two peptides, bradykinin and buccalin, was accomplished in less than 120 s by placing a 30 pM (pH approximately 6.2) droplet onto the polymer brush substrate.	Polymers	151-158	kininogen 1	Homo sapiens	31-41
19123797-3	2009	The eluant containing the anionic buccalin is pipetted away for MALDI analysis while the cationic bradykinin adsorbed to the swollen anionic brush and was subsequently released by adding a droplet of formic acid to the substrate.	formic acid	200-211	kininogen 1	Homo sapiens	98-108
19040351-4	2009	When biotin-HK is incubated with rabbit aorta endothelial cells (RAECs) and CHO-K1 cells, it is internalized into acidic intracellular vesicles, whereas when incubated with CHO-745 cells, which express reduced levels of glycosaminoglycans, HK is not internalized.	Biotin	5-11	kininogen 1	Homo sapiens	12-14
19040351-4	2009	When biotin-HK is incubated with rabbit aorta endothelial cells (RAECs) and CHO-K1 cells, it is internalized into acidic intracellular vesicles, whereas when incubated with CHO-745 cells, which express reduced levels of glycosaminoglycans, HK is not internalized.	Biotin	5-11	kininogen 1	Homo sapiens	240-242
19040351-4	2009	When biotin-HK is incubated with rabbit aorta endothelial cells (RAECs) and CHO-K1 cells, it is internalized into acidic intracellular vesicles, whereas when incubated with CHO-745 cells, which express reduced levels of glycosaminoglycans, HK is not internalized.	CAV protocol	76-79	kininogen 1	Homo sapiens	12-14
19040351-4	2009	When biotin-HK is incubated with rabbit aorta endothelial cells (RAECs) and CHO-K1 cells, it is internalized into acidic intracellular vesicles, whereas when incubated with CHO-745 cells, which express reduced levels of glycosaminoglycans, HK is not internalized.	Glycosaminoglycans	220-238	kininogen 1	Homo sapiens	12-14
19040351-5	2009	To further verify the hypothesis that HSPG-dependent mechanisms are involved in HK uptake and proteolytic processing in lysosomes, we tested chloroquine, which blocks Alexa 488- HK colocalization with Lyso Tracker in acidic endosomal vesicles.	Chloroquine	141-152	kininogen 1	Homo sapiens	80-82
19040351-5	2009	To further verify the hypothesis that HSPG-dependent mechanisms are involved in HK uptake and proteolytic processing in lysosomes, we tested chloroquine, which blocks Alexa 488- HK colocalization with Lyso Tracker in acidic endosomal vesicles.	Chloroquine	141-152	kininogen 1	Homo sapiens	178-180
19040351-5	2009	To further verify the hypothesis that HSPG-dependent mechanisms are involved in HK uptake and proteolytic processing in lysosomes, we tested chloroquine, which blocks Alexa 488- HK colocalization with Lyso Tracker in acidic endosomal vesicles.	Alexa-488	167-176	kininogen 1	Homo sapiens	178-180
19040351-6	2009	The process of HK internalization was blocked by low temperatures, methyl-beta-cyclodextrin, FCCP and 2-deoxy-D-glucose, implying that HK uptake into acidic vesicles is energy-dependent and most likely involves binding to HSPG structures localized in cholesterol-rich domains present in the plasma membrane.	methyl-beta-cyclodextrin	67-91	kininogen 1	Homo sapiens	15-17
19040351-6	2009	The process of HK internalization was blocked by low temperatures, methyl-beta-cyclodextrin, FCCP and 2-deoxy-D-glucose, implying that HK uptake into acidic vesicles is energy-dependent and most likely involves binding to HSPG structures localized in cholesterol-rich domains present in the plasma membrane.	methyl-beta-cyclodextrin	67-91	kininogen 1	Homo sapiens	135-137
19040351-6	2009	The process of HK internalization was blocked by low temperatures, methyl-beta-cyclodextrin, FCCP and 2-deoxy-D-glucose, implying that HK uptake into acidic vesicles is energy-dependent and most likely involves binding to HSPG structures localized in cholesterol-rich domains present in the plasma membrane.	Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone	93-97	kininogen 1	Homo sapiens	15-17
19040351-6	2009	The process of HK internalization was blocked by low temperatures, methyl-beta-cyclodextrin, FCCP and 2-deoxy-D-glucose, implying that HK uptake into acidic vesicles is energy-dependent and most likely involves binding to HSPG structures localized in cholesterol-rich domains present in the plasma membrane.	Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone	93-97	kininogen 1	Homo sapiens	135-137
19040351-6	2009	The process of HK internalization was blocked by low temperatures, methyl-beta-cyclodextrin, FCCP and 2-deoxy-D-glucose, implying that HK uptake into acidic vesicles is energy-dependent and most likely involves binding to HSPG structures localized in cholesterol-rich domains present in the plasma membrane.	Deoxyglucose	102-119	kininogen 1	Homo sapiens	15-17
19040351-6	2009	The process of HK internalization was blocked by low temperatures, methyl-beta-cyclodextrin, FCCP and 2-deoxy-D-glucose, implying that HK uptake into acidic vesicles is energy-dependent and most likely involves binding to HSPG structures localized in cholesterol-rich domains present in the plasma membrane.	Deoxyglucose	102-119	kininogen 1	Homo sapiens	135-137
19040351-6	2009	The process of HK internalization was blocked by low temperatures, methyl-beta-cyclodextrin, FCCP and 2-deoxy-D-glucose, implying that HK uptake into acidic vesicles is energy-dependent and most likely involves binding to HSPG structures localized in cholesterol-rich domains present in the plasma membrane.	Cholesterol	251-262	kininogen 1	Homo sapiens	15-17
19040351-6	2009	The process of HK internalization was blocked by low temperatures, methyl-beta-cyclodextrin, FCCP and 2-deoxy-D-glucose, implying that HK uptake into acidic vesicles is energy-dependent and most likely involves binding to HSPG structures localized in cholesterol-rich domains present in the plasma membrane.	Cholesterol	251-262	kininogen 1	Homo sapiens	135-137
19115248-0	2009	Effect of tamoxifen and retinoic acid on bradykinin induced proliferation in MCF-7 cells.	Tretinoin	24-37	kininogen 1	Homo sapiens	41-51
18938142-7	2009	To establish that BK receptors are functional, we employed fluorescent measurements of intracellular Ca(2+), measured changes in extracellular acidification rate (ECAR) as a reflection of the Na(+)/H(+) exchange (NHE) with a Cytosensortrade microphysiometer, and assessed ERK activation by Western blotting with a phospho-specific ERK antibody.	cytosensortrade	225-240	kininogen 1	Homo sapiens	18-20
19275271-13	2009	We therefore have clinical results showing that perindopril normalizes the angiotensin II/bradykinin balance, reduces inflammation and prevents endothelial apoptosis.	Perindopril	48-59	kininogen 1	Homo sapiens	90-100
18689441-6	2008	Furthermore, isoflurane directly activates TRPV1 after stimulation of protein kinase C. Likewise, isoflurane excites TRPV1 and sensory neurons during concomitant application of bradykinin, a key inflammatory mediator formed during tissue injury.	Isoflurane	13-23	kininogen 1	Homo sapiens	177-187
18938142-8	2009	Exposure of HEK293 cells to BK produced a concentration-dependent rise in intracellular Ca(2+) (EC(50)=36.5+/-8.0 x 10(-9)M), a rapid increase in tyrosine phosphorylation of ERK (EC(50)=9.8+/-0.4 x 10(-9)M), and elevation in ECAR by approximately 20%.	Tyrosine	146-154	kininogen 1	Homo sapiens	28-30
19145781-3	2009	METHODS: Here, we tested the hypothesis that bradykinin and its second messenger cAMP upregulate TRPM7, which stimulates activation of annexin-1 (TRPM7 substrate) and increases transmembrane Mg2+ transport and vascular smooth muscle cell (VSMC) migration.	Cyclic AMP	81-85	kininogen 1	Homo sapiens	45-55
19145781-3	2009	METHODS: Here, we tested the hypothesis that bradykinin and its second messenger cAMP upregulate TRPM7, which stimulates activation of annexin-1 (TRPM7 substrate) and increases transmembrane Mg2+ transport and vascular smooth muscle cell (VSMC) migration.	magnesium ion	191-195	kininogen 1	Homo sapiens	45-55
19145781-12	2009	[Mg2+]i was increased in bradykinin-stimulated cells (0.53 versus 0.68 mmol/l, basal versus bradykinin, P &lt; 0.01).	magnesium ion	1-5	kininogen 1	Homo sapiens	25-35
19145781-12	2009	[Mg2+]i was increased in bradykinin-stimulated cells (0.53 versus 0.68 mmol/l, basal versus bradykinin, P &lt; 0.01).	magnesium ion	1-5	kininogen 1	Homo sapiens	92-102
19145781-14	2009	Although Hoe 140 (B2 receptor antagonist), U-73122 (phospholipase C inhibitor), 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (c-Src inhibitor) and chelerythrine (protein kinase C inhibitor) blocked bradykinin actions, dibutyryl-c-AMP was without effect.	AG 1879	80-143	kininogen 1	Homo sapiens	217-227
19145781-15	2009	In small interfering RNA-transfected and in 2-aminoethoxydiphenyl borate-treated cells, bradykinin-induced Mg2+ influx and VSMC migration were reduced.	2-aminoethoxydiphenyl borate	44-72	kininogen 1	Homo sapiens	88-98
19145781-15	2009	In small interfering RNA-transfected and in 2-aminoethoxydiphenyl borate-treated cells, bradykinin-induced Mg2+ influx and VSMC migration were reduced.	magnesium ion	107-111	kininogen 1	Homo sapiens	88-98
19145781-15	2009	In small interfering RNA-transfected and in 2-aminoethoxydiphenyl borate-treated cells, bradykinin-induced Mg2+ influx and VSMC migration were reduced.	vsmc	123-127	kininogen 1	Homo sapiens	88-98
19145781-16	2009	CONCLUSION: Our results demonstrate that bradykinin regulates TRPM7 and its downstream target annexin-1 through phospholipase C-dependent, protein kinase C-dependent and c-Src-dependent and cAMP-independent pathways; effects are mediated through bradykinin type 2 receptor; and bradykinin regulates VSMC [Mg2+]i and migration through TRPM7.	Cyclic AMP	190-194	kininogen 1	Homo sapiens	41-51
19145781-16	2009	CONCLUSION: Our results demonstrate that bradykinin regulates TRPM7 and its downstream target annexin-1 through phospholipase C-dependent, protein kinase C-dependent and c-Src-dependent and cAMP-independent pathways; effects are mediated through bradykinin type 2 receptor; and bradykinin regulates VSMC [Mg2+]i and migration through TRPM7.	vsmc	299-303	kininogen 1	Homo sapiens	41-51
19145781-16	2009	CONCLUSION: Our results demonstrate that bradykinin regulates TRPM7 and its downstream target annexin-1 through phospholipase C-dependent, protein kinase C-dependent and c-Src-dependent and cAMP-independent pathways; effects are mediated through bradykinin type 2 receptor; and bradykinin regulates VSMC [Mg2+]i and migration through TRPM7.	magnesium ion	305-309	kininogen 1	Homo sapiens	41-51
19145781-17	2009	These data identify TRPM7/annexin-1/Mg2+ as a novel pathway in bradykinin signaling.	magnesium ion	36-40	kininogen 1	Homo sapiens	63-73
19028051-10	2009	However, endothelium-dependent vasorelaxation with bradykinin (10(-6) M) was significantly reduced by 34% with Hcy compared with controls (P &lt; .05).	Homocysteine	111-114	kininogen 1	Homo sapiens	51-61
19114959-5	2009	In response to bradykinin (10(-6) M), ritonavir-treated rings showed a significant reduction of endothelium-dependent vasorelaxation by 32% compared with untreated control vessels (P&lt;0.05, n=5, Student t-test).	Ritonavir	38-47	kininogen 1	Homo sapiens	15-25
18986166-5	2008	IDE specifically degrades bradykinin and kallidin at the Pro/Phe site.	Proline	57-60	kininogen 1	Homo sapiens	26-36
18986166-5	2008	IDE specifically degrades bradykinin and kallidin at the Pro/Phe site.	Phenylalanine	61-64	kininogen 1	Homo sapiens	26-36
18986166-6	2008	A 1.9 A crystal structure of bradykinin-bound IDE reveals the binding of bradykinin to the exosite and not to the catalytic site.	exosite	91-98	kininogen 1	Homo sapiens	29-39
18986166-6	2008	A 1.9 A crystal structure of bradykinin-bound IDE reveals the binding of bradykinin to the exosite and not to the catalytic site.	exosite	91-98	kininogen 1	Homo sapiens	73-83
19956340-6	2008	Additionally, singly charged Bradykinin, Substance P and Fibrinopeptide A molecular ions were fragmented via interaction with electronically excited metastable helium atoms.	Helium	160-166	kininogen 1	Homo sapiens	29-39
19074839-10	2008	In HNSCC cells, the bradykinin-induced expression of COX-2 was inhibited by the EGFR kinase inhibitor gefitinib or mitogen-activated protein kinase kinase inhibitors (PD98059 or U0126).	Gefitinib	102-111	kininogen 1	Homo sapiens	20-30
19074839-10	2008	In HNSCC cells, the bradykinin-induced expression of COX-2 was inhibited by the EGFR kinase inhibitor gefitinib or mitogen-activated protein kinase kinase inhibitors (PD98059 or U0126).	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	167-174	kininogen 1	Homo sapiens	20-30
19074839-10	2008	In HNSCC cells, the bradykinin-induced expression of COX-2 was inhibited by the EGFR kinase inhibitor gefitinib or mitogen-activated protein kinase kinase inhibitors (PD98059 or U0126).	U 0126	178-183	kininogen 1	Homo sapiens	20-30
20030444-4	2009	We hypothesized that increased levels of bradykinin could be responsible for the decrease in citric acid cough threshold on exposure to altitude and a possible etiologic factor in altitude-related cough.	Citric Acid	93-104	kininogen 1	Homo sapiens	41-51
18948121-0	2008	Bradykinin stimulates glutamate uptake via both B1R and B2R activation in a human retinal pigment epithelial cells.	Glutamic Acid	22-31	kininogen 1	Homo sapiens	0-10
18948121-3	2008	KEY FINDINGS: BK stimulated glutamate uptake as well as the mRNA expression of excitatory amino acid transporter 4 (EAAT4) and excitatory amino acid carrier 1 (EAAC1), which was blocked by treatment with bradykinin 1 receptor (B1R) and bradykinin 2 receptor (B2R) siRNA, suggesting the role of B1R and B2R in this process.	Glutamic Acid	28-37	kininogen 1	Homo sapiens	14-16
18948121-6	2008	Furthermore, the BK-induced increase in COX-2 expression was blocked by the PI-3 kinase inhibitors wortmannin and LY294002, Akt inhibitor, and the protein kinase C (PKC) inhibitors staurosporine and bisindolylmaleimide I, suggesting the role of PI-3 kinase and PKC in this process.	Wortmannin	99-109	kininogen 1	Homo sapiens	17-19
18948121-6	2008	Furthermore, the BK-induced increase in COX-2 expression was blocked by the PI-3 kinase inhibitors wortmannin and LY294002, Akt inhibitor, and the protein kinase C (PKC) inhibitors staurosporine and bisindolylmaleimide I, suggesting the role of PI-3 kinase and PKC in this process.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	114-122	kininogen 1	Homo sapiens	17-19
18948121-6	2008	Furthermore, the BK-induced increase in COX-2 expression was blocked by the PI-3 kinase inhibitors wortmannin and LY294002, Akt inhibitor, and the protein kinase C (PKC) inhibitors staurosporine and bisindolylmaleimide I, suggesting the role of PI-3 kinase and PKC in this process.	Staurosporine	181-194	kininogen 1	Homo sapiens	17-19
18948121-6	2008	Furthermore, the BK-induced increase in COX-2 expression was blocked by the PI-3 kinase inhibitors wortmannin and LY294002, Akt inhibitor, and the protein kinase C (PKC) inhibitors staurosporine and bisindolylmaleimide I, suggesting the role of PI-3 kinase and PKC in this process.	bisindolylmaleimide I	199-220	kininogen 1	Homo sapiens	17-19
18948121-8	2008	SIGNIFICANCE: BK stimulates glutamate uptake through a PKC-Akt-COX-2 signaling cascade in ARPE cells.	Glutamic Acid	28-37	kininogen 1	Homo sapiens	14-16
18927465-7	2008	CPCs from cardiovascular disease patients showed low B(2)R levels and decreased migratory capacity toward BK.	cpcs	0-4	kininogen 1	Homo sapiens	106-108
18689441-6	2008	Furthermore, isoflurane directly activates TRPV1 after stimulation of protein kinase C. Likewise, isoflurane excites TRPV1 and sensory neurons during concomitant application of bradykinin, a key inflammatory mediator formed during tissue injury.	Isoflurane	98-108	kininogen 1	Homo sapiens	177-187
18565624-1	2008	B-9430 (d-Arg-[Hyp3, Igl5, D-Igl7, Oic8]-bradykinin), where Hyp is trans-4-hydroxyproline, Igl is alpha-(2-indanyl)glycine and Oic is (3as, 7as)-octahydroindol-2-yl-carbonyl is a high affinity bradykinin B2 receptor antagonist with effects extended to the B1 receptors at high concentrations.	D-Arginine	8-13	kininogen 1	Homo sapiens	41-51
18789901-7	2008	Acetylcholine, bradykinin and sodium nitroprusside all caused dose-dependent vasodilatation in the presence and absence of aspirin and the "nitric oxide clamp" (P&lt; or =0.005 for all).	Aspirin	123-130	kininogen 1	Homo sapiens	15-25
18789901-7	2008	Acetylcholine, bradykinin and sodium nitroprusside all caused dose-dependent vasodilatation in the presence and absence of aspirin and the "nitric oxide clamp" (P&lt; or =0.005 for all).	Nitric Oxide	140-152	kininogen 1	Homo sapiens	15-25
18598727-0	2008	A novel physiological property of snake bradykinin-potentiating peptides-reversion of MK-801 inhibition of nicotinic acetylcholine receptors.	Dizocilpine Maleate	86-92	kininogen 1	Homo sapiens	40-50
18598727-1	2008	The first naturally occurring angiotensin-converting enzyme (ACE) inhibitors described are pyroglutamyl proline-rich oligopeptides, found in the venom of the viper Bothrops jararaca, and named as bradykinin-potentiating peptides (BPPs).	Proline	104-111	kininogen 1	Homo sapiens	196-206
18615566-6	2008	Finally, treatment of astrocytes with the Ca2+-ionophore A23187, glutamate agonists, or bradykinin trigger translocation of synaptobrevin/VAMP2 to the plasma membrane with a concomitant disappearance of D-serine from the regulated secretory pathway.	D-serine	203-211	kininogen 1	Homo sapiens	88-98
18539593-6	2008	All transfected lines showed constitutive enhancement of bradykinin (BDK)-induced calcium release, because of a decrease in BDK ED50 values.	Calcium	82-89	kininogen 1	Homo sapiens	57-67
18539593-6	2008	All transfected lines showed constitutive enhancement of bradykinin (BDK)-induced calcium release, because of a decrease in BDK ED50 values.	Calcium	82-89	kininogen 1	Homo sapiens	69-72
18539593-9	2008	Like BDK, vasopressin- and ATP-induced calcium release was enhanced with the same pattern in cell lines.	Adenosine Triphosphate	27-30	kininogen 1	Homo sapiens	5-8
18539593-9	2008	Like BDK, vasopressin- and ATP-induced calcium release was enhanced with the same pattern in cell lines.	Calcium	39-46	kininogen 1	Homo sapiens	5-8
18604228-8	2008	BK-induced responses were largely due to Cl(-) secretion as shown by their sensitivity to bumetanide and removal of Cl(-) from the bathing solution.	Bumetanide	90-100	kininogen 1	Homo sapiens	0-2
18604228-10	2008	Finally, responses to basolateral BK in intact tissues were inhibited by tetrodotoxin (1 microM), atropine (1 microM), capsaicin (100 microM) and piroxicam (10 microM).	Tetrodotoxin	73-85	kininogen 1	Homo sapiens	34-36
18604228-10	2008	Finally, responses to basolateral BK in intact tissues were inhibited by tetrodotoxin (1 microM), atropine (1 microM), capsaicin (100 microM) and piroxicam (10 microM).	Atropine	98-106	kininogen 1	Homo sapiens	34-36
18604228-10	2008	Finally, responses to basolateral BK in intact tissues were inhibited by tetrodotoxin (1 microM), atropine (1 microM), capsaicin (100 microM) and piroxicam (10 microM).	Capsaicin	119-128	kininogen 1	Homo sapiens	34-36
18604228-10	2008	Finally, responses to basolateral BK in intact tissues were inhibited by tetrodotoxin (1 microM), atropine (1 microM), capsaicin (100 microM) and piroxicam (10 microM).	Piroxicam	146-155	kininogen 1	Homo sapiens	34-36
18604228-11	2008	BK-stimulated prostaglandin (PG)E(2) release from colonic tissue.	Dinoprostone	14-36	kininogen 1	Homo sapiens	0-2
18604228-13	2008	Responses to apical BK reflect a direct action on epithelial cells, whereas those to basolateral BK are amplified by stimulation of enteric nerves and PG synthesis.	Prostaglandins	151-153	kininogen 1	Homo sapiens	97-99
18480467-2	2008	Although vas deferens epithelial cells reportedly express high levels of cyclooxygenases (Ptgs), and activation of bradykinin (BK) receptors can lead to upregulation of PTGS activity in epididymal epithelia, it remains unknown whether BKs and/or PTGSs have any role in modulating epithelial ion transport across vas deferens epithelia.	Berkelium	235-238	kininogen 1	Homo sapiens	115-125
18480467-2	2008	Although vas deferens epithelial cells reportedly express high levels of cyclooxygenases (Ptgs), and activation of bradykinin (BK) receptors can lead to upregulation of PTGS activity in epididymal epithelia, it remains unknown whether BKs and/or PTGSs have any role in modulating epithelial ion transport across vas deferens epithelia.	Berkelium	235-238	kininogen 1	Homo sapiens	127-129
18480467-2	2008	Although vas deferens epithelial cells reportedly express high levels of cyclooxygenases (Ptgs), and activation of bradykinin (BK) receptors can lead to upregulation of PTGS activity in epididymal epithelia, it remains unknown whether BKs and/or PTGSs have any role in modulating epithelial ion transport across vas deferens epithelia.	ptgss	246-251	kininogen 1	Homo sapiens	115-125
18480467-2	2008	Although vas deferens epithelial cells reportedly express high levels of cyclooxygenases (Ptgs), and activation of bradykinin (BK) receptors can lead to upregulation of PTGS activity in epididymal epithelia, it remains unknown whether BKs and/or PTGSs have any role in modulating epithelial ion transport across vas deferens epithelia.	ptgss	246-251	kininogen 1	Homo sapiens	127-129
18781599-1	2008	Acutely decompensated heart failure (ADHF) represents an episodic failure of cardiorenal homeostasis that may resolve with upregulation of natriuretic peptides, bradykinin, and certain prostacyclins.	adhf	37-41	kininogen 1	Homo sapiens	161-171
18565624-1	2008	B-9430 (d-Arg-[Hyp3, Igl5, D-Igl7, Oic8]-bradykinin), where Hyp is trans-4-hydroxyproline, Igl is alpha-(2-indanyl)glycine and Oic is (3as, 7as)-octahydroindol-2-yl-carbonyl is a high affinity bradykinin B2 receptor antagonist with effects extended to the B1 receptors at high concentrations.	d-igl7	27-33	kininogen 1	Homo sapiens	41-51
18434646-5	2008	RESULTS: The OSCS found in contaminated lots of unfractionated heparin, as well as a synthetically generated OSCS reference standard, directly activated the kinin-kallikrein pathway in human plasma, which can lead to the generation of bradykinin, a potent vasoactive mediator.	Heparin	63-70	kininogen 1	Homo sapiens	235-245
18621420-6	2008	BK-mediated IL-6 production was attenuated by phospholipase C inhibitor (U73122), protein kinase Cdelta inhibitor (rottlerin), NF-kappaB inhibitor (PDTC), IkappaB protease inhibitor (TPCK) and NF-kappaB inhibitor peptide.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	73-79	kininogen 1	Homo sapiens	0-2
18621420-6	2008	BK-mediated IL-6 production was attenuated by phospholipase C inhibitor (U73122), protein kinase Cdelta inhibitor (rottlerin), NF-kappaB inhibitor (PDTC), IkappaB protease inhibitor (TPCK) and NF-kappaB inhibitor peptide.	rottlerin	115-124	kininogen 1	Homo sapiens	0-2
18621420-7	2008	Stimulation of synovial fibroblasts with BK activated IkappaB kinase alpha/beta (IKK alpha/beta), IkappaBalpha phosphorylation, IkappaBalpha degradation, p65 phosphorylation at Ser(276), p65 and p50 translocation from the cytosol to the nucleus and kappaB-luciferase activity.	Serine	177-180	kininogen 1	Homo sapiens	41-43
18430865-6	2008	Cell surface-bound BK remained intact in cells overexpressing EP24.15 but was degraded intracellularly in an EP24.15-dependent manner upon B(2)R-mediated endocytosis.	b(2)r	139-144	kininogen 1	Homo sapiens	19-21
18406528-8	2008	Bradykinin stimulates IP3R-activated CICR-to test the effect of LEV on IP3R-mediated CICR, bradykinin (1 microM) was used to stimulate cells pre-treated with LEV (100 microM).	cicr	37-41	kininogen 1	Homo sapiens	0-10
18406528-8	2008	Bradykinin stimulates IP3R-activated CICR-to test the effect of LEV on IP3R-mediated CICR, bradykinin (1 microM) was used to stimulate cells pre-treated with LEV (100 microM).	Levetiracetam	158-161	kininogen 1	Homo sapiens	0-10
18406528-8	2008	Bradykinin stimulates IP3R-activated CICR-to test the effect of LEV on IP3R-mediated CICR, bradykinin (1 microM) was used to stimulate cells pre-treated with LEV (100 microM).	Levetiracetam	158-161	kininogen 1	Homo sapiens	91-101
18291093-7	2008	These results reveal a new mechanism by which BK can modulate renal sodium excretion: coupling between B2 receptor and activation of membrane-associated iPLA2.	Sodium	68-74	kininogen 1	Homo sapiens	46-48
18355801-6	2008	In addition, aspirin reduces the capacity of unlabeled bradykinin or the B2 receptor antagonist icatibant to destabilize pre-formed [3H]-bradykinin-receptor complexes.	Tritium	133-135	kininogen 1	Homo sapiens	137-147
19804327-1	2008	Perindopril, a prodrug ester of perindoprilat, is an angiotensin-converting enzyme inhibitor that lowers angiotensin II and potentiates bradykinin.	Perindopril	0-11	kininogen 1	Homo sapiens	136-146
18355801-0	2008	Aspirin inhibits human bradykinin B2 receptor ligand binding function.	Aspirin	0-7	kininogen 1	Homo sapiens	23-33
18355801-2	2008	The effect of aspirin on bradykinin binding to cell-surface receptor and on signal transduction were studied in CHO-K1 cells, stably expressing the human B2 receptor.	Aspirin	14-21	kininogen 1	Homo sapiens	25-35
18355801-5	2008	Aspirin reduces the apparent affinity of the receptor for [3H]-bradykinin by accelerating the dissociation rate of [3H]-bradykinin-receptor complexes.	Aspirin	0-7	kininogen 1	Homo sapiens	63-73
18355801-5	2008	Aspirin reduces the apparent affinity of the receptor for [3H]-bradykinin by accelerating the dissociation rate of [3H]-bradykinin-receptor complexes.	Aspirin	0-7	kininogen 1	Homo sapiens	120-130
18355801-5	2008	Aspirin reduces the apparent affinity of the receptor for [3H]-bradykinin by accelerating the dissociation rate of [3H]-bradykinin-receptor complexes.	Tritium	59-61	kininogen 1	Homo sapiens	63-73
18355801-5	2008	Aspirin reduces the apparent affinity of the receptor for [3H]-bradykinin by accelerating the dissociation rate of [3H]-bradykinin-receptor complexes.	Tritium	59-61	kininogen 1	Homo sapiens	120-130
18355801-6	2008	In addition, aspirin reduces the capacity of unlabeled bradykinin or the B2 receptor antagonist icatibant to destabilize pre-formed [3H]-bradykinin-receptor complexes.	Aspirin	13-20	kininogen 1	Homo sapiens	55-65
18355801-6	2008	In addition, aspirin reduces the capacity of unlabeled bradykinin or the B2 receptor antagonist icatibant to destabilize pre-formed [3H]-bradykinin-receptor complexes.	Aspirin	13-20	kininogen 1	Homo sapiens	137-147
18355801-6	2008	In addition, aspirin reduces the capacity of unlabeled bradykinin or the B2 receptor antagonist icatibant to destabilize pre-formed [3H]-bradykinin-receptor complexes.	Tritium	133-135	kininogen 1	Homo sapiens	55-65
18356188-4	2008	We found that bradykinin increased the TRPA1 currents evoked by allyl isothiocyanate (AITC) or cinnamaldehyde in HEK293 cells expressing TRPA1 and bradykinin receptor 2 (B2R).	allyl isothiocyanate	64-84	kininogen 1	Homo sapiens	14-24
18356188-4	2008	We found that bradykinin increased the TRPA1 currents evoked by allyl isothiocyanate (AITC) or cinnamaldehyde in HEK293 cells expressing TRPA1 and bradykinin receptor 2 (B2R).	allyl isothiocyanate	64-84	kininogen 1	Homo sapiens	147-157
18356188-4	2008	We found that bradykinin increased the TRPA1 currents evoked by allyl isothiocyanate (AITC) or cinnamaldehyde in HEK293 cells expressing TRPA1 and bradykinin receptor 2 (B2R).	allyl isothiocyanate	86-90	kininogen 1	Homo sapiens	14-24
18356188-4	2008	We found that bradykinin increased the TRPA1 currents evoked by allyl isothiocyanate (AITC) or cinnamaldehyde in HEK293 cells expressing TRPA1 and bradykinin receptor 2 (B2R).	allyl isothiocyanate	86-90	kininogen 1	Homo sapiens	147-157
18356188-4	2008	We found that bradykinin increased the TRPA1 currents evoked by allyl isothiocyanate (AITC) or cinnamaldehyde in HEK293 cells expressing TRPA1 and bradykinin receptor 2 (B2R).	cinnamaldehyde	95-109	kininogen 1	Homo sapiens	14-24
18356188-9	2008	Finally, subcutaneous pre-injection of a sub-inflammatory dose of bradykinin into rat hind paw enhanced AITC-induced pain behaviours, which was consistent with the observations in vitro.	allyl isothiocyanate	104-108	kininogen 1	Homo sapiens	66-76
18182589-5	2008	RESULTS: Lys-Des-Arg(9)-bradykinin concentration-dependently contracted strips of control gallbladders and its motor effect was higher in inflamed gallbladders.	lys-des-arg	9-20	kininogen 1	Homo sapiens	24-34
18182589-7	2008	In contrast, the Lys-Des-Arg(9)-bradykinin-induced motor response was significantly reduced by the selective B(1) receptor antagonist, R-715.	lys-des-arg	17-28	kininogen 1	Homo sapiens	32-42
18307734-10	2008	The biochemical consequences of renin inhibition differ from those of angiotensin I-converting enzyme (ACE) inhibition and Ang II antagonism, particularly in terms of angiotensin profiles and interactions with the bradykinin-nitric oxide-cyclic guanosine monophosphate pathway and possibly the (pro)renin receptor.	Nitric Oxide	225-237	kininogen 1	Homo sapiens	214-224
19804327-1	2008	Perindopril, a prodrug ester of perindoprilat, is an angiotensin-converting enzyme inhibitor that lowers angiotensin II and potentiates bradykinin.	perindoprilat	32-45	kininogen 1	Homo sapiens	136-146
18182589-4	2008	Cumulative concentration-response curves with the selective B(1) receptor agonist, Lys-Des-Arg(9)-bradykinin, cholecystokinin and carbachol were performed in control and cholecystitis specimens.	lys-des-arg	83-94	kininogen 1	Homo sapiens	98-108
18007586-9	2008	Finally, PTHrP fragments potentiated bradykinin-induced calcium transients, suggesting a role in inflammation in the skin.	Calcium	56-63	kininogen 1	Homo sapiens	37-47
18252813-6	2008	Enhanced transcription of eNOS by AVE9488 in primary human umbilical vein endothelial cells was associated with increased levels of eNOS mRNA and protein expression, as well as increased bradykinin-stimulated NO production.	4-fluoro-N-indan-2-yl-benzamide	34-41	kininogen 1	Homo sapiens	187-197
18434532-1	2008	Bradykinin potentiates synaptic glutamate release and action in the spinal cord via presynaptic and postsynaptic B(2) receptors, contributing thereby to activity-dependent central sensitization and pain hypersensitivity (Wang et al., 2005).	Glutamic Acid	32-41	kininogen 1	Homo sapiens	0-10
18307734-10	2008	The biochemical consequences of renin inhibition differ from those of angiotensin I-converting enzyme (ACE) inhibition and Ang II antagonism, particularly in terms of angiotensin profiles and interactions with the bradykinin-nitric oxide-cyclic guanosine monophosphate pathway and possibly the (pro)renin receptor.	Cyclic GMP	238-268	kininogen 1	Homo sapiens	214-224
18187413-10	2008	A B1R- and CPM-dependent calcium signal in response to B2R agonist bradykinin was also found in endothelial cells that express both proteins.	Calcium	25-32	kininogen 1	Homo sapiens	67-77
18259028-8	2008	Enalaprilat potentiated bradykinin-stimulated vasodilation and t-PA antigen and activity release similarly during placebo and 17beta-estradiol treatment.	Enalaprilat	0-11	kininogen 1	Homo sapiens	24-34
18336903-7	2008	In the presence of the nitric oxide synthase (NOS) inhibitor l-NNA (100 microM) the amplitude was significantly reduced (40+/-13% to 18+/-8%, P&lt;0.05, n=6), frequency was unaltered and the bradykinin-dependent vasodilator response was reduced (68+/-13% to 40+/-19%, P&lt;0.05, n=6).	Nitroarginine	61-66	kininogen 1	Homo sapiens	191-201
18187413-2	2008	Kinins cleaved from kininogen are agonists of the B2R and must be processed by a carboxypeptidase to generate B1R agonists des-Arg(9)-bradykinin or des-Arg(10)-kallidin.	des-arg	123-130	kininogen 1	Homo sapiens	134-144
18156442-0	2008	IL-1beta, BK, and TGF-beta1 attenuate PGI2-mediated cAMP formation in human pulmonary artery smooth muscle cells by multiple mechanisms involving p38 MAP kinase and PKA.	Epoprostenol	38-42	kininogen 1	Homo sapiens	10-12
18156442-0	2008	IL-1beta, BK, and TGF-beta1 attenuate PGI2-mediated cAMP formation in human pulmonary artery smooth muscle cells by multiple mechanisms involving p38 MAP kinase and PKA.	Cyclic AMP	52-56	kininogen 1	Homo sapiens	10-12
18156442-1	2008	We have previously shown that interleukin (IL)-1beta, transforming growth factor (TGF)-beta1, or bradykinin (BK) impair cAMP generation in response to prostacyclin analogs in human pulmonary artery smooth muscle (PASM), suggesting that inflammation can impair the effects of prostacyclin analogs on PASM in pulmonary hypertension.	Cyclic AMP	120-124	kininogen 1	Homo sapiens	97-107
18156442-1	2008	We have previously shown that interleukin (IL)-1beta, transforming growth factor (TGF)-beta1, or bradykinin (BK) impair cAMP generation in response to prostacyclin analogs in human pulmonary artery smooth muscle (PASM), suggesting that inflammation can impair the effects of prostacyclin analogs on PASM in pulmonary hypertension.	Cyclic AMP	120-124	kininogen 1	Homo sapiens	109-111
18156442-1	2008	We have previously shown that interleukin (IL)-1beta, transforming growth factor (TGF)-beta1, or bradykinin (BK) impair cAMP generation in response to prostacyclin analogs in human pulmonary artery smooth muscle (PASM), suggesting that inflammation can impair the effects of prostacyclin analogs on PASM in pulmonary hypertension.	Epoprostenol	151-163	kininogen 1	Homo sapiens	97-107
18156442-1	2008	We have previously shown that interleukin (IL)-1beta, transforming growth factor (TGF)-beta1, or bradykinin (BK) impair cAMP generation in response to prostacyclin analogs in human pulmonary artery smooth muscle (PASM), suggesting that inflammation can impair the effects of prostacyclin analogs on PASM in pulmonary hypertension.	Epoprostenol	151-163	kininogen 1	Homo sapiens	109-111
18156442-1	2008	We have previously shown that interleukin (IL)-1beta, transforming growth factor (TGF)-beta1, or bradykinin (BK) impair cAMP generation in response to prostacyclin analogs in human pulmonary artery smooth muscle (PASM), suggesting that inflammation can impair the effects of prostacyclin analogs on PASM in pulmonary hypertension.	Epoprostenol	275-287	kininogen 1	Homo sapiens	97-107
18156442-1	2008	We have previously shown that interleukin (IL)-1beta, transforming growth factor (TGF)-beta1, or bradykinin (BK) impair cAMP generation in response to prostacyclin analogs in human pulmonary artery smooth muscle (PASM), suggesting that inflammation can impair the effects of prostacyclin analogs on PASM in pulmonary hypertension.	Epoprostenol	275-287	kininogen 1	Homo sapiens	109-111
18156442-6	2008	Fluorescent kemptide assay and Western blotting confirmed that PKA and p38 MAP kinase were activated by IL-1beta, BK, and TGF-beta1.	kemptide	12-20	kininogen 1	Homo sapiens	114-116
18156442-7	2008	These studies suggest that IL-1beta, BK, and TGF-beta1 impair IP receptor-mediated cAMP accumulation by multiple effects on different components of the signaling pathway and that these effects are PKA and p38 MAP kinase dependent.	Cyclic AMP	83-87	kininogen 1	Homo sapiens	37-39
18084312-1	2008	BACKGROUND AND PURPOSE: Inhibition of bradykinin metabolizing enzymes (BMEs) can cause acute angioedema, as demonstrated in a recent clinical trial in patients administered the antihypertensive, omapatrilat.	omapatrilat	195-206	kininogen 1	Homo sapiens	38-48
18084312-5	2008	In the presence of lisinopril (ACE inhibitor), but not candoxatril (NEP inhibitor) or apstatin (APP inhibitor), bradykinin also elicited hypotension.	Lisinopril	19-29	kininogen 1	Homo sapiens	112-122
18288780-2	2008	BK-related peptides were derivatized with FITC prior to CE-LIF analysis.	Fluorescein-5-isothiocyanate	42-46	kininogen 1	Homo sapiens	0-2
17909849-8	2008	At 37 degrees C, bradykinin enhanced fluorescein isothiocyanate-dextran permeability by 48 +/- 11%.	fluorescein isothiocyanate dextran	37-71	kininogen 1	Homo sapiens	17-27
18083112-6	2008	BK is a potent inflammatory peptide which stimulates constitutive bradykinin B2 and inducible B1 receptors to release nitric oxide and prostacyclin.	Nitric Oxide	118-130	kininogen 1	Homo sapiens	0-2
18083112-6	2008	BK is a potent inflammatory peptide which stimulates constitutive bradykinin B2 and inducible B1 receptors to release nitric oxide and prostacyclin.	Nitric Oxide	118-130	kininogen 1	Homo sapiens	66-76
18083112-6	2008	BK is a potent inflammatory peptide which stimulates constitutive bradykinin B2 and inducible B1 receptors to release nitric oxide and prostacyclin.	Epoprostenol	135-147	kininogen 1	Homo sapiens	0-2
18083112-6	2008	BK is a potent inflammatory peptide which stimulates constitutive bradykinin B2 and inducible B1 receptors to release nitric oxide and prostacyclin.	Epoprostenol	135-147	kininogen 1	Homo sapiens	66-76
18037911-5	2008	KEY RESULTS: Bradykinin-induced relaxation in both sets of vessels was mediated entirely by EDHF whilst that generated by acetylcholine, though principally generated by EDHF, also had contribution from prostacyclin and possibly nitric oxide in mesenteric and subcutaneous vessels, respectively.	Acetylcholine	122-135	kininogen 1	Homo sapiens	13-23
18037911-5	2008	KEY RESULTS: Bradykinin-induced relaxation in both sets of vessels was mediated entirely by EDHF whilst that generated by acetylcholine, though principally generated by EDHF, also had contribution from prostacyclin and possibly nitric oxide in mesenteric and subcutaneous vessels, respectively.	Epoprostenol	202-214	kininogen 1	Homo sapiens	13-23
18037911-5	2008	KEY RESULTS: Bradykinin-induced relaxation in both sets of vessels was mediated entirely by EDHF whilst that generated by acetylcholine, though principally generated by EDHF, also had contribution from prostacyclin and possibly nitric oxide in mesenteric and subcutaneous vessels, respectively.	Nitric Oxide	228-240	kininogen 1	Homo sapiens	13-23
18037911-6	2008	A 2-h incubation of high glucose impaired bradykinin-induced relaxation of subcutaneous vessels whilst, in contrast, the relaxation generated by bradykinin in mesenteric vessels was enhanced at the same time point.	Glucose	25-32	kininogen 1	Homo sapiens	42-52
18037911-6	2008	A 2-h incubation of high glucose impaired bradykinin-induced relaxation of subcutaneous vessels whilst, in contrast, the relaxation generated by bradykinin in mesenteric vessels was enhanced at the same time point.	Glucose	25-32	kininogen 1	Homo sapiens	145-155
18180402-6	2008	Enalaprilat enhanced the effect of bradykinin on forearm blood flow, forearm vascular resistance, and t-PA release (all P&lt;0.001).	Enalaprilat	0-11	kininogen 1	Homo sapiens	35-45
18182246-3	2008	Using an animal model of hypertension, we have demonstrated that Ang II produces a vasodilator effect through the AT2 receptor via the bradykinin (BK)-dependent activation of endothelial nitric oxide (NO) synthase.	Nitric Oxide	187-199	kininogen 1	Homo sapiens	135-145
18182240-9	2008	The aim of the present study was to investigate intracellular calcium mobilization to quantify mouse, rat and human B1- and B2-receptor activation by bradykinin, kallidin, des-Arg9-bradykinin, des-Arg10-kallidin, and of the two novel rat kinins, kallidin-like-peptide and des-Arg10-kallidin-like-peptide.	Calcium	62-69	kininogen 1	Homo sapiens	150-160
18182246-3	2008	Using an animal model of hypertension, we have demonstrated that Ang II produces a vasodilator effect through the AT2 receptor via the bradykinin (BK)-dependent activation of endothelial nitric oxide (NO) synthase.	Nitric Oxide	187-199	kininogen 1	Homo sapiens	147-149
18158172-1	2008	BACKGROUND: Aminopeptidase P (APP) plays an important role in the catabolism of kinins in human plasma, mostly for des-Arg(9)-bradykinin.	des-arg	115-122	kininogen 1	Homo sapiens	126-136
18158172-3	2008	The pathophysiology of hereditary angioedema is presently attributed only to a quantitative/qualitative C1 inhibitor (CI-INH) defect with increased bradykinin release.	ci-inh	118-124	kininogen 1	Homo sapiens	148-158
17975109-4	2008	Bradykinin induced vascular superoxide and H2O2 production in an endothelium-dependent manner and elicited a concentration-dependent dilation that was reduced by catalase but not by 14,15-epoxyeicosa-5(Z)-enoic acid (EEZE), 6-(2-propargyloxyphenyl)hexanoic acid, sulfaphenazole, or iberiotoxin.	Superoxides	28-38	kininogen 1	Homo sapiens	0-10
18036587-0	2008	MEN16132, a kinin B2 receptor antagonist, prevents the endogenous bradykinin effects in guinea-pig airways.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	0-8	kininogen 1	Homo sapiens	66-76
18036587-2	2008	MEN16132 is a non-peptide kinin B(2) receptor antagonist able to inhibit the responses produced by intravenous bradykinin into the airways, as bronchoconstriction and microvascular leakage; we tested the effect of MEN16132 on endogenously generated bradykinin through the dextran sulfate-induced contact activation of kinin-kallikrein cascade in guinea-pigs.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	0-8	kininogen 1	Homo sapiens	111-121
18036587-2	2008	MEN16132 is a non-peptide kinin B(2) receptor antagonist able to inhibit the responses produced by intravenous bradykinin into the airways, as bronchoconstriction and microvascular leakage; we tested the effect of MEN16132 on endogenously generated bradykinin through the dextran sulfate-induced contact activation of kinin-kallikrein cascade in guinea-pigs.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	0-8	kininogen 1	Homo sapiens	249-259
18036587-6	2008	We conclude that local application of MEN16132 into the airways abolishes the responses produced by the endogenous generation of bradykinin and it can be useful as new pharmacological tool to check the role of kinins in human diseases.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	38-46	kininogen 1	Homo sapiens	129-139
17975109-4	2008	Bradykinin induced vascular superoxide and H2O2 production in an endothelium-dependent manner and elicited a concentration-dependent dilation that was reduced by catalase but not by 14,15-epoxyeicosa-5(Z)-enoic acid (EEZE), 6-(2-propargyloxyphenyl)hexanoic acid, sulfaphenazole, or iberiotoxin.	Hydrogen Peroxide	43-47	kininogen 1	Homo sapiens	0-10
17975109-4	2008	Bradykinin induced vascular superoxide and H2O2 production in an endothelium-dependent manner and elicited a concentration-dependent dilation that was reduced by catalase but not by 14,15-epoxyeicosa-5(Z)-enoic acid (EEZE), 6-(2-propargyloxyphenyl)hexanoic acid, sulfaphenazole, or iberiotoxin.	14,15-episulfide eicosatrienoic acid	217-221	kininogen 1	Homo sapiens	0-10
17975109-4	2008	Bradykinin induced vascular superoxide and H2O2 production in an endothelium-dependent manner and elicited a concentration-dependent dilation that was reduced by catalase but not by 14,15-epoxyeicosa-5(Z)-enoic acid (EEZE), 6-(2-propargyloxyphenyl)hexanoic acid, sulfaphenazole, or iberiotoxin.	6-(2-propargyloxyphenyl)hexanoic acid	224-261	kininogen 1	Homo sapiens	0-10
17975109-4	2008	Bradykinin induced vascular superoxide and H2O2 production in an endothelium-dependent manner and elicited a concentration-dependent dilation that was reduced by catalase but not by 14,15-epoxyeicosa-5(Z)-enoic acid (EEZE), 6-(2-propargyloxyphenyl)hexanoic acid, sulfaphenazole, or iberiotoxin.	Sulfaphenazole	263-277	kininogen 1	Homo sapiens	0-10
17975109-4	2008	Bradykinin induced vascular superoxide and H2O2 production in an endothelium-dependent manner and elicited a concentration-dependent dilation that was reduced by catalase but not by 14,15-epoxyeicosa-5(Z)-enoic acid (EEZE), 6-(2-propargyloxyphenyl)hexanoic acid, sulfaphenazole, or iberiotoxin.	iberiotoxin	282-293	kininogen 1	Homo sapiens	0-10
17619863-1	2008	Bradykinin and substance P have been derivatised with cyclic diethylenetriaminepentaacetic anhydride (cDTPA) and subsequently labelled with natural and isotopically enriched Eu(3+).	cyclic diethylenetriaminepentaacetic anhydride	54-100	kininogen 1	Homo sapiens	0-10
17619863-1	2008	Bradykinin and substance P have been derivatised with cyclic diethylenetriaminepentaacetic anhydride (cDTPA) and subsequently labelled with natural and isotopically enriched Eu(3+).	cdtpa	102-107	kininogen 1	Homo sapiens	0-10
18240142-5	2008	Solid-phase produced bradykinin thioester was ligated to the surface in the presence of variable concentrations of 4-mercaptophenylacetic acid as transthioesterification catalyst.	4-Mercaptophenylacetic acid	115-142	kininogen 1	Homo sapiens	21-31
18090541-2	2008	In the present study, we tested the hypothesis that the beta fragment of human coagulation factor XIIa (beta-FXIIa) induces adrenal catecholamine-mediated pressor and chronotropic responses via bradykinin generated from the plasma kallikrein-kinin system.	Catecholamines	132-145	kininogen 1	Homo sapiens	194-204
18036509-2	2008	Stimulation with either methacholine or bradykinin resulted in maximal increases in CREB phosphorylation within 1 min, with either a rapid subsequent decrease (bradykinin) to basal levels, or a sustained response (methacholine).	Methacholine Chloride	24-36	kininogen 1	Homo sapiens	160-170
18036509-2	2008	Stimulation with either methacholine or bradykinin resulted in maximal increases in CREB phosphorylation within 1 min, with either a rapid subsequent decrease (bradykinin) to basal levels, or a sustained response (methacholine).	Methacholine Chloride	214-226	kininogen 1	Homo sapiens	40-50
18036509-5	2008	In contrast, inhibition of MEK1/2 by U0126 resulted in significantly reduced CREB phosphorylation levels after B2 bradykinin, but not M3 mACh receptor activation.	U 0126	37-42	kininogen 1	Homo sapiens	114-124
18090541-6	2008	Exogenous bradykinin dose-dependently reproduced these catecholamine and haemodynamic responses in Brown Norway and BNK rats, but not in Brown Norway adrenal medullectomized rats.	Catecholamines	55-68	kininogen 1	Homo sapiens	10-20
18052679-0	2008	Cognac polyphenolic compounds increase bradykinin-induced nitric oxide production in endothelial cells.	Nitric Oxide	58-70	kininogen 1	Homo sapiens	39-49
18052679-8	2008	The capacity of CPC plus BK to increase NO signal was blunted by the NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester, and was enhanced in the presence either of superoxide dismutase or catalase.	NG-Nitroarginine Methyl Ester	92-126	kininogen 1	Homo sapiens	25-27
18052679-9	2008	Moreover, CPC plus BK response was greater after inhibition of either NADPH oxidase by apocynin or xanthine oxidase by allopurinol but it was not affected by rotenone.	acetovanillone	87-95	kininogen 1	Homo sapiens	19-21
18052679-9	2008	Moreover, CPC plus BK response was greater after inhibition of either NADPH oxidase by apocynin or xanthine oxidase by allopurinol but it was not affected by rotenone.	Allopurinol	119-130	kininogen 1	Homo sapiens	19-21
18052679-11	2008	Finally, the capacity of BK alone to increase NO was enhanced either by apocynin or allopurinol.	acetovanillone	72-80	kininogen 1	Homo sapiens	25-27
18052679-11	2008	Finally, the capacity of BK alone to increase NO was enhanced either by apocynin or allopurinol.	Allopurinol	84-95	kininogen 1	Homo sapiens	25-27
18052679-12	2008	Altogether, these data demonstrate that CPC is able to directly increase NO production without affecting O(2)(-) and enhances the BK-induced NO production in human endothelial cells.	cpc	40-43	kininogen 1	Homo sapiens	130-132
18052679-13	2008	The data highlight the ability of BK to stimulate not only NADPH oxidase- but also xanthine oxidase-inhibitor sensitive mechanisms that reduce its efficiency in increasing NO either alone or in the presence of CPC.	cpc	210-213	kininogen 1	Homo sapiens	34-36
18052679-14	2008	These results bring pharmacological evidence for vascular protection by CPC via its potentiating effect of BK response in terms of endothelial NO release.	cpc	72-75	kininogen 1	Homo sapiens	107-109
17716647-5	2007	The bradykinin/angiotensin I selectivity ratios calculated from double displacement experiments were: perindoprilat, 1.44; ramiprilat, 1.16; quinaprilat, 1.09; trandolaprilat, 1.08; enalaprilat, 1.00.	perindoprilat	102-115	kininogen 1	Homo sapiens	4-14
17716647-5	2007	The bradykinin/angiotensin I selectivity ratios calculated from double displacement experiments were: perindoprilat, 1.44; ramiprilat, 1.16; quinaprilat, 1.09; trandolaprilat, 1.08; enalaprilat, 1.00.	ramiprilat	123-133	kininogen 1	Homo sapiens	4-14
17716647-5	2007	The bradykinin/angiotensin I selectivity ratios calculated from double displacement experiments were: perindoprilat, 1.44; ramiprilat, 1.16; quinaprilat, 1.09; trandolaprilat, 1.08; enalaprilat, 1.00.	quinaprilat	141-152	kininogen 1	Homo sapiens	4-14
17716647-5	2007	The bradykinin/angiotensin I selectivity ratios calculated from double displacement experiments were: perindoprilat, 1.44; ramiprilat, 1.16; quinaprilat, 1.09; trandolaprilat, 1.08; enalaprilat, 1.00.	trandolaprilat	160-174	kininogen 1	Homo sapiens	4-14
17716647-5	2007	The bradykinin/angiotensin I selectivity ratios calculated from double displacement experiments were: perindoprilat, 1.44; ramiprilat, 1.16; quinaprilat, 1.09; trandolaprilat, 1.08; enalaprilat, 1.00.	Enalaprilat	182-193	kininogen 1	Homo sapiens	4-14
17716647-7	2007	Perindoprilat had the highest selectivity for bradykinin versus angiotensin I binding sites, and enalaprilat has the lowest.	perindoprilat	0-13	kininogen 1	Homo sapiens	46-56
17699739-0	2007	B-9972 (D-Arg-[Hyp3,Igl5,Oic7,Igl8]-bradykinin) is an inactivation-resistant agonist of the bradykinin B2 receptor derived from the peptide antagonist B-9430 (D-Arg-[Hyp3,Igl5,D-Igl7,Oic8]-bradykinin): pharmacologic profile and effective induction of receptor degradation.	D-Arginine	8-13	kininogen 1	Homo sapiens	36-46
18514752-4	2008	In cultured human ASM cells, where CD38 has been involved in TNFalpha-induced enhanced calcium signals to carbachol and bradykinin, we found that neutralizing anti-IFNbeta prevented TNFalpha enhancing action only on carbachol responses but not to that induced by bradykinin.	Calcium	87-94	kininogen 1	Homo sapiens	120-130
17872452-3	2007	METHODS AND RESULTS: In native CYP2C-expressing endothelial cells, bradykinin elicited a Ca(2+) influx that was potentiated by the soluble epoxide hydrolase inhibitor, 1-adamantyl-3-cyclohexylurea (ACU), and attenuated by CYP inhibition.	CHEMBL242255	168-196	kininogen 1	Homo sapiens	67-77
17961503-5	2007	It is demonstrated that a reduction in experiment time by a factor of 4 can be achieved for the case of a 13C-13C correlation spectrum on the nonapeptide bradykinin.	13c-13c	106-113	kininogen 1	Homo sapiens	154-164
17694592-4	2007	The sensitivities for the two peptides were significantly improved, increasing between 12 and 160 times, for bradykinin and gramicidin, respectively, on an NH(2)-modified silicon surface prepared in toluene, over that on a conventional gold substrate.	nh(2)	156-161	kininogen 1	Homo sapiens	109-119
17694592-4	2007	The sensitivities for the two peptides were significantly improved, increasing between 12 and 160 times, for bradykinin and gramicidin, respectively, on an NH(2)-modified silicon surface prepared in toluene, over that on a conventional gold substrate.	Toluene	199-206	kininogen 1	Homo sapiens	109-119
18085569-2	2007	We show that bradykinin and three modified peptides containing the basic residue arginine or lysine form stable interactions with single-stranded oligonucleotides.	Arginine	81-89	kininogen 1	Homo sapiens	13-23
18085569-2	2007	We show that bradykinin and three modified peptides containing the basic residue arginine or lysine form stable interactions with single-stranded oligonucleotides.	Lysine	93-99	kininogen 1	Homo sapiens	13-23
18085569-2	2007	We show that bradykinin and three modified peptides containing the basic residue arginine or lysine form stable interactions with single-stranded oligonucleotides.	Oligonucleotides	146-162	kininogen 1	Homo sapiens	13-23
18160362-4	2007	Bradykinin enhances nitric oxide and vasodilatory prostaglandins.	Nitric Oxide	20-32	kininogen 1	Homo sapiens	0-10
18160362-4	2007	Bradykinin enhances nitric oxide and vasodilatory prostaglandins.	Prostaglandins	50-64	kininogen 1	Homo sapiens	0-10
18160362-5	2007	Theoretically, aspirin, which inhibits cyclooxygenase enzyme, may reduce bradykinin mediated prostaglandin synthesis and blunt the beneficial effects of ACE inhibitors, when used together.	Aspirin	15-22	kininogen 1	Homo sapiens	73-83
18160362-5	2007	Theoretically, aspirin, which inhibits cyclooxygenase enzyme, may reduce bradykinin mediated prostaglandin synthesis and blunt the beneficial effects of ACE inhibitors, when used together.	Prostaglandins	93-106	kininogen 1	Homo sapiens	73-83
17704188-6	2007	In fura 2-loaded ASM cells, [Ca(2+)](i) responses to 1 microM ACh, 10 microM histamine, and 10 nM bradykinin, as well as SOCE, were attenuated (each to a different extent) after disruption of caveolae by the cholesterol-chelating drug methyl-beta-cyclodextrin.	Fura-2	3-9	kininogen 1	Homo sapiens	98-108
17823369-3	2007	Among normotensives we found that dilations to bradykinin (BK) and the NO-donor, sodium-nitroprusside (SNP) were reduced in obese subjects (BK, 10(-7) mol/L, lean: 90+/-4%, obese: 64+/-7%; SNP, 10(-6) mol/L, lean: 89+/-7%, obese: 76+/-5%).	Nitroprusside	81-101	kininogen 1	Homo sapiens	140-142
17699739-0	2007	B-9972 (D-Arg-[Hyp3,Igl5,Oic7,Igl8]-bradykinin) is an inactivation-resistant agonist of the bradykinin B2 receptor derived from the peptide antagonist B-9430 (D-Arg-[Hyp3,Igl5,D-Igl7,Oic8]-bradykinin): pharmacologic profile and effective induction of receptor degradation.	D-Arginine	8-13	kininogen 1	Homo sapiens	92-102
17885553-12	2007	Thus, beside the known influence of H2S on SMC KATP-channels, the observed direct ACE inhibitory effect may add to the vasorelaxant effect of H2S in the vasculature by reducing angiotensin II production and inhibiting bradykinin degradation.	Hydrogen Sulfide	142-145	kininogen 1	Homo sapiens	218-228
17447081-3	2007	In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)P(2), whereas closure by bradykinin B(2)-receptors (B2-BKRs) appears to result from formation of IP(3) and release of Ca(2+), implying that BKR stimulation does not deplete PI(4,5)P(2).	ip	242-244	kininogen 1	Homo sapiens	170-180
17447081-3	2007	In sympathetic neurons, closure induced by stimulating M1-muscarinic acetylcholine receptors (mAChRs) has been attributed to depletion of PI(4,5)P(2), whereas closure by bradykinin B(2)-receptors (B2-BKRs) appears to result from formation of IP(3) and release of Ca(2+), implying that BKR stimulation does not deplete PI(4,5)P(2).	pi(4,5)p	318-326	kininogen 1	Homo sapiens	170-180
17447081-5	2007	We find that the mAChR agonist, oxotremorine-M (oxo-M), produces a near-complete translocation of tubby-R332H-cYFP into the cytoplasm, whereas bradykinin (BK) produced about one third as much translocation.	Oxotremorine	32-44	kininogen 1	Homo sapiens	143-153
19668475-7	2007	Bradykinin displays protective actions against glutamate neurotoxicity through bradykinin-B(2) receptors in cultured retinal neurons.	Glutamic Acid	47-56	kininogen 1	Homo sapiens	0-10
17903241-4	2007	The effect of cytokine or asthma medication on histamine or bradykinin induced IPx signalling was assessed by [3H] inositol incorporation.	1,2-benzisothiazoline-3-one	79-82	kininogen 1	Homo sapiens	60-70
17903241-4	2007	The effect of cytokine or asthma medication on histamine or bradykinin induced IPx signalling was assessed by [3H] inositol incorporation.	3h] inositol	111-123	kininogen 1	Homo sapiens	60-70
17903241-8	2007	Similarly, TNFalpha, IFN gamma or salmeterol treatment augmented bradykinin induced IPx responses (127.4 +/- 8.3, 128.0 +/- 8.4 and 111.7 +/- 5.0%, P &lt; 0.05).	Salmeterol Xinafoate	34-44	kininogen 1	Homo sapiens	65-75
17903241-8	2007	Similarly, TNFalpha, IFN gamma or salmeterol treatment augmented bradykinin induced IPx responses (127.4 +/- 8.3, 128.0 +/- 8.4 and 111.7 +/- 5.0%, P &lt; 0.05).	1,2-benzisothiazoline-3-one	84-87	kininogen 1	Homo sapiens	65-75
17618301-10	2007	17beta-Estradiol (3-10 nM) also enhanced bradykinin-induced relaxation, which was inhibited by ICI 182,780.	Estradiol	0-16	kininogen 1	Homo sapiens	41-51
17618301-12	2007	Raloxifene, 17beta-estradiol, and bradykinin increased eNOS phosphorylation at Ser-1177 and ICI 182,780 prevented effects of raloxifene or 17beta-estradiol but not that of bradykinin.	Raloxifene Hydrochloride	0-10	kininogen 1	Homo sapiens	172-182
17618301-12	2007	Raloxifene, 17beta-estradiol, and bradykinin increased eNOS phosphorylation at Ser-1177 and ICI 182,780 prevented effects of raloxifene or 17beta-estradiol but not that of bradykinin.	Serine	79-82	kininogen 1	Homo sapiens	34-44
17618301-12	2007	Raloxifene, 17beta-estradiol, and bradykinin increased eNOS phosphorylation at Ser-1177 and ICI 182,780 prevented effects of raloxifene or 17beta-estradiol but not that of bradykinin.	Raloxifene Hydrochloride	125-135	kininogen 1	Homo sapiens	34-44
17618301-12	2007	Raloxifene, 17beta-estradiol, and bradykinin increased eNOS phosphorylation at Ser-1177 and ICI 182,780 prevented effects of raloxifene or 17beta-estradiol but not that of bradykinin.	Estradiol	139-155	kininogen 1	Homo sapiens	34-44
19668475-7	2007	Bradykinin displays protective actions against glutamate neurotoxicity through bradykinin-B(2) receptors in cultured retinal neurons.	Glutamic Acid	47-56	kininogen 1	Homo sapiens	79-89
17664134-0	2007	Bradykinin enhances reactive oxygen species generation, mitochondrial injury, and cell death induced by ATP depletion--a role of the phospholipase C-Ca(2+) pathway.	Reactive Oxygen Species	20-43	kininogen 1	Homo sapiens	0-10
17664134-0	2007	Bradykinin enhances reactive oxygen species generation, mitochondrial injury, and cell death induced by ATP depletion--a role of the phospholipase C-Ca(2+) pathway.	Adenosine Triphosphate	104-107	kininogen 1	Homo sapiens	0-10
17664134-1	2007	This study aimed to study the effect of bradykinin on reactive oxygen species (ROS) generation, mitochondrial injury, and cell death induced by ATP depletion in cell culture.	Reactive Oxygen Species	54-77	kininogen 1	Homo sapiens	40-50
17664134-1	2007	This study aimed to study the effect of bradykinin on reactive oxygen species (ROS) generation, mitochondrial injury, and cell death induced by ATP depletion in cell culture.	Reactive Oxygen Species	79-82	kininogen 1	Homo sapiens	40-50
17664134-1	2007	This study aimed to study the effect of bradykinin on reactive oxygen species (ROS) generation, mitochondrial injury, and cell death induced by ATP depletion in cell culture.	Adenosine Triphosphate	144-147	kininogen 1	Homo sapiens	40-50
17664134-7	2007	Bradykinin enhanced cellular LDH release, apoptosis, generation of superoxide, and hydrogen peroxide induced by ATP depletion.	Superoxides	67-77	kininogen 1	Homo sapiens	0-10
17664134-7	2007	Bradykinin enhanced cellular LDH release, apoptosis, generation of superoxide, and hydrogen peroxide induced by ATP depletion.	Hydrogen Peroxide	83-100	kininogen 1	Homo sapiens	0-10
17664134-7	2007	Bradykinin enhanced cellular LDH release, apoptosis, generation of superoxide, and hydrogen peroxide induced by ATP depletion.	Adenosine Triphosphate	112-115	kininogen 1	Homo sapiens	0-10
17664134-9	2007	The intracellular/mitochondrial calcium was higher in bradykinin-treated cells.	Calcium	32-39	kininogen 1	Homo sapiens	54-64
17664134-11	2007	Besides, blocking the phospholipase C (PLC) could reverse the synergistic effect of bradykinin with ATP depletion on ROS generation, mitochondrial damage, accumulation of intracellular/mitochondrial calcium, and apoptosis.	Reactive Oxygen Species	117-120	kininogen 1	Homo sapiens	84-94
17664134-11	2007	Besides, blocking the phospholipase C (PLC) could reverse the synergistic effect of bradykinin with ATP depletion on ROS generation, mitochondrial damage, accumulation of intracellular/mitochondrial calcium, and apoptosis.	Calcium	199-206	kininogen 1	Homo sapiens	84-94
17878762-7	2007	Intrabrachial infusions of bradykinin, acetylcholine, and sodium nitroprusside all caused dose-dependent increases in forearm blood flow (P &lt; 0.05) that were unaltered by hydrocortisone infusions.Short-term variations in plasma cortisol concentrations within the physiological range do not affect endothelial fibrinolytic or vasomotor function in healthy volunteers.	Hydrocortisone	231-239	kininogen 1	Homo sapiens	27-37
17868792-7	2007	Although similar intensity of RAS blockade can be achieved by either combination therapy or by using high doses of an AT1-receptor antagonist given alone, the ACE inhibitor present in the combination interferes with the bradykinin-nitric oxide pathway and the N-acetyl-Ser-Asp-Lys-Pro metabolism, which both may have additional biological effects.	Nitric Oxide	231-243	kininogen 1	Homo sapiens	220-230
17827868-0	2007	Endoplasmic reticulum is a key organella in bradykinin-triggered ATP release from cultured smooth muscle cells.	Adenosine Triphosphate	65-68	kininogen 1	Homo sapiens	44-54
17827868-3	2007	Here we show that bradykinin via B(2)-receptor stimulation induces the extracellular release of ATP via the inositol 1,4,5-trisphosphate [Ins(1,4,5)P(3)]-signaling pathway in cultured taenia coli smooth muscle cells.	Adenosine Triphosphate	96-99	kininogen 1	Homo sapiens	18-28
17827868-3	2007	Here we show that bradykinin via B(2)-receptor stimulation induces the extracellular release of ATP via the inositol 1,4,5-trisphosphate [Ins(1,4,5)P(3)]-signaling pathway in cultured taenia coli smooth muscle cells.	Inositol 1,4,5-Trisphosphate	108-136	kininogen 1	Homo sapiens	18-28
17827868-3	2007	Here we show that bradykinin via B(2)-receptor stimulation induces the extracellular release of ATP via the inositol 1,4,5-trisphosphate [Ins(1,4,5)P(3)]-signaling pathway in cultured taenia coli smooth muscle cells.	Inositol 1,4,5-Trisphosphate	138-152	kininogen 1	Homo sapiens	18-28
17827868-4	2007	It was found that bradykinin also increased the production of Ins(1,4,5)P(3) and 2-APB-inhibitable [Ca(2+)](i).	ins(1,4,5)p	62-73	kininogen 1	Homo sapiens	18-28
17827868-4	2007	It was found that bradykinin also increased the production of Ins(1,4,5)P(3) and 2-APB-inhibitable [Ca(2+)](i).	2-aminoethoxydiphenyl borate	81-86	kininogen 1	Homo sapiens	18-28
17827868-7	2007	Bradykinin caused a quick and transient accumulation of intracellular ATP from cells treated with 1% perchloric acid solution (PCA), but not with the cell lysis buffer.	Adenosine Triphosphate	70-73	kininogen 1	Homo sapiens	0-10
17827868-7	2007	Bradykinin caused a quick and transient accumulation of intracellular ATP from cells treated with 1% perchloric acid solution (PCA), but not with the cell lysis buffer.	Perchloric Acid	101-116	kininogen 1	Homo sapiens	0-10
17827868-9	2007	These findings suggest that bradykinin elicits the extracellular release of ATP that is mediated by the Ins(1,4,5)P(3)-induced Ca(2+) signaling and, finally, leads to a Ca(2+)-dependent export of ATP from the cells.	Adenosine Triphosphate	76-79	kininogen 1	Homo sapiens	28-38
17827868-9	2007	These findings suggest that bradykinin elicits the extracellular release of ATP that is mediated by the Ins(1,4,5)P(3)-induced Ca(2+) signaling and, finally, leads to a Ca(2+)-dependent export of ATP from the cells.	Inositol 1,4,5-Trisphosphate	104-118	kininogen 1	Homo sapiens	28-38
17827868-9	2007	These findings suggest that bradykinin elicits the extracellular release of ATP that is mediated by the Ins(1,4,5)P(3)-induced Ca(2+) signaling and, finally, leads to a Ca(2+)-dependent export of ATP from the cells.	Adenosine Triphosphate	196-199	kininogen 1	Homo sapiens	28-38
17827868-10	2007	Furthermore, the bradykinin-induced transient accumulation of ATP in the cells treated with PCA may imply a possible release of ATP from the endoplasmic reticulum.	Adenosine Triphosphate	62-65	kininogen 1	Homo sapiens	17-27
17827868-10	2007	Furthermore, the bradykinin-induced transient accumulation of ATP in the cells treated with PCA may imply a possible release of ATP from the endoplasmic reticulum.	Adenosine Triphosphate	128-131	kininogen 1	Homo sapiens	17-27
17956025-8	2007	Pilocarpine premedication led to a significant reduction of the contralateral secretory reflex to bradykinin.	Pilocarpine	0-11	kininogen 1	Homo sapiens	98-108
17558293-3	2007	Rises of [Ca2+]i evoked by bradykinin, and subsequent capacitative Ca2+ entry, were enhanced by prior hypoxia (1% O2, 24 h) without effect on reduced glutathione levels.	Oxygen	114-116	kininogen 1	Homo sapiens	27-37
17666194-3	2007	ACE inhibitors reduce circulating and tissue angiotensin II levels and potentiate the beneficial effects of bradykinin, including generation of nitric oxide (NO).	Nitric Oxide	144-156	kininogen 1	Homo sapiens	108-118
17666198-3	2007	However, ACE inhibitors interrupt bradykinin breakdown, which in turn potentially enhances nitric oxide and prostacyclin mechanisms.	Nitric Oxide	91-103	kininogen 1	Homo sapiens	34-44
17666198-3	2007	However, ACE inhibitors interrupt bradykinin breakdown, which in turn potentially enhances nitric oxide and prostacyclin mechanisms.	Epoprostenol	108-120	kininogen 1	Homo sapiens	34-44
17395626-5	2007	However, in sympathetic neurons, M-current inhibition by bradykinin appears to be mediated through the release and action of intracellular Ca(2)+ by inositol-1,4,5-trisphosphate (IP(3)), a product of PIP(2) hydrolysis, rather than by PIP(2) depletion.	Inositol 1,4,5-Trisphosphate	149-177	kininogen 1	Homo sapiens	57-67
17395626-5	2007	However, in sympathetic neurons, M-current inhibition by bradykinin appears to be mediated through the release and action of intracellular Ca(2)+ by inositol-1,4,5-trisphosphate (IP(3)), a product of PIP(2) hydrolysis, rather than by PIP(2) depletion.	ip	179-181	kininogen 1	Homo sapiens	57-67
17395626-7	2007	In concentrations producing equal M-current inhibition, bradykinin produced about one-quarter of the reduction in PIP(2) produced by oxotremorine-M, but equal reduction when PIP(2) synthesis was blocked with wortmannin.	oxotremorine M	133-147	kininogen 1	Homo sapiens	56-66
17395626-7	2007	In concentrations producing equal M-current inhibition, bradykinin produced about one-quarter of the reduction in PIP(2) produced by oxotremorine-M, but equal reduction when PIP(2) synthesis was blocked with wortmannin.	Wortmannin	208-218	kininogen 1	Homo sapiens	56-66
17395626-8	2007	Likewise, wortmannin restored bradykinin-induced M-current inhibition when Ca(2)+ release was prevented with thapsigargin.	Wortmannin	10-20	kininogen 1	Homo sapiens	30-40
17395626-8	2007	Likewise, wortmannin restored bradykinin-induced M-current inhibition when Ca(2)+ release was prevented with thapsigargin.	Thapsigargin	109-121	kininogen 1	Homo sapiens	30-40
17395626-9	2007	Thus, inhibition by bradykinin can use product (IP(3)/Ca(2)+)-dependent or substrate (PIP(2)) dependent mechanisms, depending on Ca(2)+ availability and PIP(2) synthesis rates.	Inositol 1,4,5-Trisphosphate	48-53	kininogen 1	Homo sapiens	20-30
17482459-0	2007	Bradykinin B1 antagonists: biphenyl SAR studies in the cyclopropanecarboxamide series.	cyclopropanecarboxamide	55-78	kininogen 1	Homo sapiens	0-10
17482459-1	2007	SAR study of the biphenyl region of cyclopropanecarboxamide derived bradykinin B(1) antagonists was examined.	cyclopropanecarboxamide	36-59	kininogen 1	Homo sapiens	68-78
17517102-5	2007	In 16-HBE 14o- cells, treatment with calcium ionophore A23187, bradykinin or LPS up-regulated the expression of these enzymes.	Calcium	37-44	kininogen 1	Homo sapiens	63-73
17379645-6	2007	Short-term treatment with rapamycin, an mTOR (mammalian target of rapamycin) inhibitor, completely abrogated the ability of insulin to increase the rate and magnitude of Ca2+ signaling and production of inositol 1,4,5-trisphosphate in response to bradykinin stimulation, indicating that insulin potentiates Gq protein-coupled receptor signaling through an mTOR-dependent pathway.	Sirolimus	26-35	kininogen 1	Homo sapiens	247-257
17379645-6	2007	Short-term treatment with rapamycin, an mTOR (mammalian target of rapamycin) inhibitor, completely abrogated the ability of insulin to increase the rate and magnitude of Ca2+ signaling and production of inositol 1,4,5-trisphosphate in response to bradykinin stimulation, indicating that insulin potentiates Gq protein-coupled receptor signaling through an mTOR-dependent pathway.	Inositol 1,4,5-Trisphosphate	203-231	kininogen 1	Homo sapiens	247-257
17470727-7	2007	17beta-Estradiol and PPT, but not DPN, attenuated the responses to U46619 and bradykinin.	Estradiol	0-16	kininogen 1	Homo sapiens	78-88
17412766-2	2007	By using the highly sensitive sniffer-patch technique, we demonstrate that the activation of P2Y receptors, bradykinin receptors and protease activated receptors all stimulate glutamate release from cultured or acutely dissociated astrocytes.	Glutamic Acid	176-185	kininogen 1	Homo sapiens	108-118
17327486-1	2007	The kinins, bradykinin (BK) and Lys-des[Arg(9)]-BK, are important inflammatory mediators that act via two specific G protein-coupled kinins, B(1) and B(2) receptors (B(2)R).	Arginine	40-43	kininogen 1	Homo sapiens	48-50
17327486-6	2007	The kinin agonists BK and Lys-des[Arg(9)]-BK up-regulated the expression of their respective receptors.	Lysine	26-29	kininogen 1	Homo sapiens	42-44
17327486-6	2007	The kinin agonists BK and Lys-des[Arg(9)]-BK up-regulated the expression of their respective receptors.	Arginine	34-37	kininogen 1	Homo sapiens	42-44
17327486-7	2007	BK, acting via the B(2)R, increased intracellular Ca(2+), as visualized by confocal microscopy using the fluorescent Ca(2+) dye, Fluor-4 AM.	fluor-4 am	129-139	kininogen 1	Homo sapiens	0-2
17470727-7	2007	17beta-Estradiol and PPT, but not DPN, attenuated the responses to U46619 and bradykinin.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	21-24	kininogen 1	Homo sapiens	78-88
17276727-6	2007	These effects of angiotensin-converting enzyme inhibitors and AT(1) receptor blockers can be mediated by activation of bradykinin pathways, resulting in the generation of vascular endothelial growth factor, nitric oxide and, consequently, angiogenesis.	Nitric Oxide	207-219	kininogen 1	Homo sapiens	119-129
17411080-7	2007	Protease inhibitors within an EDTA-plasma-collection device inhibit both intrinsic plasma peptidases and proteases and moderate the time-dependent changes of the plasma peptides, including bradykinin, and complement C4- and C3- derived peptides.	Edetic Acid	30-34	kininogen 1	Homo sapiens	189-199
17158598-7	2007	Both nickel and SKF-96365 (10 microM) inhibited the increase of the I(K(Ca)) induced by BK; however, the l-type Ca2+ channel blocker, nifedipine, had no effect.	Nickel	5-11	kininogen 1	Homo sapiens	88-90
17158598-7	2007	Both nickel and SKF-96365 (10 microM) inhibited the increase of the I(K(Ca)) induced by BK; however, the l-type Ca2+ channel blocker, nifedipine, had no effect.	1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole	16-25	kininogen 1	Homo sapiens	88-90
17158598-8	2007	Activation of the BK-induced current was inhibited by heparin, indicating dependence on intact inositol 1,4,5-triphosphate (IP3)-sensitive intracellular Ca2+ stores.	Heparin	54-61	kininogen 1	Homo sapiens	18-20
17158598-8	2007	Activation of the BK-induced current was inhibited by heparin, indicating dependence on intact inositol 1,4,5-triphosphate (IP3)-sensitive intracellular Ca2+ stores.	Inositol 1,4,5-Trisphosphate	95-122	kininogen 1	Homo sapiens	18-20
17158598-8	2007	Activation of the BK-induced current was inhibited by heparin, indicating dependence on intact inositol 1,4,5-triphosphate (IP3)-sensitive intracellular Ca2+ stores.	Inositol 1,4,5-Trisphosphate	124-127	kininogen 1	Homo sapiens	18-20
17158598-9	2007	BK also increased inositol phosphate accumulation and induced a transient Ca2+-activated chloride current (CACC) and a sustained nonselective cation current (I(CAT)).	Inositol Phosphates	18-36	kininogen 1	Homo sapiens	0-2
17158598-9	2007	BK also increased inositol phosphate accumulation and induced a transient Ca2+-activated chloride current (CACC) and a sustained nonselective cation current (I(CAT)).	Chlorides	89-97	kininogen 1	Homo sapiens	0-2
17158598-10	2007	In summary, BK activates BKCa, SKCa, CACC, and I(CAT) via IP3-sensitive stores in human ASM.	Inositol 1,4,5-Trisphosphate	58-61	kininogen 1	Homo sapiens	12-14
17391066-5	2007	The enzyme acts upon bradykinin mainly as a carboxydipeptidase, preferentially cleaving Pro-Phe over the Gly-Phe bond in a 9:1 ratio, whereas Abz-RPPGFSPFRQ-EDDnp was hydrolyzed at the same bonds but at an inverted proportion of 1:9.	H-Pro-Phe-OH	88-95	kininogen 1	Homo sapiens	21-31
17391066-5	2007	The enzyme acts upon bradykinin mainly as a carboxydipeptidase, preferentially cleaving Pro-Phe over the Gly-Phe bond in a 9:1 ratio, whereas Abz-RPPGFSPFRQ-EDDnp was hydrolyzed at the same bonds but at an inverted proportion of 1:9.	Glycine	105-108	kininogen 1	Homo sapiens	21-31
17391066-5	2007	The enzyme acts upon bradykinin mainly as a carboxydipeptidase, preferentially cleaving Pro-Phe over the Gly-Phe bond in a 9:1 ratio, whereas Abz-RPPGFSPFRQ-EDDnp was hydrolyzed at the same bonds but at an inverted proportion of 1:9.	Phenylalanine	92-95	kininogen 1	Homo sapiens	21-31
17391066-5	2007	The enzyme acts upon bradykinin mainly as a carboxydipeptidase, preferentially cleaving Pro-Phe over the Gly-Phe bond in a 9:1 ratio, whereas Abz-RPPGFSPFRQ-EDDnp was hydrolyzed at the same bonds but at an inverted proportion of 1:9.	4-[4-AMINO-6-(5-CHLORO-1H-INDOL-4-YLMETHYL)-[1,3,5]TRIAZIN-2-YLAMINO]-BENZONITRILE	142-145	kininogen 1	Homo sapiens	21-31
17391066-5	2007	The enzyme acts upon bradykinin mainly as a carboxydipeptidase, preferentially cleaving Pro-Phe over the Gly-Phe bond in a 9:1 ratio, whereas Abz-RPPGFSPFRQ-EDDnp was hydrolyzed at the same bonds but at an inverted proportion of 1:9.	-eddnp	156-162	kininogen 1	Homo sapiens	21-31
17200437-6	2007	Acetylcholine and bradykinin stimulate epoxyeicosatrienoic acid release from endothelial cells and arteries.	epoxyeicosatrienoic acid	39-63	kininogen 1	Homo sapiens	18-28
17402969-5	2007	BK also enhanced formation of prostaglandin E(2) and expression of microsomal prostaglandin E synthase.	Prostaglandins E	30-45	kininogen 1	Homo sapiens	0-2
17381681-3	2007	Results show that bradykinin increases NO release from mitral valves (DeltaBradykinin: 33.71 +/- 10.41 nm NO, P &lt; 0.001, n = 10), whereas N-nitro-l-arginine methyl esther (l-NAME) decreases NO release when compared with basal level (Deltal-NAME: 82.69 +/- 15.66 nm NO, P &lt; 0.005, n = 4).	NG-Nitroarginine Methyl Ester	175-181	kininogen 1	Homo sapiens	18-28
17381681-3	2007	Results show that bradykinin increases NO release from mitral valves (DeltaBradykinin: 33.71 +/- 10.41 nm NO, P &lt; 0.001, n = 10), whereas N-nitro-l-arginine methyl esther (l-NAME) decreases NO release when compared with basal level (Deltal-NAME: 82.69 +/- 15.66 nm NO, P &lt; 0.005, n = 4).	deltal-name	236-247	kininogen 1	Homo sapiens	18-28
17328065-0	2007	Bradykinin potentiates cytokine-induced prostaglandin biosynthesis in osteoblasts by enhanced expression of cyclooxygenase 2, resulting in increased RANKL expression.	Prostaglandins	40-53	kininogen 1	Homo sapiens	0-10
17328065-1	2007	OBJECTIVE: Bradykinin (BK) stimulates bone resorption in vitro and synergistically potentiates interleukin-1 (IL-1)-induced bone resorption and prostaglandin (PG) formation, suggesting that kinins are important in inflammation-induced bone loss.	Prostaglandins	144-157	kininogen 1	Homo sapiens	11-21
17328065-1	2007	OBJECTIVE: Bradykinin (BK) stimulates bone resorption in vitro and synergistically potentiates interleukin-1 (IL-1)-induced bone resorption and prostaglandin (PG) formation, suggesting that kinins are important in inflammation-induced bone loss.	Prostaglandins	144-157	kininogen 1	Homo sapiens	23-25
17328065-1	2007	OBJECTIVE: Bradykinin (BK) stimulates bone resorption in vitro and synergistically potentiates interleukin-1 (IL-1)-induced bone resorption and prostaglandin (PG) formation, suggesting that kinins are important in inflammation-induced bone loss.	Prostaglandins	159-161	kininogen 1	Homo sapiens	11-21
17328065-1	2007	OBJECTIVE: Bradykinin (BK) stimulates bone resorption in vitro and synergistically potentiates interleukin-1 (IL-1)-induced bone resorption and prostaglandin (PG) formation, suggesting that kinins are important in inflammation-induced bone loss.	Prostaglandins	159-161	kininogen 1	Homo sapiens	23-25
17340126-6	2007	The conducted hyperpolarizations and relaxations to BK were unaffected by L-NOARG, but were abolished by apamin and charybdotoxin.	Charybdotoxin	116-129	kininogen 1	Homo sapiens	52-54
17389890-3	2007	Kinins (bradykinin and lys-bradykinin) are endogenous vasodilators and natriuretic peptides known best for their ability to antagonize angiotensin-induced vasoconstriction and sodium retention.	Sodium	176-182	kininogen 1	Homo sapiens	8-18
17389890-3	2007	Kinins (bradykinin and lys-bradykinin) are endogenous vasodilators and natriuretic peptides known best for their ability to antagonize angiotensin-induced vasoconstriction and sodium retention.	Sodium	176-182	kininogen 1	Homo sapiens	27-37
17359538-4	2007	We showed that intravenous infusion of NS1619, a KCa channel agonist, and bradykinin selectively enhanced BTB permeability in brain tumors, but not in normal brain.	btb	106-109	kininogen 1	Homo sapiens	74-84
17182977-9	2007	Plasma cGMP was increased significantly during chronic valsartan (P = 0.048) through a bradykinin receptor-independent mechanism (effect of HOE-140, P = 0.13).	Cyclic GMP	7-11	kininogen 1	Homo sapiens	87-97
17266049-0	2007	Bradykinin analogs containing the 4-amino-2-benzazepin-3-one scaffold at the C-terminus.	4-amino-2-benzazepin-3-one	34-60	kininogen 1	Homo sapiens	0-10
17266049-1	2007	High affinity peptide ligands for the bradykinin (BK) B(2) subtype receptor have been shown to adopt a beta-turn conformation of the C-terminal tetrapeptide (H-Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)-OH).	Arginine	160-163	kininogen 1	Homo sapiens	38-48
17266049-1	2007	High affinity peptide ligands for the bradykinin (BK) B(2) subtype receptor have been shown to adopt a beta-turn conformation of the C-terminal tetrapeptide (H-Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)-OH).	Glycine	181-184	kininogen 1	Homo sapiens	38-48
17266049-1	2007	High affinity peptide ligands for the bradykinin (BK) B(2) subtype receptor have been shown to adopt a beta-turn conformation of the C-terminal tetrapeptide (H-Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)-OH).	Phenylalanine	188-191	kininogen 1	Homo sapiens	38-48
17266049-1	2007	High affinity peptide ligands for the bradykinin (BK) B(2) subtype receptor have been shown to adopt a beta-turn conformation of the C-terminal tetrapeptide (H-Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)-OH).	Serine	195-198	kininogen 1	Homo sapiens	38-48
17266049-1	2007	High affinity peptide ligands for the bradykinin (BK) B(2) subtype receptor have been shown to adopt a beta-turn conformation of the C-terminal tetrapeptide (H-Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)-OH).	Phenylalanine	209-212	kininogen 1	Homo sapiens	38-48
17319820-2	2007	STUDY DESIGN AND METHODS: The concentration of BK and one of its vasoactive metabolites, des-arginine(9)-BK (des-Arg(9)-BK), was measured in a large number of PCs as a function of leukoreduction and storage duration with specific enzyme immunoassays and complementary techniques.	des-arginine	89-101	kininogen 1	Homo sapiens	105-107
17319820-2	2007	STUDY DESIGN AND METHODS: The concentration of BK and one of its vasoactive metabolites, des-arginine(9)-BK (des-Arg(9)-BK), was measured in a large number of PCs as a function of leukoreduction and storage duration with specific enzyme immunoassays and complementary techniques.	des-arg	109-116	kininogen 1	Homo sapiens	47-49
17319820-2	2007	STUDY DESIGN AND METHODS: The concentration of BK and one of its vasoactive metabolites, des-arginine(9)-BK (des-Arg(9)-BK), was measured in a large number of PCs as a function of leukoreduction and storage duration with specific enzyme immunoassays and complementary techniques.	des-arg	109-116	kininogen 1	Homo sapiens	105-107
17157876-6	2007	Modeling of the Pro-Phe-Arg C-terminal end of the natural substrate bradykinin into the active site shows that the S1" pocket of CPN1 might better accommodate P1"-Lys than Arg residues, in agreement with CPN"s preference for cleaving off C-terminal Lys residues.	Pro-Phe-Arg	16-27	kininogen 1	Homo sapiens	68-78
17157876-6	2007	Modeling of the Pro-Phe-Arg C-terminal end of the natural substrate bradykinin into the active site shows that the S1" pocket of CPN1 might better accommodate P1"-Lys than Arg residues, in agreement with CPN"s preference for cleaving off C-terminal Lys residues.	Lysine	163-166	kininogen 1	Homo sapiens	68-78
17157876-6	2007	Modeling of the Pro-Phe-Arg C-terminal end of the natural substrate bradykinin into the active site shows that the S1" pocket of CPN1 might better accommodate P1"-Lys than Arg residues, in agreement with CPN"s preference for cleaving off C-terminal Lys residues.	Arginine	24-27	kininogen 1	Homo sapiens	68-78
17157876-6	2007	Modeling of the Pro-Phe-Arg C-terminal end of the natural substrate bradykinin into the active site shows that the S1" pocket of CPN1 might better accommodate P1"-Lys than Arg residues, in agreement with CPN"s preference for cleaving off C-terminal Lys residues.	Lysine	249-252	kininogen 1	Homo sapiens	68-78
17297930-8	2007	In certain configurations, cleavage products are produced in less than 10 s. Reproducible product patterns consistent with cleavage of the peptide bond at proline for angiotensin I, Lys-bradykinin, and myoglobin are demonstrated using capillary electrophoresis.	Proline	155-162	kininogen 1	Homo sapiens	186-196
17085540-4	2007	N(omega)-nitro-l-arginine methyl ester (l-NAME) and indomethacin (nitric oxide synthase and cyclooxygenase inhibitors, respectively) attenuated maximal relaxation to BK (R(max)) by approximately 50%.	NG-Nitroarginine Methyl Ester	0-38	kininogen 1	Homo sapiens	166-168
17085540-4	2007	N(omega)-nitro-l-arginine methyl ester (l-NAME) and indomethacin (nitric oxide synthase and cyclooxygenase inhibitors, respectively) attenuated maximal relaxation to BK (R(max)) by approximately 50%.	NG-Nitroarginine Methyl Ester	40-46	kininogen 1	Homo sapiens	166-168
17085540-4	2007	N(omega)-nitro-l-arginine methyl ester (l-NAME) and indomethacin (nitric oxide synthase and cyclooxygenase inhibitors, respectively) attenuated maximal relaxation to BK (R(max)) by approximately 50%.	Indomethacin	52-64	kininogen 1	Homo sapiens	166-168
17085540-5	2007	Coincubation with l-NAME, indomethacin, and the combined CMPs ((37,43)Gap27, (40)Gap27, and (43)Gap26) almost abolished relaxation to BK (R(max) = 12.2 +/- 3.7%).	NG-Nitroarginine Methyl Ester	18-24	kininogen 1	Homo sapiens	134-136
17085540-5	2007	Coincubation with l-NAME, indomethacin, and the combined CMPs ((37,43)Gap27, (40)Gap27, and (43)Gap26) almost abolished relaxation to BK (R(max) = 12.2 +/- 3.7%).	Indomethacin	26-38	kininogen 1	Homo sapiens	134-136
17694800-6	2007	On the contrary, minimal myometrial response to oxytocin, PG2alpha, ET-1, and bradykinin were observed during luteal phase when progesterone levels are increased.	Progesterone	128-140	kininogen 1	Homo sapiens	78-88
17319820-2	2007	STUDY DESIGN AND METHODS: The concentration of BK and one of its vasoactive metabolites, des-arginine(9)-BK (des-Arg(9)-BK), was measured in a large number of PCs as a function of leukoreduction and storage duration with specific enzyme immunoassays and complementary techniques.	des-arginine	89-101	kininogen 1	Homo sapiens	47-49
17145192-5	2007	gACE was potently inhibited by EDTA, 1,10-phenanthroline, captopril and lisinopril, and it promptly released the dipeptides His-Leu and Phe-Arg from angiotensin I and bradykinin.	Dipeptides	113-123	kininogen 1	Homo sapiens	167-177
17145192-5	2007	gACE was potently inhibited by EDTA, 1,10-phenanthroline, captopril and lisinopril, and it promptly released the dipeptides His-Leu and Phe-Arg from angiotensin I and bradykinin.	Arginine	140-143	kininogen 1	Homo sapiens	167-177
17105827-5	2007	Clofibrate (10 microM) reduced basal ET-1 from 0.36 +/- 0.08 (control) to 0.03 +/- 0.01 and blunted vasoactive agent-induced increase to 0.12 +/- 0.07 (PMA), 0.6 +/- 0.04 (BK), 0.25 +/- 0.03 (AII), or 0.12 +/- 0.03 (Hem) fM/microg protein (p &lt; 0.05).	Clofibrate	0-10	kininogen 1	Homo sapiens	172-174
17785966-8	2007	NM alone (30-50 mg) or LMWH + NM (1 mg) inhibited bradykinin production, whereas heparin alone or LMWH alone significantly accelerated it.	Heparin, Low-Molecular-Weight	23-27	kininogen 1	Homo sapiens	50-60
17305412-4	2007	Although both groups of drugs lower blood pressure, studies of the ACE inhibitor perindopril have revealed preservation of beneficial vascular and endothelial effects mediated by bradykinin and nitric oxide.	Perindopril	81-92	kininogen 1	Homo sapiens	179-189
16842920-9	2006	It is concluded that serotonin and bradykinin, classic endogenous algogens, can turn into potent histamine-independent pruritogens in lesional skin of atopic dermatitis.	Histamine	97-106	kininogen 1	Homo sapiens	35-45
18219959-10	2007	The most prominent therapeutic effect of perindopril is a result of its high affinity to endothelial ACE and the inhibition of bradykinin degradation.	Perindopril	41-52	kininogen 1	Homo sapiens	127-137
17636215-2	2007	Systemic arteries, isolated from women with healthy pregnancies, relax to the endothelial-dependent agonist bradykinin via a nonprostacyclin and non-nitric oxide pathway attributable to EDHF.	Nitric Oxide	149-161	kininogen 1	Homo sapiens	108-118
17636215-2	2007	Systemic arteries, isolated from women with healthy pregnancies, relax to the endothelial-dependent agonist bradykinin via a nonprostacyclin and non-nitric oxide pathway attributable to EDHF.	edhf	186-190	kininogen 1	Homo sapiens	108-118
17202847-4	2006	Bradykinin (BK)-stimulated Ca2+ entry, previously shown to be via SOCE, is enhanced by the addition of vanadate, an inhibitor of tyrosine phosphatases.	Vanadates	103-111	kininogen 1	Homo sapiens	0-10
17202847-4	2006	Bradykinin (BK)-stimulated Ca2+ entry, previously shown to be via SOCE, is enhanced by the addition of vanadate, an inhibitor of tyrosine phosphatases.	Vanadates	103-111	kininogen 1	Homo sapiens	12-14
17202847-5	2006	Furthermore, SOCE is regulated by cytochrome P-450, as demonstrated by the fact that the products of cytochrome P-450 activity (14,15 EET) stimulated SOCE while econazole, an inhibitor of cytochrome P450, suppressed BK-stimulated Ca2+ entry.	Econazole	161-170	kininogen 1	Homo sapiens	216-218
17113976-1	2006	G protein-coupled receptors (GPCRs) such as angiotensin II, bradykinin and endothelin-1 (ET-1) are critically involved in the regulation of adrenal function, including aldosterone production from zona glomerulosa cells.	Aldosterone	168-179	kininogen 1	Homo sapiens	60-70
17085429-6	2006	In response to inflammatory agonists such as thrombin and bradykinin, the generation of inositol 1,4,5-trisphosphate transiently depletes endoplasmic reticulum calcium and activates the TRPC1/TRPC4 channel.	Inositol 1,4,5-Trisphosphate	88-116	kininogen 1	Homo sapiens	58-68
17003818-4	2006	We found significantly decreased plasma APP activity (P=0.013) in HSR+ subjects as well as altered degradation of endogenous des-Arginine(9)-bradykinin, with a significantly lower beta value (P&lt;0.001).	des-arginine	125-137	kininogen 1	Homo sapiens	141-151
16898954-8	2006	In vitro tyrosine dephosphorylation of platelet eNOS using a recombinant protein tyrosine phosphatase enhanced thrombin-induced activity compared to thrombin alone, but had no effect on endothelial eNOS activity either at basal or after stimulation with bradykinin.	Tyrosine	9-17	kininogen 1	Homo sapiens	254-264
17047985-5	2006	The two phases can be assigned to second messengers of the BK-signalling pathway: Ca(2+) for the decrease and cyclic adenosine monophosphate for the rise of resistance, respectively.	Cyclic AMP	110-140	kininogen 1	Homo sapiens	59-61
18221093-4	2006	Perindopril is a third-generation long acting, once-daily lipophilic angiotensin-converting enzyme inhibitor with high tissue angiotensin-converting enzyme affinity, lowering angiotensin II and potentiating bradykinin.	Perindopril	0-11	kininogen 1	Homo sapiens	207-217
16957554-1	2006	BACKGROUND: Tissue kallikrein (TK) generates Lys-bradykinin, which is then converted to bradykinin and releases nitric oxide (NO) from endothelial cells via B2 receptors.	Nitric Oxide	112-124	kininogen 1	Homo sapiens	49-59
16616057-1	2006	BACKGROUND: Carboxypeptidase N is a plasma zinc metallocarboxypeptidase which is constitutively expressed in the liver and was identified as the enzyme responsible for inactivating bradykinin and kallidin by removing the C-terminal arginine.	Arginine	232-240	kininogen 1	Homo sapiens	181-191
16905135-0	2006	Bradykinin activates ADP-ribosyl cyclase in neuroblastoma cells: intracellular concentration decrease in NAD and increase in cyclic ADP-ribose.	NAD	105-108	kininogen 1	Homo sapiens	0-10
16905135-0	2006	Bradykinin activates ADP-ribosyl cyclase in neuroblastoma cells: intracellular concentration decrease in NAD and increase in cyclic ADP-ribose.	Cyclic ADP-Ribose	125-142	kininogen 1	Homo sapiens	0-10
16905135-3	2006	Application of 300nM BK to living NGPM1-27 cells decreased NAD(+) to 78% of the prestimulation level at 30s.	NAD	59-65	kininogen 1	Homo sapiens	21-23
16766609-6	2006	A mathematical model is developed to link the bradykinin-mediated DMR signals to the dynamic relocation of intracellular proteins and the receptor internalization during B2 receptor signaling cycle.	aspartylmethionylarginine	66-69	kininogen 1	Homo sapiens	46-56
16916274-4	2006	DX-88 (ecallantide, Dyax Corp.) is a highly specific recombinant plasma kallikrein inhibitor that halts the production of bradykinin and can be dosed subcutaneously.	ecallantide	0-5	kininogen 1	Homo sapiens	122-132
16917094-7	2006	In arterioles of DM(+), but not those of DM(-), patients" bradykinin-induced dilations were reduced by the nonselective COX inhibitor indomethacin or by the selective COX-2 inhibitor NS-398 (DM(+) at 10 nmol/L: to 20+/-4% and 29+/-7%, respectively).	Indomethacin	134-146	kininogen 1	Homo sapiens	58-68
16917094-7	2006	In arterioles of DM(+), but not those of DM(-), patients" bradykinin-induced dilations were reduced by the nonselective COX inhibitor indomethacin or by the selective COX-2 inhibitor NS-398 (DM(+) at 10 nmol/L: to 20+/-4% and 29+/-7%, respectively).	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	183-189	kininogen 1	Homo sapiens	58-68
16917094-9	2006	We conclude that in coronary arterioles of diabetic patients bradykinin induces enhanced COX-2-derived prostaglandin-mediated dilation.	Prostaglandins	103-116	kininogen 1	Homo sapiens	61-71
16916274-4	2006	DX-88 (ecallantide, Dyax Corp.) is a highly specific recombinant plasma kallikrein inhibitor that halts the production of bradykinin and can be dosed subcutaneously.	ecallantide	7-18	kininogen 1	Homo sapiens	122-132
16607560-8	2006	Maximum nitric-oxide-mediated dilation to bradykinin was significantly higher in patients with SDB who had received antihypertensive drug treatment compared to normotensive SDB patients.	Nitric Oxide	8-20	kininogen 1	Homo sapiens	42-52
16598774-8	2006	Furthermore, siRNA suppression of HSP27 expression significantly decreased KNG inhibition of etoposide-induced caspase-3 activation and apoptosis in these cells.	Etoposide	93-102	kininogen 1	Homo sapiens	75-78
16598774-9	2006	In summary, KNG modulate bone marrow derived stromal/preosteoblast cell proliferation and suppress etoposide-induced apoptosis through ERK and HSP27 activation, respectively.	Etoposide	99-108	kininogen 1	Homo sapiens	12-15
16529929-0	2006	5-Piperazinyl pyridine carboxamide bradykinin B1 antagonists.	5-piperazinyl pyridine	0-22	kininogen 1	Homo sapiens	35-45
16554405-1	2006	Previously, we reported that both the bradykinin (Bk)-induced increase in mitochondrial ATP concentration ([ATP]M) and the rate of cytosolic Ca2+ removal are significantly decreased in skin fibroblasts from a patient with an isolated complex I deficiency.	Adenosine Triphosphate	88-91	kininogen 1	Homo sapiens	38-48
16554405-1	2006	Previously, we reported that both the bradykinin (Bk)-induced increase in mitochondrial ATP concentration ([ATP]M) and the rate of cytosolic Ca2+ removal are significantly decreased in skin fibroblasts from a patient with an isolated complex I deficiency.	Adenosine Triphosphate	88-91	kininogen 1	Homo sapiens	50-52
16554405-1	2006	Previously, we reported that both the bradykinin (Bk)-induced increase in mitochondrial ATP concentration ([ATP]M) and the rate of cytosolic Ca2+ removal are significantly decreased in skin fibroblasts from a patient with an isolated complex I deficiency.	Adenosine Triphosphate	108-111	kininogen 1	Homo sapiens	38-48
16554405-1	2006	Previously, we reported that both the bradykinin (Bk)-induced increase in mitochondrial ATP concentration ([ATP]M) and the rate of cytosolic Ca2+ removal are significantly decreased in skin fibroblasts from a patient with an isolated complex I deficiency.	Adenosine Triphosphate	108-111	kininogen 1	Homo sapiens	50-52
16554405-2	2006	Here we demonstrate that the mitochondrial Ca2+ indicator rhod-2 can be used to selectively buffer the Bk-induced increase in mitochondrial Ca2+ concentration ([Ca2+]M) and, consequently, the Ca2+-stimulated increase in [ATP]M, thus allowing studies of how the increase in [ATP]M and the cytosolic Ca2+ removal rate are related.	Adenosine Triphosphate	221-224	kininogen 1	Homo sapiens	103-105
16554405-2	2006	Here we demonstrate that the mitochondrial Ca2+ indicator rhod-2 can be used to selectively buffer the Bk-induced increase in mitochondrial Ca2+ concentration ([Ca2+]M) and, consequently, the Ca2+-stimulated increase in [ATP]M, thus allowing studies of how the increase in [ATP]M and the cytosolic Ca2+ removal rate are related.	Adenosine Triphosphate	274-277	kininogen 1	Homo sapiens	103-105
16554405-3	2006	Luminometry of healthy fibroblasts expressing either aequorin or luciferase in the mitochondrial matrix showed that rhod-2 dose dependently decreased the Bk-induced increase in [Ca2+]M and [ATP]M by maximally 80 and 90%, respectively.	Adenosine Triphosphate	190-193	kininogen 1	Homo sapiens	154-156
16574942-6	2006	TNF-alpha treatment also increased both the peak and plateau intracellular Ca(2+) concentration responses in HASMCs elicited by acetylcholine and bradykinin.	hasmcs	109-115	kininogen 1	Homo sapiens	146-156
16814758-5	2006	We then performed co-immunoprecipitation experiments and found that amlodipine dose-dependently disrupted the caveolin/eNOS interaction contrary to other calcium channel blockers, and potentiated the stimulation of NO production by agonists such as bradykinin and vascular endothelial growth factor (VEGF) (+138+/-28% and +183+/-27% over values obtained with the agonist alone, respectively; P&lt;0.01).	Amlodipine	68-78	kininogen 1	Homo sapiens	249-259
16875977-7	2006	RESULTS: In NT, vasodilation to ACH and BDK was blunted by L-NMMA and not changed by SUL.	omega-N-Methylarginine	59-65	kininogen 1	Homo sapiens	40-43
16875977-7	2006	RESULTS: In NT, vasodilation to ACH and BDK was blunted by L-NMMA and not changed by SUL.	Sulfaphenazole	2-5	kininogen 1	Homo sapiens	40-43
16875977-11	2006	In 2 final groups of normotensive control subjects, vasodilation to ACH or BDK residual to cyclooxygenase and L-NMMA blockade was further inhibited by simultaneous SUL infusion.	omega-N-Methylarginine	110-116	kininogen 1	Homo sapiens	75-78
16875977-13	2006	CONCLUSIONS: Cytochrome P450 epoxygenase-derived EDHF acts as a partial compensatory mechanism to sustain endothelium-dependent vasodilation in HT, particularly the BDK-mediated response, when NO activity is impaired because of oxidative stress.	edhf	49-53	kininogen 1	Homo sapiens	165-168
16815471-11	2006	Sildenafil citrate improved bradykinin-induced but not acetylcholine-induced relaxation of omental small arteries from NP women.	Sildenafil Citrate	0-18	kininogen 1	Homo sapiens	28-38
16699727-4	2006	At low concentration with no significant effect on relaxation, kaempferol (10 microM) enhanced relaxation produced by bradykinin, the calcium ionophore A23187, isoproterenol and sodium nitroprusside in endothelium-intact porcine coronary arteries.	kaempferol	63-73	kininogen 1	Homo sapiens	118-128
16621150-7	2006	A 2.022 kDa fragment of alpha-Hb (amino acids 110-128, NH2-AAHLPAEFTPAVHASLDKF-COOH) was found to potentiate smooth muscle cell contraction in response to bradykinin, oxytocin and prostaglandin-F2alpha.	Carbonic Acid	79-83	kininogen 1	Homo sapiens	155-165
16527409-3	2006	NMR and molecular modeling studies were performed to investigate the influence of the bulk, flexibility and hydrophobicity of polyphenols on the association with bradykinin, the peptide model.	Polyphenols	126-137	kininogen 1	Homo sapiens	162-172
16418331-0	2006	Endothelial-cell apoptosis induced by cleaved high-molecular-weight kininogen (HKa) is matrix dependent and requires the generation of reactive oxygen species.	Reactive Oxygen Species	135-158	kininogen 1	Homo sapiens	46-77
16529929-1	2006	A series of 2,3-diaminopyridine bradykinin B(1) antagonists was modified to mitigate the potential for bioactivation.	,3-diaminopyridine	13-31	kininogen 1	Homo sapiens	32-42
16626818-3	2006	It was postulated that the insertion and the disulfide bond, also found in other receptors such as those for bradykinin, endothelin, purine and other ligands, might play a role in regulating the function of the AT1 receptor.	Disulfides	45-54	kininogen 1	Homo sapiens	109-119
16626818-3	2006	It was postulated that the insertion and the disulfide bond, also found in other receptors such as those for bradykinin, endothelin, purine and other ligands, might play a role in regulating the function of the AT1 receptor.	purine	133-139	kininogen 1	Homo sapiens	109-119
16631660-4	2006	The microvein was precontracted with thromboxane A2 mimetic U46619 (-7 log M) and the EDHF-mediated relaxation was induced by bradykinin (-10 to -6 log M) in the presence of indomethacin, NG-nitro-L-arginine, and oxyhemoglobin before and after H-R.	edhf	86-90	kininogen 1	Homo sapiens	126-136
16504505-0	2006	Bradykinin antagonists modified with dipeptide mimetic beta-turn inducers.	Dipeptides	37-46	kininogen 1	Homo sapiens	0-10
16740128-7	2006	Bradykinin-stimulated accumulation of inositol phosphate was observed in BHK cells expressing the recombinant receptor, which indicated the activation of endogenous G alpha(q) protein by the recombinant B2R.	Inositol Phosphates	38-56	kininogen 1	Homo sapiens	0-10
16540342-1	2006	The dissociation reactions of [M + H]+, [M + Na]+, and [M + Cu]+ ions of bradykinin (amino acid sequence RPPGFSPFR) and three bradykinin analogues (RPPGF, RPPGFSPF, PPGFSPFR) are examined by using 193-nm photodissociation and post-source decay (PSD) TOF-TOF-MS techniques.	Copper	60-62	kininogen 1	Homo sapiens	73-83
16601572-8	2006	Interestingly, AT1-receptor blockade appears to stimulate the bradykinin-nitric oxide pathway by increased angiotensin II type 2 receptor activation.	Nitric Oxide	73-85	kininogen 1	Homo sapiens	62-72
16766855-6	2006	The imidapril treatment significantly inhibited serum ACE activity and increased plasma bradykinin concentration.	imidapril	4-13	kininogen 1	Homo sapiens	88-98
16766855-7	2006	Furthermore, the extent of inhibition of serum ACE activity and the extent of increase in plasma bradykinin concentration in response to the imidapril treatment were both significantly correlated with the extent of increase in plasma NOx concentration.	imidapril	141-150	kininogen 1	Homo sapiens	97-107
16766855-7	2006	Furthermore, the extent of inhibition of serum ACE activity and the extent of increase in plasma bradykinin concentration in response to the imidapril treatment were both significantly correlated with the extent of increase in plasma NOx concentration.	nicotine 1-N-oxide	234-237	kininogen 1	Homo sapiens	97-107
16766855-11	2006	The increase in bradykinin concentration may be involved in the enhancing effect of the ACE inhibitor on NOx production in vivo.	nicotine 1-N-oxide	105-108	kininogen 1	Homo sapiens	16-26
16599534-1	2006	The conformers of gaseous bradykinin, BK, (Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) and its protonated forms, [BK + H](+), [BK + 2H](2+), and [BK + 3H](3+), were examined theoretically using a combination of the Merck molecular force field, Hartree-Fock, and density functional theory.	Proline	50-53	kininogen 1	Homo sapiens	26-36
16599534-1	2006	The conformers of gaseous bradykinin, BK, (Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) and its protonated forms, [BK + H](+), [BK + 2H](2+), and [BK + 3H](3+), were examined theoretically using a combination of the Merck molecular force field, Hartree-Fock, and density functional theory.	2)-pro	54-60	kininogen 1	Homo sapiens	26-36
16599534-1	2006	The conformers of gaseous bradykinin, BK, (Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) and its protonated forms, [BK + H](+), [BK + 2H](2+), and [BK + 3H](3+), were examined theoretically using a combination of the Merck molecular force field, Hartree-Fock, and density functional theory.	3)-gly	61-67	kininogen 1	Homo sapiens	26-36
16599534-1	2006	The conformers of gaseous bradykinin, BK, (Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) and its protonated forms, [BK + H](+), [BK + 2H](2+), and [BK + 3H](3+), were examined theoretically using a combination of the Merck molecular force field, Hartree-Fock, and density functional theory.	Phenylalanine	71-74	kininogen 1	Homo sapiens	26-36
16599534-1	2006	The conformers of gaseous bradykinin, BK, (Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) and its protonated forms, [BK + H](+), [BK + 2H](2+), and [BK + 3H](3+), were examined theoretically using a combination of the Merck molecular force field, Hartree-Fock, and density functional theory.	Serine	78-81	kininogen 1	Homo sapiens	26-36
16599534-1	2006	The conformers of gaseous bradykinin, BK, (Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) and its protonated forms, [BK + H](+), [BK + 2H](2+), and [BK + 3H](3+), were examined theoretically using a combination of the Merck molecular force field, Hartree-Fock, and density functional theory.	Proline	57-60	kininogen 1	Homo sapiens	26-36
16599534-1	2006	The conformers of gaseous bradykinin, BK, (Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) and its protonated forms, [BK + H](+), [BK + 2H](2+), and [BK + 3H](3+), were examined theoretically using a combination of the Merck molecular force field, Hartree-Fock, and density functional theory.	Phenylalanine	92-95	kininogen 1	Homo sapiens	26-36
16599534-1	2006	The conformers of gaseous bradykinin, BK, (Arg(1)-Pro(2)-Pro(3)-Gly(4)-Phe(5)-Ser(6)-Pro(7)-Phe(8)-Arg(9)) and its protonated forms, [BK + H](+), [BK + 2H](2+), and [BK + 3H](3+), were examined theoretically using a combination of the Merck molecular force field, Hartree-Fock, and density functional theory.	Arginine	99-102	kininogen 1	Homo sapiens	26-36
16376871-10	2006	However, when intracellular Ca(2+) was chelated with BAPTA/AM (100 microM), bradykinin caused ER Ca(2+) depletion and apoptosis without accompanying caspase-12 cleavage.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	53-58	kininogen 1	Homo sapiens	76-86
16448859-6	2006	BK-induced release of NO was 160.4+/-10.3 nmol/L in PA (n=8) and 103.0+/-14.7 nmol/L in PV (n=8, p&lt;0.001) with longer releasing duration in PA than in PV (14.3+/-1.3 vs. 12.1+/-0.8 min, p&lt;0.01).	Protactinium	52-54	kininogen 1	Homo sapiens	0-2
16448859-6	2006	BK-induced release of NO was 160.4+/-10.3 nmol/L in PA (n=8) and 103.0+/-14.7 nmol/L in PV (n=8, p&lt;0.001) with longer releasing duration in PA than in PV (14.3+/-1.3 vs. 12.1+/-0.8 min, p&lt;0.01).	Protactinium	143-145	kininogen 1	Homo sapiens	0-2
16291754-5	2006	Bradykinin-dependent Ca2+ release from the endoplasmic reticulum was rescued by wild-type calreticulin and by the Glu(238), Glu(239), Asp(241), and Glu(243) mutants.	Glutamic Acid	114-117	kininogen 1	Homo sapiens	0-10
16461819-10	2006	Pioglitazone treatment significantly improved endothelium-dependent dilation to bradykinin (P=0.01) without affecting the response to sodium nitroprusside (P=0.31).	Pioglitazone	0-12	kininogen 1	Homo sapiens	80-90
16497154-6	2006	The receptor binds [3H]Lys-des-Arg9-bradykinin in a saturable manner (K(d) 0.36 nM) and exhibits a pharmacological profile similar to that of human B(1)R.	Tritium	20-22	kininogen 1	Homo sapiens	36-46
16497154-6	2006	The receptor binds [3H]Lys-des-Arg9-bradykinin in a saturable manner (K(d) 0.36 nM) and exhibits a pharmacological profile similar to that of human B(1)R.	Lysine	23-26	kininogen 1	Homo sapiens	36-46
16497154-6	2006	The receptor binds [3H]Lys-des-Arg9-bradykinin in a saturable manner (K(d) 0.36 nM) and exhibits a pharmacological profile similar to that of human B(1)R.	des-arg9	27-35	kininogen 1	Homo sapiens	36-46
16446219-11	2006	The vasoconstrictive action on epicardial coronary arteries of des-Arg(9)-bradykinin in humans argues for a predominant action of B1-receptor stimulation at the level of smooth muscle cells.	des-arg	63-70	kininogen 1	Homo sapiens	74-84
16291754-5	2006	Bradykinin-dependent Ca2+ release from the endoplasmic reticulum was rescued by wild-type calreticulin and by the Glu(238), Glu(239), Asp(241), and Glu(243) mutants.	Glutamic Acid	124-127	kininogen 1	Homo sapiens	0-10
16291754-5	2006	Bradykinin-dependent Ca2+ release from the endoplasmic reticulum was rescued by wild-type calreticulin and by the Glu(238), Glu(239), Asp(241), and Glu(243) mutants.	Aspartic Acid	134-137	kininogen 1	Homo sapiens	0-10
16291754-5	2006	Bradykinin-dependent Ca2+ release from the endoplasmic reticulum was rescued by wild-type calreticulin and by the Glu(238), Glu(239), Asp(241), and Glu(243) mutants.	Glutamic Acid	124-127	kininogen 1	Homo sapiens	0-10
16324696-0	2005	MEN16132, a novel potent and selective nonpeptide antagonist for the human bradykinin B2 receptor.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	0-8	kininogen 1	Homo sapiens	75-85
16313901-7	2006	Thus, dihydropyridines and angiotensin converting enzyme inhibitors limit high glucose-induced superoxide formation and improve NO bioavailability in human endothelial cells, in part via bradykinin and p38MAPK.	Dihydropyridines	6-22	kininogen 1	Homo sapiens	187-197
16313901-7	2006	Thus, dihydropyridines and angiotensin converting enzyme inhibitors limit high glucose-induced superoxide formation and improve NO bioavailability in human endothelial cells, in part via bradykinin and p38MAPK.	Glucose	79-86	kininogen 1	Homo sapiens	187-197
17192135-1	2006	Ramipril is an oral, non-sulfhydryl ACE inhibitor thought to act in the renin-angiotensin-aldosterone system to decrease vasopressor activity, aldosterone secretion, and bradykinin degradation.	Ramipril	0-8	kininogen 1	Homo sapiens	170-180
16143655-3	2006	Bradykinin (BK), a vasoactive peptide increased in inflammation, induces the formation of prostaglandins through specific receptor activation.	Prostaglandins	90-104	kininogen 1	Homo sapiens	0-10
16143655-3	2006	Bradykinin (BK), a vasoactive peptide increased in inflammation, induces the formation of prostaglandins through specific receptor activation.	Prostaglandins	90-104	kininogen 1	Homo sapiens	12-14
16143655-4	2006	We hypothesized that BK plays an important role in the regulation of COX-2, contributing to the increase in production of prostaglandins in vascular smooth muscle cells.	Prostaglandins	122-136	kininogen 1	Homo sapiens	21-23
16213125-2	2006	We previously showed that the bradykinin (Bk)-induced increase in mitochondrial [ATP] ([ATP](M)) is significantly reduced in primary skin fibroblasts from a patient with an isolated complex I deficiency.	Adenosine Triphosphate	81-84	kininogen 1	Homo sapiens	30-40
16213125-2	2006	We previously showed that the bradykinin (Bk)-induced increase in mitochondrial [ATP] ([ATP](M)) is significantly reduced in primary skin fibroblasts from a patient with an isolated complex I deficiency.	Adenosine Triphosphate	88-91	kininogen 1	Homo sapiens	30-40
16256194-3	2006	This pool can also be mobilized by bradykinin, which acts via phospholipase C and inositol trisphosphate production.	inositol 1,2,3-trisphosphate	82-104	kininogen 1	Homo sapiens	35-45
17170519-5	2006	Bradykinin levels in contrast were increased by MPCM and treatment with omapatrilat further augmented levels.	omapatrilat	72-83	kininogen 1	Homo sapiens	0-10
17170519-6	2006	Co-incubation with the bradykinin B2 receptor antagonist HOE 140 attenuated the omapatrilat-induced lowering of fibronectin.	4-hydroxy-2-octenal	57-60	kininogen 1	Homo sapiens	23-33
17170519-6	2006	Co-incubation with the bradykinin B2 receptor antagonist HOE 140 attenuated the omapatrilat-induced lowering of fibronectin.	omapatrilat	80-91	kininogen 1	Homo sapiens	23-33
16428706-2	2006	The mechanism of ACE inhibitor-induced cough remains unresolved, but likely involves the protussive mediators bradykinin and substance P, agents that are degraded by ACE and therefore accumulate in the upper respiratory tract or lung when the enzyme is inhibited, and prostaglandins, the production of which may be stimulated by bradykinin.	Prostaglandins	268-282	kininogen 1	Homo sapiens	110-120
16340662-5	2006	For example, its potential for endothelium-dependent vasodilation, and for improvement of glucose transport and utilization, make bradykinin an important mediator for reducing the consequences of diabetes-related oxidative stress on both the myocardium and vessels.	Glucose	90-97	kininogen 1	Homo sapiens	130-140
16403023-8	2006	This, together with ionic interactions between the guanidino group of Arg9 of BK and the side chains of Asp360 and Glu150 in the S(2)" pocket, are possible reasons for the high-affinity binding of BK.	guanidino	51-60	kininogen 1	Homo sapiens	78-80
18802500-1	2006	Doubly-protonated bradykinin (RPPGFSPFR) and an angiotensin III analogue (RVYIFPF) were subjected to hydrogen/deuterium (H/D) exchange with CD(3)OD in a Fourier transform ion cyclotron resonance (FT-ICR) mass spectrometer.	Deuterium	110-119	kininogen 1	Homo sapiens	18-28
18802500-2	2006	A bimodal distribution of deuterium incorporation was present for bradykinin after H/D exchange for 90 s at a CD(3)OD pressure of 4 x 10(-7) Torr, indicating the existence of at least two distinct populations.	Deuterium	26-35	kininogen 1	Homo sapiens	66-76
18802500-3	2006	Bradykinin ion populations corresponding to 0-2 and 5-11 deuteriums (i.e., D(0), D(1), D(2), D(5), D(6), D(7), D(8), D(9), D(10), and D(11)) were each monoisotopically selected and fragmented via sustained off-resonance irradiation (SORI) collision-induced dissociation (CID).	Deuterium	57-67	kininogen 1	Homo sapiens	0-10
16186248-4	2006	The ACE-associated MYH9 immunoprecipitated from (32)P-labeled endothelial cells was basally phosphorylated and cell stimulation with ACE inhibitors, or with bradykinin, increased the phosphorylation of MYH9.	Phosphorus-32	48-53	kininogen 1	Homo sapiens	157-167
16497109-9	2006	After inhibition of the hyperpolarizing pathway by 4-aminopyridine, hypotension induced by ACh 10 microg achieved 64.6+/-2.5 mm Hg vs control value 78.4+/-2.8 mm Hg P&lt;0.001 and that induced by BK 100 microg 56.6+/-5.3 mm Hg vs control value 72.3+/-2.5 mm Hg P&lt;0.001 .	Acetylcholine	91-94	kininogen 1	Homo sapiens	196-198
16497109-13	2006	A different basal BP response, but equally attenuated hypotension to Ach and BK, was detected after the inhibition of two selected hyperpolarizing pathways.	Benzo(a)pyrene	18-20	kininogen 1	Homo sapiens	77-79
17332682-3	2006	On the other hand, they modify synthesis and release of PGI(2) and NO via increasing production of other biologically important peptides like bradykinin, Ang-(1-7) or Ang-(1-9).	Prostaglandins I	56-59	kininogen 1	Homo sapiens	142-152
16324696-3	2005	The affinity of MEN16132 for the bradykinin B2 receptor has been investigated by means of competition studies at [3H]bradykinin binding to membranes prepared from Chinese Hamster Ovary (CHO) cells expressing the human bradykinin B2 receptor (pKi 10.5), human lung fibroblasts (pKi 10.5), guinea pig airways (pKi 10.0), guinea pig ileum longitudinal smooth muscle (pKi 10.2), or guinea pig cultured colonic myocytes (pKi 10.3).	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	16-24	kininogen 1	Homo sapiens	33-43
16324696-3	2005	The affinity of MEN16132 for the bradykinin B2 receptor has been investigated by means of competition studies at [3H]bradykinin binding to membranes prepared from Chinese Hamster Ovary (CHO) cells expressing the human bradykinin B2 receptor (pKi 10.5), human lung fibroblasts (pKi 10.5), guinea pig airways (pKi 10.0), guinea pig ileum longitudinal smooth muscle (pKi 10.2), or guinea pig cultured colonic myocytes (pKi 10.3).	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	16-24	kininogen 1	Homo sapiens	117-127
16324696-3	2005	The affinity of MEN16132 for the bradykinin B2 receptor has been investigated by means of competition studies at [3H]bradykinin binding to membranes prepared from Chinese Hamster Ovary (CHO) cells expressing the human bradykinin B2 receptor (pKi 10.5), human lung fibroblasts (pKi 10.5), guinea pig airways (pKi 10.0), guinea pig ileum longitudinal smooth muscle (pKi 10.2), or guinea pig cultured colonic myocytes (pKi 10.3).	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	16-24	kininogen 1	Homo sapiens	117-127
16324696-6	2005	The antagonist potency was measured in functional assays, i.e., in blocking the bradykinin induced inositolphosphates (IP) accumulation at the human (CHO: pKB 10.3) and guinea pig (colonic myocytes: pKB 10.3) B2 receptor, or in antagonizing the bradykinin induced contractile responses in human (detrusor smooth muscle: pKB 9.9) and guinea pig (ileum longitudinal smooth muscle: pKB 10.1) tissues.	Inositol Phosphates	119-121	kininogen 1	Homo sapiens	80-90
16324696-6	2005	The antagonist potency was measured in functional assays, i.e., in blocking the bradykinin induced inositolphosphates (IP) accumulation at the human (CHO: pKB 10.3) and guinea pig (colonic myocytes: pKB 10.3) B2 receptor, or in antagonizing the bradykinin induced contractile responses in human (detrusor smooth muscle: pKB 9.9) and guinea pig (ileum longitudinal smooth muscle: pKB 10.1) tissues.	cho	150-153	kininogen 1	Homo sapiens	80-90
16324696-7	2005	In both functional assay types MEN16132 exerted a different antagonist pattern, i.e., surmountable at the human and insurmountable at the guinea pig bradykinin B2 receptors.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	31-39	kininogen 1	Homo sapiens	149-159
16324696-8	2005	Moreover, the receptor determinants important for the high affinity interaction of MEN16132 with the human bradykinin B2 receptor were investigated by means of radioligand binding studies performed at 24 point-mutated receptors.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	83-91	kininogen 1	Homo sapiens	107-117
16324696-10	2005	In conclusion, MEN16132 is a new, potent, and selective nonpeptide bradykinin B2 receptor antagonist.	(4-amino-5-(4-(4-(2,4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido)tetrahydro-2H-4-pyranoylcarbonyl)piperazino)-5-oxopentyl)(trimethyl)ammonium	15-23	kininogen 1	Homo sapiens	67-77
16378073-2	2005	METHODS: The EDHF-mediated relaxation was induced by bradykinin (BK, -10 to -6.5 logM) in the presence of inhibitors of nitric oxide and prostacyclin in porcine small resistance coronary arteries, before and after incubation in ST (Group Ia, n=11), Celsior (Group Ib, n=13), or Krebs (Group Ic, control, n=12) at 4 degrees C for 4 hr.	edhf	13-17	kininogen 1	Homo sapiens	53-63
16378073-2	2005	METHODS: The EDHF-mediated relaxation was induced by bradykinin (BK, -10 to -6.5 logM) in the presence of inhibitors of nitric oxide and prostacyclin in porcine small resistance coronary arteries, before and after incubation in ST (Group Ia, n=11), Celsior (Group Ib, n=13), or Krebs (Group Ic, control, n=12) at 4 degrees C for 4 hr.	edhf	13-17	kininogen 1	Homo sapiens	65-67
16319926-2	2005	This process, called sensitization or hyperalgesia, is mediated by a variety of proinflammatory factors, including bradykinin, ATP and NGF, which cause sensitization to noxious heat stimuli by enhancing the membrane current carried by the heat- and capsaicin-gated ion channel, TRPV1.	Capsaicin	249-258	kininogen 1	Homo sapiens	115-125
16262265-5	2005	Both purified and hyperexpressed tropolysin hydrolyzed bradykinin-derived fluorogenic peptide substrates at restricted sites, with an alkaline pH optimum, and were activated by dithiothreitol and reduced glutathione and by divalent metal cations, in the order Zn(2+) &gt; Co(2+) &gt; Mn(2+).	Dithiothreitol	177-191	kininogen 1	Homo sapiens	55-65
16365212-6	2005	Although there was a dose-dependent increase in blood flow with each vasodilator (P&lt;0.0001 for all), this response was attenuated with bradykinin (P&lt;0.05), acetylcholine (P&lt;0.05), and sodium nitroprusside (P&lt;0.001) infusions 2 hours after exposure to diesel exhaust, which persisted at 6 hours.	Nitroprusside	193-213	kininogen 1	Homo sapiens	138-148
16242459-3	2005	The EDHF-mediated relaxation by bradykinin (-10 to approximately -6 logM) with inhibitors of nitric oxide and prostacyclin was studied.	edhf	4-8	kininogen 1	Homo sapiens	32-42
16242459-3	2005	The EDHF-mediated relaxation by bradykinin (-10 to approximately -6 logM) with inhibitors of nitric oxide and prostacyclin was studied.	Epoprostenol	110-122	kininogen 1	Homo sapiens	32-42
16166566-6	2005	Enalaprilat potentiated the effect of exogenous BK on FBF similarly in all groups.	Enalaprilat	0-11	kininogen 1	Homo sapiens	48-50
16485516-1	2005	Perindopril is a long-acting, once-daily lipophilic angiotensin-converting enzyme inhibitor with high tissue angiotensin-converting enzyme affinity, lowering angiotensin II and potentiating bradykinin.	Perindopril	0-11	kininogen 1	Homo sapiens	190-200
16202859-7	2005	In the HRT group, significant increases were found in PRA, Ang I, and Ang II (all P &lt; .05) and a significant decrease in bradykinin (P &lt; .01) with candesartan treatment.	candesartan	153-164	kininogen 1	Homo sapiens	124-134
16093449-0	2005	Bradykinin signaling counteracts cAMP-elicited aquaporin 2 translocation in renal cells.	Cyclic AMP	33-37	kininogen 1	Homo sapiens	0-10
16093449-1	2005	Bradykinin (BK) is one of the most important peptides regulating vascular tone, water, and ionic balance in the body, playing a key role in controlling BP.	Benzo(a)pyrene	152-154	kininogen 1	Homo sapiens	0-10
16093449-1	2005	Bradykinin (BK) is one of the most important peptides regulating vascular tone, water, and ionic balance in the body, playing a key role in controlling BP.	Benzo(a)pyrene	152-154	kininogen 1	Homo sapiens	12-14
16093449-3	2005	For elucidating the mechanism by which BK regulates renal water transport that contributes to its antihypertensive effect, aquaporin 2 (AQP2)-transfected collecting duct CD8 cells, expressing the BK type II receptor (BK2R), were used as an experimental model.	Water	58-63	kininogen 1	Homo sapiens	39-41
16093449-4	2005	In CD8 cells, BK pretreatment impaired forskolin-induced AQP2 translocation to the apical plasma membrane.	Colforsin	39-48	kininogen 1	Homo sapiens	14-16
16093449-5	2005	For clarifying the signal transduction cascade associated with this effect, whether BK induced an increase in cytosolic calcium, via the G protein Gq, known to be coupled to BK2R, first was investigated.	Calcium	120-127	kininogen 1	Homo sapiens	84-86
16093449-6	2005	Spectrofluorometry using fura-2-AM revealed that 100 nM BK elicited a significant increase in Ca(i), which was abolished by the receptor antagonist HOE-140.	fura-2-am	25-34	kininogen 1	Homo sapiens	56-58
16093449-6	2005	Spectrofluorometry using fura-2-AM revealed that 100 nM BK elicited a significant increase in Ca(i), which was abolished by the receptor antagonist HOE-140.	carboxyamido-triazole	94-99	kininogen 1	Homo sapiens	56-58
16093449-6	2005	Spectrofluorometry using fura-2-AM revealed that 100 nM BK elicited a significant increase in Ca(i), which was abolished by the receptor antagonist HOE-140.	4-hydroxy-2-octenal	148-151	kininogen 1	Homo sapiens	56-58
15985616-7	2005	Prostaglandin E2 (PGE2), NOR-3 [(+/-)-(E)-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexeneamine] (NO donor), and bradykinin stimulated the secretion of HCO3(-), and the effect of bradykinin was blocked by indomethacin and L-NAME as well as FR172357.	nor-3 [(+/-)-(e)-ethyl-2-[(e)-hydroxyimino]-5-nitro-3-hexeneamine	25-90	kininogen 1	Homo sapiens	174-184
20527397-3	2005	Tissue ACE-I, through their high affinity to endothelium, considerably stronger prevents the local synthesis of angiotensin II (Ang II) and by inhibition of kininase II causes the subsequent increase of bradykinin level and mediated by BK2 receptor release of nitric oxide (NO), prostacycline (PGI2) and tissue type plasminogen activator (t-PA).	Nitric Oxide	260-272	kininogen 1	Homo sapiens	203-213
20527397-3	2005	Tissue ACE-I, through their high affinity to endothelium, considerably stronger prevents the local synthesis of angiotensin II (Ang II) and by inhibition of kininase II causes the subsequent increase of bradykinin level and mediated by BK2 receptor release of nitric oxide (NO), prostacycline (PGI2) and tissue type plasminogen activator (t-PA).	Epoprostenol (TN)	279-292	kininogen 1	Homo sapiens	203-213
20527397-3	2005	Tissue ACE-I, through their high affinity to endothelium, considerably stronger prevents the local synthesis of angiotensin II (Ang II) and by inhibition of kininase II causes the subsequent increase of bradykinin level and mediated by BK2 receptor release of nitric oxide (NO), prostacycline (PGI2) and tissue type plasminogen activator (t-PA).	Epoprostenol	294-298	kininogen 1	Homo sapiens	203-213
16125051-1	2005	Perindopril is a long-acting, once-daily lipophilic angiotensin-converting enzyme inhibitor with high tissue angiotensin-converting enzyme affinity, lowering angiotensin II and potentiating bradykinin.	Perindopril	0-11	kininogen 1	Homo sapiens	190-200
16272778-3	2005	However, the role of nitric oxide (NO) in the early phase protection of preconditioning with BK is not well understood.	Nitric Oxide	21-33	kininogen 1	Homo sapiens	93-95
16272778-10	2005	Protection by BK was abolished by coadministration of CH, 5-HD, or L-NAME.	NG-Nitroarginine Methyl Ester	67-73	kininogen 1	Homo sapiens	14-16
16204762-0	2005	ACE inhibitor and AT1 antagonist stimulate duodenal HCO3- secretion mediated by a common pathway - involvement of PG, NO and bradykinin.	Bicarbonates	52-56	kininogen 1	Homo sapiens	125-135
16204762-4	2005	Enalapril increased the HCO3- secretion in a dose-dependent manner, with a decrease in arterial blood pressure (MBP), and these effects were significantly attenuated by pretreatment with indomethacin, L-NAME and FR172357 (a selective bradykinin B2 receptor antagonist).	Enalapril	0-9	kininogen 1	Homo sapiens	234-244
16204762-4	2005	Enalapril increased the HCO3- secretion in a dose-dependent manner, with a decrease in arterial blood pressure (MBP), and these effects were significantly attenuated by pretreatment with indomethacin, L-NAME and FR172357 (a selective bradykinin B2 receptor antagonist).	Bicarbonates	24-28	kininogen 1	Homo sapiens	234-244
16204762-4	2005	Enalapril increased the HCO3- secretion in a dose-dependent manner, with a decrease in arterial blood pressure (MBP), and these effects were significantly attenuated by pretreatment with indomethacin, L-NAME and FR172357 (a selective bradykinin B2 receptor antagonist).	Indomethacin	187-199	kininogen 1	Homo sapiens	234-244
16204762-4	2005	Enalapril increased the HCO3- secretion in a dose-dependent manner, with a decrease in arterial blood pressure (MBP), and these effects were significantly attenuated by pretreatment with indomethacin, L-NAME and FR172357 (a selective bradykinin B2 receptor antagonist).	NG-Nitroarginine Methyl Ester	201-207	kininogen 1	Homo sapiens	234-244
16204762-4	2005	Enalapril increased the HCO3- secretion in a dose-dependent manner, with a decrease in arterial blood pressure (MBP), and these effects were significantly attenuated by pretreatment with indomethacin, L-NAME and FR172357 (a selective bradykinin B2 receptor antagonist).	FR 167344	212-220	kininogen 1	Homo sapiens	234-244
16204762-6	2005	Bradykinin also dose-dependently increased the HCO3- secretion with no change in MBP, though transient, and again the effects were blocked by indomethacin, L-NAME and FR172357.	Bicarbonates	47-51	kininogen 1	Homo sapiens	0-10
16088213-8	2005	Diminished AT 1 expression and adhesion molecule expression in response to ramiprilat treatment were partially reversed after incubation with a bradykinin 2 receptor antagonist, suggesting that elevated bradykinin levels under ACE inhibition may be involved in the beneficial effect of ACE inhibitors.	ramiprilat	75-85	kininogen 1	Homo sapiens	144-154
16088213-8	2005	Diminished AT 1 expression and adhesion molecule expression in response to ramiprilat treatment were partially reversed after incubation with a bradykinin 2 receptor antagonist, suggesting that elevated bradykinin levels under ACE inhibition may be involved in the beneficial effect of ACE inhibitors.	ramiprilat	75-85	kininogen 1	Homo sapiens	203-213
16262265-5	2005	Both purified and hyperexpressed tropolysin hydrolyzed bradykinin-derived fluorogenic peptide substrates at restricted sites, with an alkaline pH optimum, and were activated by dithiothreitol and reduced glutathione and by divalent metal cations, in the order Zn(2+) &gt; Co(2+) &gt; Mn(2+).	Glutathione	204-215	kininogen 1	Homo sapiens	55-65
16262265-5	2005	Both purified and hyperexpressed tropolysin hydrolyzed bradykinin-derived fluorogenic peptide substrates at restricted sites, with an alkaline pH optimum, and were activated by dithiothreitol and reduced glutathione and by divalent metal cations, in the order Zn(2+) &gt; Co(2+) &gt; Mn(2+).	Metals	232-237	kininogen 1	Homo sapiens	55-65
16262265-5	2005	Both purified and hyperexpressed tropolysin hydrolyzed bradykinin-derived fluorogenic peptide substrates at restricted sites, with an alkaline pH optimum, and were activated by dithiothreitol and reduced glutathione and by divalent metal cations, in the order Zn(2+) &gt; Co(2+) &gt; Mn(2+).	Zinc	260-266	kininogen 1	Homo sapiens	55-65
16262265-5	2005	Both purified and hyperexpressed tropolysin hydrolyzed bradykinin-derived fluorogenic peptide substrates at restricted sites, with an alkaline pH optimum, and were activated by dithiothreitol and reduced glutathione and by divalent metal cations, in the order Zn(2+) &gt; Co(2+) &gt; Mn(2+).	Cobalt(2+)	272-278	kininogen 1	Homo sapiens	55-65
16262265-5	2005	Both purified and hyperexpressed tropolysin hydrolyzed bradykinin-derived fluorogenic peptide substrates at restricted sites, with an alkaline pH optimum, and were activated by dithiothreitol and reduced glutathione and by divalent metal cations, in the order Zn(2+) &gt; Co(2+) &gt; Mn(2+).	Manganese(2+)	284-290	kininogen 1	Homo sapiens	55-65
16014619-11	2005	When the cells were pretreated with glibenclamide, an ATP-sensitive potassium channel blocker, the CGRP actions on bradykinin-induced Ca2+ influx were profoundly inhibited.	Glyburide	36-49	kininogen 1	Homo sapiens	115-125
16054523-4	2005	The isolated protein, named natterin, was able to induce edema, nociception and cleave human kininogen and kininogen-derived synthetic peptides, releasing kallidin (Lys-bradykinin).	natterin	28-36	kininogen 1	Homo sapiens	169-179
16333382-6	2005	The net intracellular calcium responses to 10 nmol/L bradykinin were measured in HASM cells by fluorescence imaging.	Calcium	22-29	kininogen 1	Homo sapiens	53-63
16083785-2	2005	This response is attenuated after repeated inhalation of bradykinin, suggesting that AMP may act in part by the release of neuropeptides.	Adenosine Monophosphate	85-88	kininogen 1	Homo sapiens	57-67
16079255-3	2005	BK provoked cell proliferation, increase in cytosolic calcium, activation of protein kinase C (PKC)-alpha, -beta, -delta, -epsilon and -eta and phosphorylation of the extracellular-regulated kinases 1 and 2 (ERK1/2).	Calcium	54-61	kininogen 1	Homo sapiens	0-2
16109080-3	2005	Previous work in our laboratory has shown that noscapine, an antitussive drug, inhibits the effect of bradykinin.	Noscapine	47-56	kininogen 1	Homo sapiens	102-112
16109080-9	2005	CONCLUSION: Noscapine, possibly by inhibition of bradykinin synthesis, eliminates ACEI-induced cough in the majority of patients and allows them to continue with ACEI therapy.	Noscapine	12-21	kininogen 1	Homo sapiens	49-59
16185420-3	2005	With methyl thiotetrazole (MTT) and trypan blue staining it was shown that the BK in dose of 1 x 10(-4) mol/L possessed most powerful inhibitory effect, and the survival rate of HKC was 69.3%.	methyl thiotetrazole	5-25	kininogen 1	Homo sapiens	79-81
16185420-3	2005	With methyl thiotetrazole (MTT) and trypan blue staining it was shown that the BK in dose of 1 x 10(-4) mol/L possessed most powerful inhibitory effect, and the survival rate of HKC was 69.3%.	monooxyethylene trimethylolpropane tristearate	27-30	kininogen 1	Homo sapiens	79-81
16185420-3	2005	With methyl thiotetrazole (MTT) and trypan blue staining it was shown that the BK in dose of 1 x 10(-4) mol/L possessed most powerful inhibitory effect, and the survival rate of HKC was 69.3%.	Trypan Blue	36-47	kininogen 1	Homo sapiens	79-81
15961376-5	2005	For the first time, we have observed that factor XII and high-molecular-weight kininogen, constituents of the blood plasma, can bind to VSMC in a Zn2+-dependent manner.	vsmc	136-140	kininogen 1	Homo sapiens	57-88
15961376-5	2005	For the first time, we have observed that factor XII and high-molecular-weight kininogen, constituents of the blood plasma, can bind to VSMC in a Zn2+-dependent manner.	Zinc	146-150	kininogen 1	Homo sapiens	57-88
15815977-2	2005	In this work we examine the binding and folding of the kinin peptide, bradykinin (BK), in the presence of the ganglioside monosialylated 1 (GM1) micelle.	Gangliosides	110-121	kininogen 1	Homo sapiens	70-80
15815977-2	2005	In this work we examine the binding and folding of the kinin peptide, bradykinin (BK), in the presence of the ganglioside monosialylated 1 (GM1) micelle.	Gangliosides	110-121	kininogen 1	Homo sapiens	82-84
15815977-2	2005	In this work we examine the binding and folding of the kinin peptide, bradykinin (BK), in the presence of the ganglioside monosialylated 1 (GM1) micelle.	gm1	140-143	kininogen 1	Homo sapiens	70-80
15815977-2	2005	In this work we examine the binding and folding of the kinin peptide, bradykinin (BK), in the presence of the ganglioside monosialylated 1 (GM1) micelle.	gm1	140-143	kininogen 1	Homo sapiens	82-84
15815977-3	2005	Using two-dimensional NMR techniques, we have shown that at low concentration, GM1 micelle is able to induce a turn conformation to BK.	gm1	79-82	kininogen 1	Homo sapiens	132-134
15895105-0	2005	Bradykinin-induced, endothelium-dependent responses in porcine coronary arteries: involvement of potassium channel activation and epoxyeicosatrienoic acids.	epoxyeicosatrienoic acids	130-155	kininogen 1	Homo sapiens	0-10
15895105-1	2005	In coronary arteries, bradykinin opens endothelial intermediate- and small-conductance Ca2+-sensitive K+ channels (IK(Ca) and SK(Ca)) and, additionally, releases epoxyeicosatrienoic acids (EETs) from the endothelium.	epoxyeicosatrienoic acids	162-187	kininogen 1	Homo sapiens	22-32
15895105-1	2005	In coronary arteries, bradykinin opens endothelial intermediate- and small-conductance Ca2+-sensitive K+ channels (IK(Ca) and SK(Ca)) and, additionally, releases epoxyeicosatrienoic acids (EETs) from the endothelium.	eets	189-193	kininogen 1	Homo sapiens	22-32
15895105-8	2005	Bradykinin (but not substance P) also hyperpolarizes myocytes by a mechanism (independent of endothelial cell hyperpolarization) which involves endothelial cell production of EETs (most likely 14,15- and/or 11,12-EET).	EET	175-178	kininogen 1	Homo sapiens	0-10
15895105-2	2005	To clarify the involvement of these pathways in endothelium-dependent myocyte hyperpolarization, bradykinin-induced electrical changes in endothelial cells and myocytes of porcine coronary arteries (following nitric oxide (NO) synthase and cyclooxygenase inhibition) were measured using sharp microelectrodes.	Nitric Oxide	209-221	kininogen 1	Homo sapiens	97-107
15895105-3	2005	Hyperpolarization of endothelial cells by bradykinin (27.0 +/- 0.9 mV, n = 4) was partially inhibited (74%) by blockade of IK(Ca) and SK(Ca) channels using 10 microM TRAM-39 (2-(2-chlorophenyl)-2,2-diphenylacetonitrile) plus 100 nM apamin (leaving an iberiotoxin-sensitive component), whereas the response to substance P was abolished.	2-(2-chlorophenyl)-2,2-diphenyl acetonitrile	175-218	kininogen 1	Homo sapiens	42-52
15895105-3	2005	Hyperpolarization of endothelial cells by bradykinin (27.0 +/- 0.9 mV, n = 4) was partially inhibited (74%) by blockade of IK(Ca) and SK(Ca) channels using 10 microM TRAM-39 (2-(2-chlorophenyl)-2,2-diphenylacetonitrile) plus 100 nM apamin (leaving an iberiotoxin-sensitive component), whereas the response to substance P was abolished.	iberiotoxin	251-262	kininogen 1	Homo sapiens	42-52
15895105-4	2005	After gap junction blockade with HEPES, (N-(2-hydroxyethyl)piperazine-N"-(2-ethanesulphonic acid)) hyperpolarization of the endothelium by 100 nM bradykinin was abolished by TRAM-39 plus apamin, whereas myocyte hyperpolarization still occurred (12.9 +/- 1.0 mV, n=4).	HEPES	33-38	kininogen 1	Homo sapiens	146-156
15895105-4	2005	After gap junction blockade with HEPES, (N-(2-hydroxyethyl)piperazine-N"-(2-ethanesulphonic acid)) hyperpolarization of the endothelium by 100 nM bradykinin was abolished by TRAM-39 plus apamin, whereas myocyte hyperpolarization still occurred (12.9 +/- 1.0 mV, n=4).	HEPES	41-97	kininogen 1	Homo sapiens	146-156
15895105-5	2005	The residual hyperpolarizations to 100 nM bradykinin were antagonized by the EET antagonist, 14,15-EEZE (14,15-epoxyeicosa-5(Z)-enoic acid) (10 microM), and abolished by iberiotoxin.	EET	77-80	kininogen 1	Homo sapiens	42-52
15895105-5	2005	The residual hyperpolarizations to 100 nM bradykinin were antagonized by the EET antagonist, 14,15-EEZE (14,15-epoxyeicosa-5(Z)-enoic acid) (10 microM), and abolished by iberiotoxin.	14,15-episulfide eicosatrienoic acid	93-103	kininogen 1	Homo sapiens	42-52
15895105-5	2005	The residual hyperpolarizations to 100 nM bradykinin were antagonized by the EET antagonist, 14,15-EEZE (14,15-epoxyeicosa-5(Z)-enoic acid) (10 microM), and abolished by iberiotoxin.	14,15-episulfide eicosatrienoic acid	105-138	kininogen 1	Homo sapiens	42-52
15895105-5	2005	The residual hyperpolarizations to 100 nM bradykinin were antagonized by the EET antagonist, 14,15-EEZE (14,15-epoxyeicosa-5(Z)-enoic acid) (10 microM), and abolished by iberiotoxin.	iberiotoxin	170-181	kininogen 1	Homo sapiens	42-52
15895105-6	2005	Bradykinin-induced myocyte hyperpolarizations were also reduced by 14,15-EEZE-mSI (14,15-EEZE-methylsulfonylimide) (5,6- and 14,15-EET antagonist), whereas those to exogenous 11,12-EET were unaffected.	14,15-eeze-msi	67-81	kininogen 1	Homo sapiens	0-10
15895105-6	2005	Bradykinin-induced myocyte hyperpolarizations were also reduced by 14,15-EEZE-mSI (14,15-EEZE-methylsulfonylimide) (5,6- and 14,15-EET antagonist), whereas those to exogenous 11,12-EET were unaffected.	14,15-eeze-methylsulfonylimide	83-113	kininogen 1	Homo sapiens	0-10
15895105-6	2005	Bradykinin-induced myocyte hyperpolarizations were also reduced by 14,15-EEZE-mSI (14,15-EEZE-methylsulfonylimide) (5,6- and 14,15-EET antagonist), whereas those to exogenous 11,12-EET were unaffected.	-eet	130-134	kininogen 1	Homo sapiens	0-10
15895105-6	2005	Bradykinin-induced myocyte hyperpolarizations were also reduced by 14,15-EEZE-mSI (14,15-EEZE-methylsulfonylimide) (5,6- and 14,15-EET antagonist), whereas those to exogenous 11,12-EET were unaffected.	11,12-epoxy-5,8,14-eicosatrienoic acid	175-184	kininogen 1	Homo sapiens	0-10
15895105-8	2005	Bradykinin (but not substance P) also hyperpolarizes myocytes by a mechanism (independent of endothelial cell hyperpolarization) which involves endothelial cell production of EETs (most likely 14,15- and/or 11,12-EET).	eets	175-179	kininogen 1	Homo sapiens	0-10
15941293-4	2005	The experimental and theoretical evidence for bradykinin fragment 1-5 tagged with K(+) suggests that the SB structure is favored; the calculations indicate a head-to-tail looped structure stabilized by a salt bridge between the protonated guanidine group and the deprotonated C-terminus, which allows K(+) to sit in a binding pocket with five C=O electrostatic interactions.	Antimony	105-107	kininogen 1	Homo sapiens	46-56
16003073-8	2005	Furthermore, a reduction of endothelial nitric oxide formation takes place, thus decreasing microvascular reactivity to dilating agents such as bradykinin, and complement function (e.g., opsonization, chemotaxis) is impaired, despite elevations of certain complement factors.	Nitric Oxide	40-52	kininogen 1	Homo sapiens	144-154
15941293-4	2005	The experimental and theoretical evidence for bradykinin fragment 1-5 tagged with K(+) suggests that the SB structure is favored; the calculations indicate a head-to-tail looped structure stabilized by a salt bridge between the protonated guanidine group and the deprotonated C-terminus, which allows K(+) to sit in a binding pocket with five C=O electrostatic interactions.	Guanidine	239-248	kininogen 1	Homo sapiens	46-56
15919417-7	2005	RESULTS: Endothelium-dependent relaxation in response to bradykinin was reduced by 36% and 81% for the rings treated with 12.5 and 25 mum of LPC, respectively, as compared with controls (P &lt; 0.05).	Lysophosphatidylcholines	141-144	kininogen 1	Homo sapiens	57-67
15665048-7	2005	Results showed that treatment of TEVM with Provinols significantly potentiated the contractile responses induced by histamine and bradykinin.	Polyphenols	43-52	kininogen 1	Homo sapiens	130-140
15983144-7	2005	The bradykinin concentrations in blood mixed with LCT and LCT/MCT propofol were significantly higher than in blood mixed with saline.	Propofol	66-74	kininogen 1	Homo sapiens	4-14
15983144-7	2005	The bradykinin concentrations in blood mixed with LCT and LCT/MCT propofol were significantly higher than in blood mixed with saline.	Sodium Chloride	126-132	kininogen 1	Homo sapiens	4-14
15910619-0	2005	The contribution of nitric oxide and vasodilatory prostanoids to bradykinin-mediated vasodilation in Type 1 diabetes.	Nitric Oxide	20-32	kininogen 1	Homo sapiens	65-75
15910619-0	2005	The contribution of nitric oxide and vasodilatory prostanoids to bradykinin-mediated vasodilation in Type 1 diabetes.	Prostaglandins	50-61	kininogen 1	Homo sapiens	65-75
15910619-5	2005	After infusion of L-NMMA and L-NMMA with indomethacin, there was a similar reduction in blood flow responses to bradykinin in both groups.	omega-N-Methylarginine	18-24	kininogen 1	Homo sapiens	112-122
15910619-5	2005	After infusion of L-NMMA and L-NMMA with indomethacin, there was a similar reduction in blood flow responses to bradykinin in both groups.	omega-N-Methylarginine	29-35	kininogen 1	Homo sapiens	112-122
15910619-5	2005	After infusion of L-NMMA and L-NMMA with indomethacin, there was a similar reduction in blood flow responses to bradykinin in both groups.	Indomethacin	41-53	kininogen 1	Homo sapiens	112-122
15910619-7	2005	CONCLUSIONS: This study demonstrates that bradykinin-stimulated vasodilation is mediated by both nitric oxide and prostaglandin release from the endothelium in patients with Type 1 diabetes and normoalbuminuria, and in healthy control subjects.	Nitric Oxide	97-109	kininogen 1	Homo sapiens	42-52
15910619-7	2005	CONCLUSIONS: This study demonstrates that bradykinin-stimulated vasodilation is mediated by both nitric oxide and prostaglandin release from the endothelium in patients with Type 1 diabetes and normoalbuminuria, and in healthy control subjects.	Prostaglandins	114-127	kininogen 1	Homo sapiens	42-52
15655136-0	2005	Losartan increases bradykinin levels in hypertensive humans.	Losartan	0-8	kininogen 1	Homo sapiens	19-29
15983144-2	2005	Alternatively, LCT propofol generates bradykinin causing the injection pain and activates complement, but these effects when using LCT/MCT propofol have not been examined.	Propofol	19-27	kininogen 1	Homo sapiens	38-48
15573401-4	2005	We initially observed that BK- and EGF-dependent activation of Src, EGFR, Akt, and p42/p44 MAPK and [3H]thymidine incorporation were mediated by Src and EGFR, because the Src inhibitor PP1 and EGFR kinase inhibitor AG1478 abrogated BK- and EGF-dependent effects.	Tritium	101-103	kininogen 1	Homo sapiens	27-29
15573401-4	2005	We initially observed that BK- and EGF-dependent activation of Src, EGFR, Akt, and p42/p44 MAPK and [3H]thymidine incorporation were mediated by Src and EGFR, because the Src inhibitor PP1 and EGFR kinase inhibitor AG1478 abrogated BK- and EGF-dependent effects.	Tritium	101-103	kininogen 1	Homo sapiens	232-234
15573401-4	2005	We initially observed that BK- and EGF-dependent activation of Src, EGFR, Akt, and p42/p44 MAPK and [3H]thymidine incorporation were mediated by Src and EGFR, because the Src inhibitor PP1 and EGFR kinase inhibitor AG1478 abrogated BK- and EGF-dependent effects.	Thymidine	104-113	kininogen 1	Homo sapiens	27-29
15573401-4	2005	We initially observed that BK- and EGF-dependent activation of Src, EGFR, Akt, and p42/p44 MAPK and [3H]thymidine incorporation were mediated by Src and EGFR, because the Src inhibitor PP1 and EGFR kinase inhibitor AG1478 abrogated BK- and EGF-dependent effects.	RTKI cpd	215-221	kininogen 1	Homo sapiens	27-29
15911880-4	2005	The IP(3)R complex functions as a focal point to promote Ca(2+) release in two ways: (1) it facilitates PKA-dependent phosphorylation of IP(3)R1 in response to BK-induced elevation of cAMP, and (2) it couples the plasmalemmal EGFR with IP(3)R1 at the Ca(2+) store located juxtaposed to the plasma membrane.	Cyclic AMP	184-188	kininogen 1	Homo sapiens	160-162
15746099-8	2005	The BK-triggered increased IL-8 secretion in SMM-treated cultures was mediated by an increased Ca(2+)(i) mobilization consequent to an ER expansion associated with increases in protein synthesis (total, cytokines, and antimicrobial factors).	smm	45-48	kininogen 1	Homo sapiens	4-6
15909515-4	2005	For example, the peak capacity for a 2.5 microg load of one bradykinin on the polymeric column was reduced to only 0.38 times its value for 0.1 microg when using 0.02 M formic acid, compared with 0.77 times its value when using the same concentration of TFA.	formic acid	169-180	kininogen 1	Homo sapiens	60-70
15909515-4	2005	For example, the peak capacity for a 2.5 microg load of one bradykinin on the polymeric column was reduced to only 0.38 times its value for 0.1 microg when using 0.02 M formic acid, compared with 0.77 times its value when using the same concentration of TFA.	Trifluoroacetic Acid	254-257	kininogen 1	Homo sapiens	60-70
15891334-11	2005	Ketamine time-dependently reduced bradykinin-enhanced intracellular calcium concentrations.	Calcium	68-75	kininogen 1	Homo sapiens	34-44
15891334-12	2005	Analysis by confocal microscopy further demonstrated the suppressive effects of ketamine on bradykinin-induced calcium mobilization.	Ketamine	80-88	kininogen 1	Homo sapiens	92-102
15891334-12	2005	Analysis by confocal microscopy further demonstrated the suppressive effects of ketamine on bradykinin-induced calcium mobilization.	Calcium	111-118	kininogen 1	Homo sapiens	92-102
15780194-6	2005	Ascorbic acid administration in the dorsal hand vein significantly increased the venodilation with bradykinin in smokers (68.3%+/-13.2% vs 89.5%+/-6.3% before and after infusion, respectively; P&lt;0.05) but not in non-smokers (93.7%+/-20.1% vs 86.4%+/-12.4% before and after infusion, respectively).	Ascorbic Acid	0-13	kininogen 1	Homo sapiens	99-109
15681300-9	2005	Compared with losartan, enalapril augmented bradykinin-mediated vasodilatation (P&lt;0.05) and t-PA release (P&lt;0.01 for all) but had no effect on B(1) receptor-mediated responses.	Enalapril	24-33	kininogen 1	Homo sapiens	44-54
15699460-1	2005	Bradykinin causes arterial relaxation and hyperpolarization, which is mediated by a transferable endothelium-derived hyperpolarizing factor (EDHF).	derived hyperpolarizing factor	109-139	kininogen 1	Homo sapiens	0-10
15699460-1	2005	Bradykinin causes arterial relaxation and hyperpolarization, which is mediated by a transferable endothelium-derived hyperpolarizing factor (EDHF).	edhf	141-145	kininogen 1	Homo sapiens	0-10
15563630-7	2005	For BK infusion, FBF increased approximately 10-fold in the control condition; L-NMMA tended to reduce BK dilation (P &lt; 0.1), and addition of ketorolac significantly reduced BK dilation.	omega-N-Methylarginine	79-85	kininogen 1	Homo sapiens	103-105
15563630-7	2005	For BK infusion, FBF increased approximately 10-fold in the control condition; L-NMMA tended to reduce BK dilation (P &lt; 0.1), and addition of ketorolac significantly reduced BK dilation.	omega-N-Methylarginine	79-85	kininogen 1	Homo sapiens	103-105
15563630-9	2005	To test the idea that NO can inhibit the NOS + COX-independent portion of dilation, we infused a dose of sodium nitroprusside (NO-clamp technique) during ACh or BK that restored the reduction in baseline blood flow due to L-NMMA.	Nitroprusside	105-125	kininogen 1	Homo sapiens	161-163
15640399-1	2005	Bradykinin (BK) is an endogenous vasoactive peptide that promotes vasodilation by stimulating the release of nitric oxide (NO) from endothelial cells via activation of endothelial NO synthase (eNOS).	Nitric Oxide	109-121	kininogen 1	Homo sapiens	0-10
15640399-1	2005	Bradykinin (BK) is an endogenous vasoactive peptide that promotes vasodilation by stimulating the release of nitric oxide (NO) from endothelial cells via activation of endothelial NO synthase (eNOS).	Nitric Oxide	109-121	kininogen 1	Homo sapiens	12-14
15740805-0	2005	Preemptive analgesia by zaltoprofen that inhibits bradykinin action and cyclooxygenase in a post-operative pain model.	pyranoprofen	24-35	kininogen 1	Homo sapiens	50-60
15740805-3	2005	2-(10,11-dihydro-10-oxo-dibenzo[b,f]thiepin-2-yl) propionic acid (zaltoprofen) is a unique compound that inhibits cyclooxygenase (COX) and exhibits anti-bradykinin activity.	CN 100	0-64	kininogen 1	Homo sapiens	153-163
15740805-3	2005	2-(10,11-dihydro-10-oxo-dibenzo[b,f]thiepin-2-yl) propionic acid (zaltoprofen) is a unique compound that inhibits cyclooxygenase (COX) and exhibits anti-bradykinin activity.	pyranoprofen	66-77	kininogen 1	Homo sapiens	153-163
16011263-5	2005	RESULTS: Using the established method, we developed accordingly QSAR models of Bitter tasting dipeptide, ACE inhibitors and bradykinin-potentiating pentapeptides and their r2 and XV-r2 were more than 0.70.	Dipeptides	94-103	kininogen 1	Homo sapiens	124-134
15664665-4	2005	The stimulatory effect of BK on the IL-1beta- or TNFalpha-stimulated IL-8 production was reduced in the presence of BK B2 receptor antagonist HOE 140, whereas the B1 receptor antagonist Lys-(des-arg9, Leu8)-BK had no effect.	Lysine	186-190	kininogen 1	Homo sapiens	26-28
15664665-4	2005	The stimulatory effect of BK on the IL-1beta- or TNFalpha-stimulated IL-8 production was reduced in the presence of BK B2 receptor antagonist HOE 140, whereas the B1 receptor antagonist Lys-(des-arg9, Leu8)-BK had no effect.	des-arg9	191-199	kininogen 1	Homo sapiens	26-28
15664665-5	2005	Similar to BK, the calcium ionophore A23187 also upregulated the stimulatory effect of IL-1beta and TNFalpha on IL-8 production.	Calcimycin	37-43	kininogen 1	Homo sapiens	11-13
15664665-6	2005	The protein kinase C (PKC) inhibitor bisindolylmaleimide, BIS, significantly reduced the stimulatory effect of BK on IL-1beta and TNFalpha increased IL-8 production but did not affect the production of IL-8 stimulated by cytokines alone.	bisindolylmaleimide	37-56	kininogen 1	Homo sapiens	111-113
15664665-6	2005	The protein kinase C (PKC) inhibitor bisindolylmaleimide, BIS, significantly reduced the stimulatory effect of BK on IL-1beta and TNFalpha increased IL-8 production but did not affect the production of IL-8 stimulated by cytokines alone.	Bismuth	58-61	kininogen 1	Homo sapiens	111-113
15664665-7	2005	The specific p38 mitogen-activated protein kinase (MAPK) inhibitor SB 203580 reduced IL-8 production stimulated by the combination of BK and IL-1beta as well as the IL-1beta-stimulated IL-8 production.	SB 203580	67-76	kininogen 1	Homo sapiens	134-136
15771546-2	2005	In the present study, electrospray ionization is used to examine the behavior of anionic clusters of triphosphate with choline, acetylcholine, and betaine, and the behaviors of cationic clusters of triphosphate with the peptides bradykinin (RPPGFSPFR) and ARRPEGRTWAQPGY.	triphosphoric acid	198-210	kininogen 1	Homo sapiens	229-239
15685206-19	2005	Corynanthine produced a greater increase in nasal blockage when in combination with bradykinin compared to its combination with R-alpha-MeH.	Yohimbine	0-12	kininogen 1	Homo sapiens	84-94
15626609-4	2005	The current responses recorded at each electrode after stimulation of glutamate and NO release by means of K+ and bradykinin clearly demonstrate the ability of the individual electrode in the array to detect the analyte towards which its sensitivity and selectivity was targeted without interference from the neighbouring electrode or other analytes present in the test mixture.	Glutamic Acid	70-79	kininogen 1	Homo sapiens	114-124
15471985-1	2005	The present study tested the hypothesis that endostatin stimulates superoxide (O2*-) production through a ceramide-mediating signaling pathway and thereby results in an uncoupling of bradykinin (BK)-induced increases in intracellular Ca2+ concentration ([Ca2+]i) from nitric oxide (NO) production in coronary endothelial cells.	Nitric Oxide	268-280	kininogen 1	Homo sapiens	195-197
15680854-8	2005	There was an interaction of SMA-CPB and MPSS to decrease both TCC (p = 0.042) and bradykinin generation (p = 0.028).	sma-cpb	28-35	kininogen 1	Homo sapiens	82-92
16204762-6	2005	Bradykinin also dose-dependently increased the HCO3- secretion with no change in MBP, though transient, and again the effects were blocked by indomethacin, L-NAME and FR172357.	Indomethacin	142-154	kininogen 1	Homo sapiens	0-10
16204762-6	2005	Bradykinin also dose-dependently increased the HCO3- secretion with no change in MBP, though transient, and again the effects were blocked by indomethacin, L-NAME and FR172357.	NG-Nitroarginine Methyl Ester	156-162	kininogen 1	Homo sapiens	0-10
16204762-6	2005	Bradykinin also dose-dependently increased the HCO3- secretion with no change in MBP, though transient, and again the effects were blocked by indomethacin, L-NAME and FR172357.	FR 167344	167-175	kininogen 1	Homo sapiens	0-10
16204762-8	2005	These results suggest that both an ACE inhibitor and AT1 antagonist (in the presence of angiotensin II) increase duodenal HCO3- secretion via a common pathway, involving bradykinin, NO and PGs.	Bicarbonates	122-126	kininogen 1	Homo sapiens	170-180
16204762-9	2005	It is also assumed that bradykinin releases NO locally, which in turns stimulates HCO3- secretion mediated by PGs.	Bicarbonates	82-86	kininogen 1	Homo sapiens	24-34
16204762-9	2005	It is also assumed that bradykinin releases NO locally, which in turns stimulates HCO3- secretion mediated by PGs.	Phosphatidylglycerols	110-113	kininogen 1	Homo sapiens	24-34
15905730-6	2005	In response to bradykinin at 10 M, ritonavir (15 and 30 microM) reduced the relaxation by 27% and 78%, respectively, as compared with controls (P &lt; 0.05).	Ritonavir	35-44	kininogen 1	Homo sapiens	15-25
15573401-5	2005	Inhibition of PI3-K by LY294002 attenuated BK-induced Akt and p42/p44 MAPK phosphorylation and [3H]thymidine incorporation, but had no effect on EGFR phosphorylation, suggesting that EGFR may be an upstream component of PI3-K/Akt and MAPK in these responses.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	23-31	kininogen 1	Homo sapiens	43-45
15573401-5	2005	Inhibition of PI3-K by LY294002 attenuated BK-induced Akt and p42/p44 MAPK phosphorylation and [3H]thymidine incorporation, but had no effect on EGFR phosphorylation, suggesting that EGFR may be an upstream component of PI3-K/Akt and MAPK in these responses.	Tritium	96-98	kininogen 1	Homo sapiens	43-45
15573401-7	2005	Pretreatment with U0126 (a MEK1/2 inhibitor) attenuated the p42/p44 MAPK phosphorylation and [3H]thymidine incorporation stimulated by BK, but had no effect on Akt activation.	U 0126	18-23	kininogen 1	Homo sapiens	135-137
15573401-7	2005	Pretreatment with U0126 (a MEK1/2 inhibitor) attenuated the p42/p44 MAPK phosphorylation and [3H]thymidine incorporation stimulated by BK, but had no effect on Akt activation.	Tritium	94-96	kininogen 1	Homo sapiens	135-137
15573401-8	2005	Moreover, BK-induced transactivation of EGFR and cell proliferation was blocked by matrix metalloproteinase inhibitor GM6001.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	118-124	kininogen 1	Homo sapiens	10-12
15573401-9	2005	These results suggest that, in VSMCs, the mechanism of BK-stimulated activation of p42/p44 MAPK and cell proliferation was mediated, at least in part, through activation of Src family kinases, EGFR transactivation, and PI3-K/Akt.	vsmcs	31-36	kininogen 1	Homo sapiens	55-57
15806012-0	2005	Montelukast protects against bradykinin-induced bronchospasm.	montelukast	0-11	kininogen 1	Homo sapiens	29-39
15591222-3	2005	Inhibition of K(IR) by barium chloride (4 micromol min(-1)) alone or with additional inhibition of Na(+)/K(+) ATPase (ouabain 2.7 micromol min(-1)) reduced responses to bradykinin (30 pmol min(-1)), by 26+/-8.3% and 36+/-7.2%, respectively (each P&lt;0 0.05).	barium chloride	23-38	kininogen 1	Homo sapiens	169-179
15591222-4	2005	Barium with ouabain plus inhibitors of prostaglandin (PG) and nitric oxide synthesis inhibited but did not abolish responses to bradykinin (51+/-2.8% inhibition; P&lt;0.01); norepinephrine (240 pmol min(-1)) caused similar reduction of baseline blood flow, as did this combination of inhibitors, but did not significantly inhibit the response to bradykinin.	Barium	0-6	kininogen 1	Homo sapiens	346-356
15591222-8	2005	Barium selectively inhibited the forearm blood flow response to bradykinin, indicating that a component of this response is mediated by KIR.	Barium	0-6	kininogen 1	Homo sapiens	64-74
15843162-4	2005	Blarinasin preferentially hydrolysed Pro-Phe-Arg-4-methylcoumaryl-7-amide (MCA) and N-tert-butyloxycarbonyl-Val-Leu-Lys-MCA, and preferentially converted human high-molecular-weight kininogen (HK) to bradykinin.	blarinasin	0-10	kininogen 1	Homo sapiens	160-191
15843162-4	2005	Blarinasin preferentially hydrolysed Pro-Phe-Arg-4-methylcoumaryl-7-amide (MCA) and N-tert-butyloxycarbonyl-Val-Leu-Lys-MCA, and preferentially converted human high-molecular-weight kininogen (HK) to bradykinin.	blarinasin	0-10	kininogen 1	Homo sapiens	200-210
15630045-0	2005	Angiotensin-(1-7) and bradykinin in norepinephrine release in the central nervous system of hypertension.	Norepinephrine	36-50	kininogen 1	Homo sapiens	22-32
15475593-6	2005	Enalaprilat induced a significant increase in bradykinin levels in the dialysate, without affecting kallidin levels.	Enalaprilat	0-11	kininogen 1	Homo sapiens	46-56
15655136-5	2005	Losartan increased blood levels of BK-(1-9) and hydroxylated BK-(1-9) by approximately 2-fold and reduced the BK-(1-7)/BK-(1-9) ratio by 55%.	Losartan	0-8	kininogen 1	Homo sapiens	35-37
15655136-5	2005	Losartan increased blood levels of BK-(1-9) and hydroxylated BK-(1-9) by approximately 2-fold and reduced the BK-(1-7)/BK-(1-9) ratio by 55%.	Losartan	0-8	kininogen 1	Homo sapiens	61-63
15655136-5	2005	Losartan increased blood levels of BK-(1-9) and hydroxylated BK-(1-9) by approximately 2-fold and reduced the BK-(1-7)/BK-(1-9) ratio by 55%.	Losartan	0-8	kininogen 1	Homo sapiens	61-63
15655136-6	2005	There was a trend for eprosartan to produce similar changes in bradykinin levels.	eprosartan	22-32	kininogen 1	Homo sapiens	63-73
15655136-12	2005	CONCLUSIONS: Losartan increases bradykinin levels.	Losartan	13-21	kininogen 1	Homo sapiens	32-42
15586018-4	2005	RECENT FINDINGS: During the past year, the evidence for an AT2 receptor microvascular dilator action has been presented that is mediated by nitric oxide (NO) generation in a bradykinin-dependent or independent manner.	Nitric Oxide	140-152	kininogen 1	Homo sapiens	174-184
15613974-6	2005	NG-monomethyl-L-arginine (L-NMMA) inhibited the responses of acetylcholine; however, L-NMMA only partially inhibited the responses to bradykinin.	omega-N-Methylarginine	85-91	kininogen 1	Homo sapiens	134-144
15723572-1	2005	Perindopril is a long-acting, once-daily lipophilic angiotensin-converting enzyme inhibitor with high tissue angiotensin-converting enzyme affinity, lowering angiotensin II and potentiating bradykinin.	Perindopril	0-11	kininogen 1	Homo sapiens	190-200
15494400-11	2004	However, with small physiological peptides such as bradykinin and dynorphin B-9, ATP and triphosphate increased the rate of hydrolysis approximately 10-fold.	Adenosine Triphosphate	81-84	kininogen 1	Homo sapiens	51-61
15494400-11	2004	However, with small physiological peptides such as bradykinin and dynorphin B-9, ATP and triphosphate increased the rate of hydrolysis approximately 10-fold.	triphosphoric acid	89-101	kininogen 1	Homo sapiens	51-61
15352135-0	2004	Modulation of bradykinin-induced calcium changes in SH-SY5Y cells by neurosteroids and sigma receptor ligands via a shared mechanism.	Calcium	33-40	kininogen 1	Homo sapiens	14-24
15665357-10	2005	EDHF also contributes significantly to bradykinin mediated relaxation in porcine ocular ciliary arteries.	edhf	0-4	kininogen 1	Homo sapiens	39-49
15492133-9	2004	Compared with placebo, thiorphan augmented bradykinin-mediated vasodilatation (1.4-fold; P&lt;0.0001) and net tissue plasminogen activator release (1.5-fold; P&lt;0.005).	Thiorphan	23-32	kininogen 1	Homo sapiens	43-53
15574748-8	2004	However, bradykinin receptors became nearly as effective as M1 receptors when PIP2 synthesis, IP3 receptors, or the activity of neuronal Ca2+ sensor-1 were blocked, suggesting that bradykinin receptor-induced intracellular Ca2+ increases stimulate PIP2 synthesis, compensating for PIP2 hydrolysis.	Phosphatidylinositol 4,5-Diphosphate	78-82	kininogen 1	Homo sapiens	9-19
15574748-8	2004	However, bradykinin receptors became nearly as effective as M1 receptors when PIP2 synthesis, IP3 receptors, or the activity of neuronal Ca2+ sensor-1 were blocked, suggesting that bradykinin receptor-induced intracellular Ca2+ increases stimulate PIP2 synthesis, compensating for PIP2 hydrolysis.	Phosphatidylinositol 4,5-Diphosphate	248-252	kininogen 1	Homo sapiens	9-19
15574748-8	2004	However, bradykinin receptors became nearly as effective as M1 receptors when PIP2 synthesis, IP3 receptors, or the activity of neuronal Ca2+ sensor-1 were blocked, suggesting that bradykinin receptor-induced intracellular Ca2+ increases stimulate PIP2 synthesis, compensating for PIP2 hydrolysis.	Phosphatidylinositol 4,5-Diphosphate	248-252	kininogen 1	Homo sapiens	181-191
15622377-8	2004	However, endothelium-dependent vasorelaxation in response to 10(-5) mol/L bradykinin was 40% in the homocysteine-treated group, as compared to 73% in the control group (P = .03).	Homocysteine	100-112	kininogen 1	Homo sapiens	74-84
15739773-2	2004	NAA shape up, in biological fluids, as normal human endogenous low- and high-weight substances, e.g. angiotensin 2, bradykinin and others, and play the regulatory role in homeostasis.	1-naphthaleneacetic acid	0-3	kininogen 1	Homo sapiens	116-126
15541417-2	2004	In primary cultured human prostate stromal cells, bradykinin, but not [des-Arg9]bradykinin or [des-Arg10]kallidin, produced calcium mobilization or inositol phosphates accumulation with potencies (pEC50) of 8.8+/-0.2 and 8.2+/-0.2, respectively.	Calcium	124-131	kininogen 1	Homo sapiens	50-60
15541417-2	2004	In primary cultured human prostate stromal cells, bradykinin, but not [des-Arg9]bradykinin or [des-Arg10]kallidin, produced calcium mobilization or inositol phosphates accumulation with potencies (pEC50) of 8.8+/-0.2 and 8.2+/-0.2, respectively.	Inositol Phosphates	148-167	kininogen 1	Homo sapiens	50-60
15538809-7	2004	Low attomole-level detection of peptides (adrenocorticotropic hormone fragment 18-39, pI 4.25) was achieved from a mixture containing other peptides (angiotensin I, pI 6.92, and bradykinin, pI 12.00) at 100 000-fold higher concentrations.	attomole	4-12	kininogen 1	Homo sapiens	178-188
15516132-5	2004	With the aid of a scanning electrochemical microscope, it was possible to use the distance sensor by recording the negative feedback effect on the reduction of molecular oxygen to "guide" the nitric oxide sensor to various known distances from a layer of adherently growing human umbilical vein endothelial cells for the detection of nitric oxide released from the cells upon stimulation with bradykinin.	Oxygen	170-176	kininogen 1	Homo sapiens	393-403
15516132-5	2004	With the aid of a scanning electrochemical microscope, it was possible to use the distance sensor by recording the negative feedback effect on the reduction of molecular oxygen to "guide" the nitric oxide sensor to various known distances from a layer of adherently growing human umbilical vein endothelial cells for the detection of nitric oxide released from the cells upon stimulation with bradykinin.	Nitric Oxide	192-204	kininogen 1	Homo sapiens	393-403
15516132-5	2004	With the aid of a scanning electrochemical microscope, it was possible to use the distance sensor by recording the negative feedback effect on the reduction of molecular oxygen to "guide" the nitric oxide sensor to various known distances from a layer of adherently growing human umbilical vein endothelial cells for the detection of nitric oxide released from the cells upon stimulation with bradykinin.	Nitric Oxide	334-346	kininogen 1	Homo sapiens	393-403
15549171-5	2004	However, ACE2 also hydrolyses dynorphin A (1-13), apelin-13 and des-Arg(9) bradykinin.	des-arg	64-71	kininogen 1	Homo sapiens	75-85
15505491-8	2004	Pretreatment with Tiron, a cell-permeable SOD-mimetic, significantly enhanced the EDHF-mediated relaxations and hyperpolarizations to bradykinin, and this effect was abolished by catalase, indicating that this enhancing effect was achieved by H2O2.	1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt	18-23	kininogen 1	Homo sapiens	134-144
15505491-8	2004	Pretreatment with Tiron, a cell-permeable SOD-mimetic, significantly enhanced the EDHF-mediated relaxations and hyperpolarizations to bradykinin, and this effect was abolished by catalase, indicating that this enhancing effect was achieved by H2O2.	edhf	82-86	kininogen 1	Homo sapiens	134-144
15352135-1	2004	In this study we investigated the effects of sigma receptor ligands and neurosteroids on bradykinin-induced intracellular calcium concentration ([Ca2+]i) changes in SH-SY5Y neuroblastoma cells.	Calcium	122-129	kininogen 1	Homo sapiens	89-99
15352135-4	2004	Preincubation of low micromolar concentrations of the neurosteroids pregnenolone, dehydroepiandrosterone (DHEA), or the prototypic sigma (sigma) receptor agonist (+)pentazocine potentiated bradykinin-induced [Ca2+]i changes in SH-SY5Y cells.	Pregnenolone	68-80	kininogen 1	Homo sapiens	189-199
15352135-4	2004	Preincubation of low micromolar concentrations of the neurosteroids pregnenolone, dehydroepiandrosterone (DHEA), or the prototypic sigma (sigma) receptor agonist (+)pentazocine potentiated bradykinin-induced [Ca2+]i changes in SH-SY5Y cells.	Dehydroepiandrosterone	82-104	kininogen 1	Homo sapiens	189-199
15352135-4	2004	Preincubation of low micromolar concentrations of the neurosteroids pregnenolone, dehydroepiandrosterone (DHEA), or the prototypic sigma (sigma) receptor agonist (+)pentazocine potentiated bradykinin-induced [Ca2+]i changes in SH-SY5Y cells.	Dehydroepiandrosterone	106-110	kininogen 1	Homo sapiens	189-199
15352135-4	2004	Preincubation of low micromolar concentrations of the neurosteroids pregnenolone, dehydroepiandrosterone (DHEA), or the prototypic sigma (sigma) receptor agonist (+)pentazocine potentiated bradykinin-induced [Ca2+]i changes in SH-SY5Y cells.	Pentazocine	165-176	kininogen 1	Homo sapiens	189-199
15470067-2	2004	BK caused concentration- and time-dependent increase in COX-2 expression, which was attenuated by a selective B2 BK receptor antagonist (HOE140), a Ras inhibitor (manumycin A), a Raf-1 inhibitor (GW 5074), a MEK inhibitor (PD 098059), an NF-kappaB inhibitor (pyrrolidine dithiocarbate), and an IkappaB protease inhibitor (L-1-tosylamido-2-phenylethyl chloromethyl ketone).	manumycin	163-174	kininogen 1	Homo sapiens	0-2
15470067-2	2004	BK caused concentration- and time-dependent increase in COX-2 expression, which was attenuated by a selective B2 BK receptor antagonist (HOE140), a Ras inhibitor (manumycin A), a Raf-1 inhibitor (GW 5074), a MEK inhibitor (PD 098059), an NF-kappaB inhibitor (pyrrolidine dithiocarbate), and an IkappaB protease inhibitor (L-1-tosylamido-2-phenylethyl chloromethyl ketone).	5-iodo-3-((3,5-dibromo-4-hydroxyphenyl)methylene)-2-indolinone	196-203	kininogen 1	Homo sapiens	0-2
15470067-2	2004	BK caused concentration- and time-dependent increase in COX-2 expression, which was attenuated by a selective B2 BK receptor antagonist (HOE140), a Ras inhibitor (manumycin A), a Raf-1 inhibitor (GW 5074), a MEK inhibitor (PD 098059), an NF-kappaB inhibitor (pyrrolidine dithiocarbate), and an IkappaB protease inhibitor (L-1-tosylamido-2-phenylethyl chloromethyl ketone).	pyrrolidine dithiocarbate	259-284	kininogen 1	Homo sapiens	0-2
15470067-2	2004	BK caused concentration- and time-dependent increase in COX-2 expression, which was attenuated by a selective B2 BK receptor antagonist (HOE140), a Ras inhibitor (manumycin A), a Raf-1 inhibitor (GW 5074), a MEK inhibitor (PD 098059), an NF-kappaB inhibitor (pyrrolidine dithiocarbate), and an IkappaB protease inhibitor (L-1-tosylamido-2-phenylethyl chloromethyl ketone).	Tosylphenylalanyl Chloromethyl Ketone	322-370	kininogen 1	Homo sapiens	0-2
15470067-5	2004	BK-induced Ras activation was inhibited by manumycin A.	manumycin	43-54	kininogen 1	Homo sapiens	0-2
15470067-6	2004	Raf-1 phosphorylation at Ser338 by BK was inhibited by manumycin A and GW 5074.	manumycin	55-66	kininogen 1	Homo sapiens	35-37
15470067-6	2004	Raf-1 phosphorylation at Ser338 by BK was inhibited by manumycin A and GW 5074.	glycyltryptophan	71-73	kininogen 1	Homo sapiens	35-37
15470067-7	2004	BK-induced ERK activation was inhibited by HOE140, manumycin A, GW 5074, and PD 098059.	manumycin	51-62	kininogen 1	Homo sapiens	0-2
15470067-7	2004	BK-induced ERK activation was inhibited by HOE140, manumycin A, GW 5074, and PD 098059.	glycyltryptophan	64-66	kininogen 1	Homo sapiens	0-2
15470067-9	2004	BK-mediated increase in IKKalphabeta activity and formation of the NF-kappaB-specific DNA-protein complex were inhibited by HOE140, a Ras dominant-negative mutant (RasN17), manumycin A, GW 5074, and PD 098059.	manumycin	173-184	kininogen 1	Homo sapiens	0-2
15470067-9	2004	BK-mediated increase in IKKalphabeta activity and formation of the NF-kappaB-specific DNA-protein complex were inhibited by HOE140, a Ras dominant-negative mutant (RasN17), manumycin A, GW 5074, and PD 098059.	glycyltryptophan	186-188	kininogen 1	Homo sapiens	0-2
15526242-6	2004	Bradykinin is thought to contribute to the cardioprotective effect of ACE inhibition through modification of nitric oxide release, calcium handling and collagen accumulation.	Nitric Oxide	109-121	kininogen 1	Homo sapiens	0-10
15345332-7	2004	BK treatment resulted in the phosphorylation of p38 MAPK and extracellular signal-regulated kinase (ERK)1/2, and 2-APB could suppress BK-induced phosphorylation of ERK1/2.	2-aminoethoxydiphenyl borate	113-118	kininogen 1	Homo sapiens	0-2
15345332-7	2004	BK treatment resulted in the phosphorylation of p38 MAPK and extracellular signal-regulated kinase (ERK)1/2, and 2-APB could suppress BK-induced phosphorylation of ERK1/2.	2-aminoethoxydiphenyl borate	113-118	kininogen 1	Homo sapiens	134-136
15345332-8	2004	These findings suggest that BK increased both IL-6 and PGE(2) synthesis in osteoblastic cells via B2R and that PLC, IP(3)-induced [Ca(2+)]i, MEK, and MAPKs were involved in the signal transduction in these cells.	Prostaglandins E	55-58	kininogen 1	Homo sapiens	28-30
15317600-1	2004	AIMS: The aim of this study was to evaluate the effect of acutely induced hyperglycaemia on renal sodium handling and to explore the role of the bradykinin-nitric oxide-cGMP signalling pathway.	Nitric Oxide	156-168	kininogen 1	Homo sapiens	145-155
15317600-1	2004	AIMS: The aim of this study was to evaluate the effect of acutely induced hyperglycaemia on renal sodium handling and to explore the role of the bradykinin-nitric oxide-cGMP signalling pathway.	Cyclic GMP	169-173	kininogen 1	Homo sapiens	145-155
15345332-1	2004	We investigated the effects of bradykinin (BK) on the production of interleukin (IL)-6 and prostaglandin PGE(2), whose molecules are capable of stimulating the development of osteoclasts from their hematopoietic precursors as well as the signal transduction systems involved, in human osteoblasts (SaM-1 cells).	Prostaglandins	91-104	kininogen 1	Homo sapiens	31-41
15345332-1	2004	We investigated the effects of bradykinin (BK) on the production of interleukin (IL)-6 and prostaglandin PGE(2), whose molecules are capable of stimulating the development of osteoclasts from their hematopoietic precursors as well as the signal transduction systems involved, in human osteoblasts (SaM-1 cells).	Prostaglandins	91-104	kininogen 1	Homo sapiens	43-45
15345332-1	2004	We investigated the effects of bradykinin (BK) on the production of interleukin (IL)-6 and prostaglandin PGE(2), whose molecules are capable of stimulating the development of osteoclasts from their hematopoietic precursors as well as the signal transduction systems involved, in human osteoblasts (SaM-1 cells).	Prostaglandins E	105-108	kininogen 1	Homo sapiens	31-41
15345332-1	2004	We investigated the effects of bradykinin (BK) on the production of interleukin (IL)-6 and prostaglandin PGE(2), whose molecules are capable of stimulating the development of osteoclasts from their hematopoietic precursors as well as the signal transduction systems involved, in human osteoblasts (SaM-1 cells).	Prostaglandins E	105-108	kininogen 1	Homo sapiens	43-45
15345332-3	2004	Treatment of SaM-1 cells with BK increased the synthesis of both IL-6 and PGE(2) and the increase in both was blocked by HOE140 (B2R antagonist), but not by Des-Arg(9)-[Leu(8)]-BK (B1R antagonist).	Prostaglandins E	74-77	kininogen 1	Homo sapiens	30-32
15345332-4	2004	U-73122, a phospholipase C (PLC) inhibitor, suppressed BK-induced IL-6 and PGE(2) synthesis in SaM-1 cells.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	0-7	kininogen 1	Homo sapiens	55-57
15345332-4	2004	U-73122, a phospholipase C (PLC) inhibitor, suppressed BK-induced IL-6 and PGE(2) synthesis in SaM-1 cells.	Prostaglandins E	75-78	kininogen 1	Homo sapiens	55-57
15345332-5	2004	In addition, BK caused an increase in the intracellular Ca(2+) concentration ([Ca(2+)]i), which was inhibited by pretreatment with HOE140 or 2-aminoethoxydiphenyl borate (2-APB), an inositol 1,4,5-trisphosphate (IP(3)) receptor (IP(3)R) blocker.	Borates	163-169	kininogen 1	Homo sapiens	13-15
15345332-5	2004	In addition, BK caused an increase in the intracellular Ca(2+) concentration ([Ca(2+)]i), which was inhibited by pretreatment with HOE140 or 2-aminoethoxydiphenyl borate (2-APB), an inositol 1,4,5-trisphosphate (IP(3)) receptor (IP(3)R) blocker.	2-aminoethoxydiphenyl borate	171-176	kininogen 1	Homo sapiens	13-15
15474695-5	2004	Eleven patients on angiotensin converting enzyme inhibitors and 10 controls were challenged with ketoprofen infusion (to inhibit PG synthesis and bradykinin activity).	Ketoprofen	97-107	kininogen 1	Homo sapiens	146-156
15474695-8	2004	The increased PG and bradykinin productions both at rest and during exercise in CHF were attenuated after ketoprofen infusion, associated with ergoreflex reduction (-5.1+/-2.2 L/min, p&lt;0.05 vs. saline).	Sodium Chloride	197-203	kininogen 1	Homo sapiens	21-31
15375773-7	2004	BK activates a G-protein coupled receptor, B2R, to regulate renal blood flow and salt and water excretion.	Salts	81-85	kininogen 1	Homo sapiens	0-2
15375773-7	2004	BK activates a G-protein coupled receptor, B2R, to regulate renal blood flow and salt and water excretion.	Water	90-95	kininogen 1	Homo sapiens	0-2
15281091-9	2004	Conversely, Go6976, an inhibitor of PKC-alpha and -beta isozymes, and the 18-h treatment of cells with PMA, that led to the complete down-regulation of PKC-alpha, -beta, -epsilon, and -eta, but not of PKC-delta, did not have any effect, thereby indicating that the PKC-delta mediates the mitogenic signalling of BK.	Go 6976	12-18	kininogen 1	Homo sapiens	312-314
15361764-1	2004	OBJECTIVE: Bradykinin-induced, endothelium-derived hyperpolarizing factor (EDHF)-mediated responses depend on Ca-dependent K-channels (KCa) of small (SKCa) and intermediate (IKCa) conductance, inwardly rectifying K (KIR) channels and/or Na-K-ATPase.	edhf	75-79	kininogen 1	Homo sapiens	11-21
15361764-5	2004	L-NAME, charybdotoxin + apamin, KCl, and ouabain shifted the bradykinin concentration-response curve (CRC) approximately 10-fold to the right.	NG-Nitroarginine Methyl Ester	0-6	kininogen 1	Homo sapiens	61-71
15361764-5	2004	L-NAME, charybdotoxin + apamin, KCl, and ouabain shifted the bradykinin concentration-response curve (CRC) approximately 10-fold to the right.	Charybdotoxin	8-21	kininogen 1	Homo sapiens	61-71
15361764-5	2004	L-NAME, charybdotoxin + apamin, KCl, and ouabain shifted the bradykinin concentration-response curve (CRC) approximately 10-fold to the right.	Potassium Chloride	32-35	kininogen 1	Homo sapiens	61-71
15361764-7	2004	Full blockade of bradykinin was obtained when combining L-NAME with charybdotoxin + apamin, KCl or ouabain + BaCl2.	NG-Nitroarginine Methyl Ester	56-62	kininogen 1	Homo sapiens	17-27
15361764-7	2004	Full blockade of bradykinin was obtained when combining L-NAME with charybdotoxin + apamin, KCl or ouabain + BaCl2.	Charybdotoxin	68-81	kininogen 1	Homo sapiens	17-27
15361764-7	2004	Full blockade of bradykinin was obtained when combining L-NAME with charybdotoxin + apamin, KCl or ouabain + BaCl2.	Potassium Chloride	92-95	kininogen 1	Homo sapiens	17-27
15361764-7	2004	Full blockade of bradykinin was obtained when combining L-NAME with charybdotoxin + apamin, KCl or ouabain + BaCl2.	Ouabain	99-106	kininogen 1	Homo sapiens	17-27
15361764-7	2004	Full blockade of bradykinin was obtained when combining L-NAME with charybdotoxin + apamin, KCl or ouabain + BaCl2.	barium chloride	109-114	kininogen 1	Homo sapiens	17-27
15361764-8	2004	PHMBA reduced the maximum effect of bradykinin.	phmba	0-5	kininogen 1	Homo sapiens	36-46
15361764-14	2004	Since S-nitrosothiols decompose to NO, stored L-S-nitrosothiols may mediate bradykinin-induced, EDHF-dependent relaxation.	S-Nitrosothiols	6-21	kininogen 1	Homo sapiens	76-86
15361764-14	2004	Since S-nitrosothiols decompose to NO, stored L-S-nitrosothiols may mediate bradykinin-induced, EDHF-dependent relaxation.	l-s-nitrosothiols	46-63	kininogen 1	Homo sapiens	76-86
15361764-14	2004	Since S-nitrosothiols decompose to NO, stored L-S-nitrosothiols may mediate bradykinin-induced, EDHF-dependent relaxation.	edhf	96-100	kininogen 1	Homo sapiens	76-86
15269216-5	2004	This effect of the inhibitor was paralleled by complete restoration of the bradykinin-induced increases in mitochondrial Ca2+ concentration and ensuing ATP production.	Adenosine Triphosphate	152-155	kininogen 1	Homo sapiens	75-85
15526242-6	2004	Bradykinin is thought to contribute to the cardioprotective effect of ACE inhibition through modification of nitric oxide release, calcium handling and collagen accumulation.	Calcium	131-138	kininogen 1	Homo sapiens	0-10
15283591-6	2004	An unprecedented detection limit of 480 molecules (800 ymol) for des-Arg(9)-bradykinin is reported on a pentafluorophenyl-functionalized DIOS chip.	des-arg	65-72	kininogen 1	Homo sapiens	76-86
15222018-0	2004	Conformational basis for the biological activity of TOAC-labeled angiotensin II and bradykinin: electron paramagnetic resonance, circular dichroism, and fluorescence studies.	2,2,6,6-tetramethylpiperidine-N-oxide-4-amino-4-carboxylic acid	52-56	kininogen 1	Homo sapiens	84-94
15222018-1	2004	N-Terminally and internally labeled analogues of the hormones angiotensin (AII, DRVYIHPF) and bradykinin (BK, RPPGFSPFR) were synthesized containing the paramagnetic amino acid 2,2,6,6-tetramethylpiperidine-1-oxyl-4-amino-4-carboxylic acid (TOAC).	amino acid 2,2,6,6-tetramethylpiperidine-1-oxyl-4-amino-4-carboxylic acid	166-239	kininogen 1	Homo sapiens	94-104
15481790-5	2004	Intracellular calcium, [Ca2+]i measured by changes in fura-2 level in response to ATP or bradykinin, was significantly inhibited in IgA-IC treated mesangial cells, compared to control cells.	Calcium	14-21	kininogen 1	Homo sapiens	89-99
15274676-9	2004	Mean bradykinin plasma levels peaked in the efferent line post-adsorber at 1000 mL of treated blood volume; 467 fmol/mL (N = 6 sessions) in the ARA-treated patients and 671 fmol/mL (N = 9 sessions) in a control group of three DALI patients without ARA medication (P = 0.69, n.s.).	Arabinose	248-251	kininogen 1	Homo sapiens	5-15
14764428-6	2004	The net intracellular calcium responses to bradykinin, thrombin, and histamine were significantly (P &lt; or = 0.05) higher in cells treated with IL-13 compared with controls.	Calcium	22-29	kininogen 1	Homo sapiens	43-53
15481790-5	2004	Intracellular calcium, [Ca2+]i measured by changes in fura-2 level in response to ATP or bradykinin, was significantly inhibited in IgA-IC treated mesangial cells, compared to control cells.	Fura-2	54-60	kininogen 1	Homo sapiens	89-99
15040788-2	2004	Bradykinin was released from these peptides by the mK1- and rK1-mediated hydrolysis of Arg-Arg and Arg-Ser (or Arg-Ala) peptide bonds.	Serine	103-106	kininogen 1	Homo sapiens	0-10
15040788-2	2004	Bradykinin was released from these peptides by the mK1- and rK1-mediated hydrolysis of Arg-Arg and Arg-Ser (or Arg-Ala) peptide bonds.	Arginine	87-90	kininogen 1	Homo sapiens	0-10
15040788-2	2004	Bradykinin was released from these peptides by the mK1- and rK1-mediated hydrolysis of Arg-Arg and Arg-Ser (or Arg-Ala) peptide bonds.	Arginine	91-94	kininogen 1	Homo sapiens	0-10
15040788-2	2004	Bradykinin was released from these peptides by the mK1- and rK1-mediated hydrolysis of Arg-Arg and Arg-Ser (or Arg-Ala) peptide bonds.	Arginine	91-94	kininogen 1	Homo sapiens	0-10
15040788-2	2004	Bradykinin was released from these peptides by the mK1- and rK1-mediated hydrolysis of Arg-Arg and Arg-Ser (or Arg-Ala) peptide bonds.	Arginine	91-94	kininogen 1	Homo sapiens	0-10
15040788-2	2004	Bradykinin was released from these peptides by the mK1- and rK1-mediated hydrolysis of Arg-Arg and Arg-Ser (or Arg-Ala) peptide bonds.	Alanine	115-118	kininogen 1	Homo sapiens	0-10
15040788-3	2004	However, owing to preferential hydrolysis of Phe-Arg compared with the Arg-Ala bond in the peptide derived from rat LMWK, hK1 released bradykinin only from the mouse LMWK fragment and preferentially released des-[Arg9]bradykinin from the rat LMWK fragment (Abz-MTSVIRRPPGFSPFRAPRV-NH2).	phenylalanylarginine	45-52	kininogen 1	Homo sapiens	135-145
15040788-4	2004	The formation of these hydrolysis products was examined in more detail by determining the kinetic parameters for the hydrolysis of synthetic, internally quenched fluorescent peptides containing six N- or C-terminal amino acids of bradykinin added to the five downstream or upstream residues of mouse and rat kininogens respectively.	Peptides	174-182	kininogen 1	Homo sapiens	230-240
15040788-5	2004	One of these peptides, Abz-GFSPFRAPRVQ-EDDnp (where EDDnp stands for ethylenediamine 2,4-dinitrophenyl), was preferentially hydrolysed at the Phe-Arg bond, confirming the potential des-[Arg9]bradykinin-releasing activity of hK1 on rat kininogen.	abz-gfspfraprvq-eddnp	23-44	kininogen 1	Homo sapiens	191-201
15040788-5	2004	One of these peptides, Abz-GFSPFRAPRVQ-EDDnp (where EDDnp stands for ethylenediamine 2,4-dinitrophenyl), was preferentially hydrolysed at the Phe-Arg bond, confirming the potential des-[Arg9]bradykinin-releasing activity of hK1 on rat kininogen.	n1-(2,4-dinitrophenyl)ethane-1,2-diamine	39-44	kininogen 1	Homo sapiens	191-201
15040788-5	2004	One of these peptides, Abz-GFSPFRAPRVQ-EDDnp (where EDDnp stands for ethylenediamine 2,4-dinitrophenyl), was preferentially hydrolysed at the Phe-Arg bond, confirming the potential des-[Arg9]bradykinin-releasing activity of hK1 on rat kininogen.	Phenylalanine	142-145	kininogen 1	Homo sapiens	191-201
15040788-5	2004	One of these peptides, Abz-GFSPFRAPRVQ-EDDnp (where EDDnp stands for ethylenediamine 2,4-dinitrophenyl), was preferentially hydrolysed at the Phe-Arg bond, confirming the potential des-[Arg9]bradykinin-releasing activity of hK1 on rat kininogen.	Arginine	146-149	kininogen 1	Homo sapiens	191-201
15040788-6	2004	The proline residue that is two residues upstream of bradykinin in rat kininogen is, in part, responsible for this pattern of hydrolysis, since the peptide Abz-GFSPFRASRVQ-EDDnp was preferentially cleaved at the Arg-Ala bond by hK1.	Proline	4-11	kininogen 1	Homo sapiens	53-63
15040788-6	2004	The proline residue that is two residues upstream of bradykinin in rat kininogen is, in part, responsible for this pattern of hydrolysis, since the peptide Abz-GFSPFRASRVQ-EDDnp was preferentially cleaved at the Arg-Ala bond by hK1.	Arginine	212-215	kininogen 1	Homo sapiens	53-63
15040788-6	2004	The proline residue that is two residues upstream of bradykinin in rat kininogen is, in part, responsible for this pattern of hydrolysis, since the peptide Abz-GFSPFRASRVQ-EDDnp was preferentially cleaved at the Arg-Ala bond by hK1.	Alanine	216-219	kininogen 1	Homo sapiens	53-63
14751845-4	2004	In norepinephrine-constricted vessels, incubation with N(G)-nitro-L-arginine methyl ester (L-NAME) resulted in a significant reduction in relaxation to BK.	Norepinephrine	3-17	kininogen 1	Homo sapiens	152-154
14751845-4	2004	In norepinephrine-constricted vessels, incubation with N(G)-nitro-L-arginine methyl ester (L-NAME) resulted in a significant reduction in relaxation to BK.	NG-Nitroarginine Methyl Ester	55-89	kininogen 1	Homo sapiens	152-154
14751845-4	2004	In norepinephrine-constricted vessels, incubation with N(G)-nitro-L-arginine methyl ester (L-NAME) resulted in a significant reduction in relaxation to BK.	NG-Nitroarginine Methyl Ester	91-97	kininogen 1	Homo sapiens	152-154
14751845-6	2004	BK-mediated dilatation in the presence of K(+)-modified solution was decreased to similar level as obtained after incubation with L-NAME.	NG-Nitroarginine Methyl Ester	130-136	kininogen 1	Homo sapiens	0-2
14751845-7	2004	Incubation with L-NAME abolished BK-induced responses in K(+)-modified solution.	NG-Nitroarginine Methyl Ester	16-22	kininogen 1	Homo sapiens	33-35
15167453-6	2004	Both NPP and bradykinin increased systolic (SBP) and diastolic (DBP) blood pressures, heart rate and plasma adrenaline and noradrenaline concentrations.	Epinephrine	108-118	kininogen 1	Homo sapiens	13-23
15255189-1	2004	We investigated the influence of pH and divalent cations (Zn2+, Mg2+ and Ca2+) on high molecular weight kininogen processing by cathepsin B.	Zinc	58-62	kininogen 1	Homo sapiens	82-113
15167453-6	2004	Both NPP and bradykinin increased systolic (SBP) and diastolic (DBP) blood pressures, heart rate and plasma adrenaline and noradrenaline concentrations.	Norepinephrine	123-136	kininogen 1	Homo sapiens	13-23
14729908-6	2004	In cultured human colonic smooth muscle cells, bradykinin (BK) elicited InsP(3)-dependent calcium transients that were repeatable and independent of extracellular calcium.	inositol 1,4-bisphosphate 5-phosphorothioate	72-79	kininogen 1	Homo sapiens	47-57
15167278-5	2004	The BK-induced hyperpolarization was significantly reduced by N-nitro-L-arginine, indomethacin, and hemoglobin in both arteries and veins and was greater in the arteries.	Nitroarginine	62-80	kininogen 1	Homo sapiens	4-6
15167278-5	2004	The BK-induced hyperpolarization was significantly reduced by N-nitro-L-arginine, indomethacin, and hemoglobin in both arteries and veins and was greater in the arteries.	Indomethacin	82-94	kininogen 1	Homo sapiens	4-6
15139763-0	2004	Discovery of the first non-peptide full agonists for the human bradykinin B(2) receptor incorporating 4-(2-picolyloxy)quinoline and 1-(2-picolyl)benzimidazole frameworks.	4-(2-picolyloxy)quinoline	102-127	kininogen 1	Homo sapiens	63-73
15139763-0	2004	Discovery of the first non-peptide full agonists for the human bradykinin B(2) receptor incorporating 4-(2-picolyloxy)quinoline and 1-(2-picolyl)benzimidazole frameworks.	1-(2-picolyl)benzimidazole	132-158	kininogen 1	Homo sapiens	63-73
15139763-1	2004	In the course of our studies on non-peptide bradykinin (BK) B(2) receptor ligands, it was suggested that the 4-substituent of the quinoline ring may play a critical role in determining binding affinities for human and guinea pig B(2) receptors, as well as agonist/antagonist properties.	quinoline	130-139	kininogen 1	Homo sapiens	44-54
15139763-6	2004	On the other hand, 22b strongly suppressed BK-induced IPs formation through the cloned human B(2) receptor.	Inositol Phosphates	54-57	kininogen 1	Homo sapiens	43-45
15139763-10	2004	The representative 1-(2-picolyl)benzimidazole derivative 47c increased PGE(2) production at a 1 microM concentration to the same level as the maximum effect of BK.	1-(2-picolyl)benzimidazole	19-45	kininogen 1	Homo sapiens	160-162
15139763-10	2004	The representative 1-(2-picolyl)benzimidazole derivative 47c increased PGE(2) production at a 1 microM concentration to the same level as the maximum effect of BK.	Dinoprostone	71-77	kininogen 1	Homo sapiens	160-162
15140628-0	2004	The N-terminal of icatibant and bradykinin interact with the same Asp residues in the human B2 receptor.	Aspartic Acid	66-69	kininogen 1	Homo sapiens	32-42
15140628-9	2004	Our results highlight a crucial role for two aspartic residues, D266 and D284, located at the top of transmembrane segments 6 and 7, in the high-affinity interaction of peptide antagonists with the human bradykinin B2 receptor.	d266	64-68	kininogen 1	Homo sapiens	204-214
15140628-9	2004	Our results highlight a crucial role for two aspartic residues, D266 and D284, located at the top of transmembrane segments 6 and 7, in the high-affinity interaction of peptide antagonists with the human bradykinin B2 receptor.	d284	73-77	kininogen 1	Homo sapiens	204-214
15167831-2	2004	Myometrial resistance arteries from women with preeclampsia show a minimal, wholly nitric oxide-mediated, bradykinin-induced relaxation.	Nitric Oxide	83-95	kininogen 1	Homo sapiens	106-116
15171468-9	2004	After 5 minutes of blood circulation bradykinin levels significantly increased in all three groups (p &lt; 0.01); however, the group with the PMEA coated oxygenators showed the lowest values.	poly(2-methoxyethylacrylate)	142-146	kininogen 1	Homo sapiens	37-47
15066907-0	2004	Bradykinin-induced relaxation of coronary microarteries: S-nitrosothiols as EDHF?	S-Nitrosothiols	57-72	kininogen 1	Homo sapiens	0-10
15066907-8	2004	The guanylyl cyclase inhibitor ODQ and the NO scavenger hydroxocobalamin induced a larger shift of the bradykinin CRC than the NO synthase inhibitor L-NAME, although all three inhibitors equally suppressed bradykinin-induced cGMP responses.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	31-34	kininogen 1	Homo sapiens	103-113
15066907-8	2004	The guanylyl cyclase inhibitor ODQ and the NO scavenger hydroxocobalamin induced a larger shift of the bradykinin CRC than the NO synthase inhibitor L-NAME, although all three inhibitors equally suppressed bradykinin-induced cGMP responses.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	31-34	kininogen 1	Homo sapiens	206-216
15066907-8	2004	The guanylyl cyclase inhibitor ODQ and the NO scavenger hydroxocobalamin induced a larger shift of the bradykinin CRC than the NO synthase inhibitor L-NAME, although all three inhibitors equally suppressed bradykinin-induced cGMP responses.	Hydroxocobalamin	56-72	kininogen 1	Homo sapiens	103-113
15066907-8	2004	The guanylyl cyclase inhibitor ODQ and the NO scavenger hydroxocobalamin induced a larger shift of the bradykinin CRC than the NO synthase inhibitor L-NAME, although all three inhibitors equally suppressed bradykinin-induced cGMP responses.	Hydroxocobalamin	56-72	kininogen 1	Homo sapiens	206-216
15066907-10	2004	Complete blockade of bradykinin-induced relaxation was obtained with L-NAME in the presence of the large- and intermediate-conductance Ca(2+)-activated K(+)-channel (BK(Ca), IK(Ca)) blocker charybdotoxin and the small-conductance Ca(2+)-activated K(+)-channel (SK(Ca)) channel blocker apamin, but not in the presence of L-NAME, apamin and the BK(Ca) channel blocker iberiotoxin.	NG-Nitroarginine Methyl Ester	69-75	kininogen 1	Homo sapiens	21-31
15066907-10	2004	Complete blockade of bradykinin-induced relaxation was obtained with L-NAME in the presence of the large- and intermediate-conductance Ca(2+)-activated K(+)-channel (BK(Ca), IK(Ca)) blocker charybdotoxin and the small-conductance Ca(2+)-activated K(+)-channel (SK(Ca)) channel blocker apamin, but not in the presence of L-NAME, apamin and the BK(Ca) channel blocker iberiotoxin.	NG-Nitroarginine Methyl Ester	320-326	kininogen 1	Homo sapiens	21-31
15066907-10	2004	Complete blockade of bradykinin-induced relaxation was obtained with L-NAME in the presence of the large- and intermediate-conductance Ca(2+)-activated K(+)-channel (BK(Ca), IK(Ca)) blocker charybdotoxin and the small-conductance Ca(2+)-activated K(+)-channel (SK(Ca)) channel blocker apamin, but not in the presence of L-NAME, apamin and the BK(Ca) channel blocker iberiotoxin.	iberiotoxin	366-377	kininogen 1	Homo sapiens	21-31
15066907-20	2004	Our results support the concept that bradykinin-induced relaxation is mediated via de novo synthesized NO and a non-NO, endothelium-derived hyperpolarizing factor (EDHF).	endothelium-derived hyperpolarizing factor	120-162	kininogen 1	Homo sapiens	37-47
14751540-5	2004	BK stimulated [3H]thymidine incorporation and p42/p44 MAPK phosphorylation in a time- and concentration-dependent manner.	Tritium	15-17	kininogen 1	Homo sapiens	0-2
14751540-5	2004	BK stimulated [3H]thymidine incorporation and p42/p44 MAPK phosphorylation in a time- and concentration-dependent manner.	Thymidine	18-27	kininogen 1	Homo sapiens	0-2
14751540-7	2004	BK-stimulated responses were attenuated by inhibitors of selective B2 receptor (Hoe 140), phosphatidylinositol (PI)-PLC (U73122), an intracellular Ca2+chelator (BAPTA/AM), PKC (GF109203X), tyrosine kinase (genistein), and MEK1/2 (PD98059).	Phosphatidylinositols	90-110	kininogen 1	Homo sapiens	0-2
14751540-7	2004	BK-stimulated responses were attenuated by inhibitors of selective B2 receptor (Hoe 140), phosphatidylinositol (PI)-PLC (U73122), an intracellular Ca2+chelator (BAPTA/AM), PKC (GF109203X), tyrosine kinase (genistein), and MEK1/2 (PD98059).	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	161-166	kininogen 1	Homo sapiens	0-2
14751540-7	2004	BK-stimulated responses were attenuated by inhibitors of selective B2 receptor (Hoe 140), phosphatidylinositol (PI)-PLC (U73122), an intracellular Ca2+chelator (BAPTA/AM), PKC (GF109203X), tyrosine kinase (genistein), and MEK1/2 (PD98059).	Genistein	206-215	kininogen 1	Homo sapiens	0-2
15319801-2	2004	The aim of this study on human umbilical arteries was: i) to compare the recognition properties of the mediating contractions of bradykinin receptors; and ii) to assess the possible role of thromboxane A2 in a bradykinin-induced contraction of smooth muscle.	Thromboxane A2	190-204	kininogen 1	Homo sapiens	210-220
15319801-7	2004	However, Hoe 140 D-Arg-[Hyp3, Thi5,D-Tic7, Oic8]-bradykinin, an antagonist of B2 responses, significantly inhibited bradykinin-induced contraction.	Arginine	19-22	kininogen 1	Homo sapiens	49-59
15319801-7	2004	However, Hoe 140 D-Arg-[Hyp3, Thi5,D-Tic7, Oic8]-bradykinin, an antagonist of B2 responses, significantly inhibited bradykinin-induced contraction.	Arginine	19-22	kininogen 1	Homo sapiens	116-126
15319801-7	2004	However, Hoe 140 D-Arg-[Hyp3, Thi5,D-Tic7, Oic8]-bradykinin, an antagonist of B2 responses, significantly inhibited bradykinin-induced contraction.	thi5	30-34	kininogen 1	Homo sapiens	49-59
15319801-7	2004	However, Hoe 140 D-Arg-[Hyp3, Thi5,D-Tic7, Oic8]-bradykinin, an antagonist of B2 responses, significantly inhibited bradykinin-induced contraction.	thi5	30-34	kininogen 1	Homo sapiens	116-126
15319801-9	2004	However, bradykinin contractions were antagonized in a noncompetitive manner by quinacrine (10(-5) mM).	Quinacrine	80-90	kininogen 1	Homo sapiens	9-19
15023566-11	2004	A 30-fold increase in PGI2 production was observed in cells stimulated with BK.	Epoprostenol	22-26	kininogen 1	Homo sapiens	76-78
15086463-8	2004	Moreover, the bradykinin B2 receptor antagonist HOE 140 attenuated the beneficial effects of perindoprilat.	perindoprilat	93-106	kininogen 1	Homo sapiens	14-24
14751845-9	2004	The inhibitor of gap junctions, 18 alpha-glycyrrhetinic acid, significantly reduced BK-mediated relaxation both without and with incubation with L-NAME.	Glycyrrhetinic Acid	35-60	kininogen 1	Homo sapiens	84-86
14751845-10	2004	We found that both NO and EDHF, but not PGI(2), are involved in the endothelium-dependent dilatation to BK.	edhf	26-30	kininogen 1	Homo sapiens	104-106
14751845-11	2004	BK-induced relaxation is almost equally mediated by NO and EDHF.	edhf	59-63	kininogen 1	Homo sapiens	0-2
14751845-12	2004	CYP450 epoxygenase metabolites of AA or H(2)O(2) do not account for EDHF-mediated response; however, gap junctions are involved in the EDHF-mediated responses to BK in subcutaneous small arteries in normal pregnancy.	edhf	135-139	kininogen 1	Homo sapiens	162-164
15093721-5	2004	RESULTS: Endothelium-dependent vasorelaxation (bradykinin) for the homocysteine alone group was 62% compared with control (P &lt; 0.05), and endothelium-dependent vasorelaxation for the estrogen alone group was 85% compared with control (P &gt; 0.05).	Homocysteine	67-79	kininogen 1	Homo sapiens	47-57
15050422-0	2004	Cyclic AMP increases bradykinin receptor binding affinity in human endothelial cells.	Cyclic AMP	0-10	kininogen 1	Homo sapiens	21-31
15050422-1	2004	We demonstrated bradykinin receptors in human endothelial cells and studied whether bradykinin receptors might be regulated by cyclic AMP.	Cyclic AMP	127-137	kininogen 1	Homo sapiens	84-94
15050422-6	2004	Stimulating cells with dibutyryl-cAMP, cholera toxin and forskolin for 24 h increased (125)I-[Tyr(8)]-bradykinin (90 pM) binding with approximately 50%.	Bucladesine	23-37	kininogen 1	Homo sapiens	102-112
15050422-6	2004	Stimulating cells with dibutyryl-cAMP, cholera toxin and forskolin for 24 h increased (125)I-[Tyr(8)]-bradykinin (90 pM) binding with approximately 50%.	Colforsin	57-66	kininogen 1	Homo sapiens	102-112
15050422-6	2004	Stimulating cells with dibutyryl-cAMP, cholera toxin and forskolin for 24 h increased (125)I-[Tyr(8)]-bradykinin (90 pM) binding with approximately 50%.	Tyrosine	94-97	kininogen 1	Homo sapiens	102-112
15050422-9	2004	These results suggest, that the dibutyryl-cAMP stimulated increase in (125)I-[Tyr(8)]-bradykinin binding is probably due to increased B(1) receptor affinity with no change in receptor capacity.	dibutyryl	32-41	kininogen 1	Homo sapiens	86-96
15050422-9	2004	These results suggest, that the dibutyryl-cAMP stimulated increase in (125)I-[Tyr(8)]-bradykinin binding is probably due to increased B(1) receptor affinity with no change in receptor capacity.	Cyclic AMP	42-46	kininogen 1	Homo sapiens	86-96
15050422-9	2004	These results suggest, that the dibutyryl-cAMP stimulated increase in (125)I-[Tyr(8)]-bradykinin binding is probably due to increased B(1) receptor affinity with no change in receptor capacity.	Tyrosine	78-81	kininogen 1	Homo sapiens	86-96
14644762-7	2004	The effect of lisinopril was prevented by pretreatment with a bradykinin antagonist (HOE-130) and dichloroisocoumarine, an inhibitor of kinine-forming enzymes.	Lisinopril	14-24	kininogen 1	Homo sapiens	62-72
14644762-7	2004	The effect of lisinopril was prevented by pretreatment with a bradykinin antagonist (HOE-130) and dichloroisocoumarine, an inhibitor of kinine-forming enzymes.	hoe-130	85-92	kininogen 1	Homo sapiens	62-72
14985092-0	2004	Conformational alteration of bradykinin in presence of GM1 micelle.	G(M1) Ganglioside	55-58	kininogen 1	Homo sapiens	29-39
14985092-1	2004	We report here the interaction of bradykinin with ganglioside GM1 by circular dichroism, steady-state fluorescence, and one-dimensional 1H NMR spectroscopy.	Gangliosides	50-61	kininogen 1	Homo sapiens	34-44
14985092-1	2004	We report here the interaction of bradykinin with ganglioside GM1 by circular dichroism, steady-state fluorescence, and one-dimensional 1H NMR spectroscopy.	G(M1) Ganglioside	62-65	kininogen 1	Homo sapiens	34-44
14985092-1	2004	We report here the interaction of bradykinin with ganglioside GM1 by circular dichroism, steady-state fluorescence, and one-dimensional 1H NMR spectroscopy.	Hydrogen	136-138	kininogen 1	Homo sapiens	34-44
14985092-2	2004	Circular dichroism spectroscopy is indicative of a turn formation of bradykinin backbone in the presence of GM1 micelle.	G(M1) Ganglioside	108-111	kininogen 1	Homo sapiens	69-79
14729908-6	2004	In cultured human colonic smooth muscle cells, bradykinin (BK) elicited InsP(3)-dependent calcium transients that were repeatable and independent of extracellular calcium.	inositol 1,4-bisphosphate 5-phosphorothioate	72-79	kininogen 1	Homo sapiens	59-61
14985092-3	2004	The fluorescence quenching efficiencies of iodide and acrylamide are substantially reduced, indicating a shielding of phenylalanine residue of bradykinin from aqueous environment.	Iodides	43-49	kininogen 1	Homo sapiens	143-153
14985092-3	2004	The fluorescence quenching efficiencies of iodide and acrylamide are substantially reduced, indicating a shielding of phenylalanine residue of bradykinin from aqueous environment.	Acrylamide	54-64	kininogen 1	Homo sapiens	143-153
14729908-6	2004	In cultured human colonic smooth muscle cells, bradykinin (BK) elicited InsP(3)-dependent calcium transients that were repeatable and independent of extracellular calcium.	Calcium	90-97	kininogen 1	Homo sapiens	47-57
14985092-3	2004	The fluorescence quenching efficiencies of iodide and acrylamide are substantially reduced, indicating a shielding of phenylalanine residue of bradykinin from aqueous environment.	Phenylalanine	118-131	kininogen 1	Homo sapiens	143-153
14729908-6	2004	In cultured human colonic smooth muscle cells, bradykinin (BK) elicited InsP(3)-dependent calcium transients that were repeatable and independent of extracellular calcium.	Calcium	90-97	kininogen 1	Homo sapiens	59-61
14729908-6	2004	In cultured human colonic smooth muscle cells, bradykinin (BK) elicited InsP(3)-dependent calcium transients that were repeatable and independent of extracellular calcium.	Calcium	163-170	kininogen 1	Homo sapiens	59-61
14729908-7	2004	The NO donor sodium nitroprusside and the specific cGK activator 8-(4-chlorophenylthio)guanosine-3",5"-cyclic-monophosphate (8-pCPT-cGMP) significantly inhibited BK-induced increase in intracellular calcium.	Nitroprusside	13-33	kininogen 1	Homo sapiens	162-164
14729908-7	2004	The NO donor sodium nitroprusside and the specific cGK activator 8-(4-chlorophenylthio)guanosine-3",5"-cyclic-monophosphate (8-pCPT-cGMP) significantly inhibited BK-induced increase in intracellular calcium.	8-((4-chlorophenyl)thio)cyclic-3',5'-GMP	65-123	kininogen 1	Homo sapiens	162-164
14729908-7	2004	The NO donor sodium nitroprusside and the specific cGK activator 8-(4-chlorophenylthio)guanosine-3",5"-cyclic-monophosphate (8-pCPT-cGMP) significantly inhibited BK-induced increase in intracellular calcium.	8-((4-chlorophenyl)thio)cyclic-3',5'-GMP	125-136	kininogen 1	Homo sapiens	162-164
15020200-3	2004	In human skin, sulindac reduces bradykinin-induced edema.	Sulindac	15-23	kininogen 1	Homo sapiens	32-42
15162074-0	2004	Omapatrilat limits infarct size and lowers the threshold for induction of myocardial preconditioning through a bradykinin receptor-mediated mechanism.	omapatrilat	0-11	kininogen 1	Homo sapiens	111-121
15162074-2	2004	Through simultaneous inhibition of neutral endopeptidase and angiotensin converting enzyme, omapatrilat prevents enzymatic degradation of bradykinin.	omapatrilat	92-103	kininogen 1	Homo sapiens	138-148
15162074-3	2004	The aim of this study was to investigate if omapatrilat, through its ability to augment bradykinin levels, can augment a subthreshold IPC stimulus (Sub-IPC) and to compare the action of omapatrilat with the angiotensin-converting enzyme inhibitor, captopril.	omapatrilat	44-55	kininogen 1	Homo sapiens	88-98
15162074-11	2004	We conclude that omapatrilat elicits cardioprotection via inhibition of bradykinin degradation and that dual inhibition of angiotensin-converting enzyme and neutral endopeptidase may have beneficial effects beyond standard angiotensin-converting enzyme inhibitor therapy in patients with acute coronary syndromes who are at risk of myocardial infarction.	omapatrilat	17-28	kininogen 1	Homo sapiens	72-82
15019645-6	2004	EDHF-mediated hyperpolarization was elicited by BK (-6.5 log M) in the presence of Indo, l-NNA and HbO.	edhf	0-4	kininogen 1	Homo sapiens	48-50
14998543-1	2004	Gas-phase complexes of triply charged metal ions with peptides may be readily produced using electrospray ionization, including for small peptides such as bradykinin and peptides with no basic residues such as insulin chain A. Attachment without charge-reduction is demonstrated for all trications studied: La(3+), Al(3+), Ga(3+), Fe(3+), V(3+), and Cr(3+).	Metals	38-43	kininogen 1	Homo sapiens	155-165
14998543-1	2004	Gas-phase complexes of triply charged metal ions with peptides may be readily produced using electrospray ionization, including for small peptides such as bradykinin and peptides with no basic residues such as insulin chain A. Attachment without charge-reduction is demonstrated for all trications studied: La(3+), Al(3+), Ga(3+), Fe(3+), V(3+), and Cr(3+).	Peptides	54-62	kininogen 1	Homo sapiens	155-165
14998543-1	2004	Gas-phase complexes of triply charged metal ions with peptides may be readily produced using electrospray ionization, including for small peptides such as bradykinin and peptides with no basic residues such as insulin chain A. Attachment without charge-reduction is demonstrated for all trications studied: La(3+), Al(3+), Ga(3+), Fe(3+), V(3+), and Cr(3+).	Gallium	0-2	kininogen 1	Homo sapiens	155-165
15019645-6	2004	EDHF-mediated hyperpolarization was elicited by BK (-6.5 log M) in the presence of Indo, l-NNA and HbO.	Indomethacin	83-87	kininogen 1	Homo sapiens	48-50
15019645-6	2004	EDHF-mediated hyperpolarization was elicited by BK (-6.5 log M) in the presence of Indo, l-NNA and HbO.	Nitroarginine	89-94	kininogen 1	Homo sapiens	48-50
15019645-6	2004	EDHF-mediated hyperpolarization was elicited by BK (-6.5 log M) in the presence of Indo, l-NNA and HbO.	2,4-dihydroxy-7-methoxy-1,4-benzoxazin-3-one	99-102	kininogen 1	Homo sapiens	48-50
15019645-7	2004	RESULTS: BK-induced, EDHF-mediated relaxation was reduced from 93.6 +/- 2.8% to 79.7 +/- 4.6% after UW preservation (p = 0.01 by unpaired t-test and p = 0.005 by 2-way analysis of variance [ANOVA]), whereas HTK incubation did not decrease EDHF-mediated relaxation (87.0 +/- 6.5%, p = 0.3 by unpaired t-test and p = 0.6 by 2-way ANOVA, compared with control, and p = 0.001 by 2-way ANOVA, compared with UW).	edhf	21-25	kininogen 1	Homo sapiens	9-11
15019645-7	2004	RESULTS: BK-induced, EDHF-mediated relaxation was reduced from 93.6 +/- 2.8% to 79.7 +/- 4.6% after UW preservation (p = 0.01 by unpaired t-test and p = 0.005 by 2-way analysis of variance [ANOVA]), whereas HTK incubation did not decrease EDHF-mediated relaxation (87.0 +/- 6.5%, p = 0.3 by unpaired t-test and p = 0.6 by 2-way ANOVA, compared with control, and p = 0.001 by 2-way ANOVA, compared with UW).	edhf	239-243	kininogen 1	Homo sapiens	9-11
14670842-0	2004	Interleukin-1beta, transforming growth factor-beta1, and bradykinin attenuate cyclic AMP production by human pulmonary artery smooth muscle cells in response to prostacyclin analogues and prostaglandin E2 by cyclooxygenase-2 induction and downregulation of adenylyl cyclase isoforms 1, 2, and 4.	Cyclic AMP	78-88	kininogen 1	Homo sapiens	57-67
14987993-0	2004	PI 3-kinase and MAP kinase regulate bradykinin induced prostaglandin E(2) release in human pulmonary artery by modulating COX-2 activity.	Dinoprostone	55-73	kininogen 1	Homo sapiens	36-46
14987993-1	2004	Here we studied the role of phosphoinositide 3-kinase (PI 3-kinase) and mitogen activated protein (MAP) kinase in regulating bradykinin (BK) induced prostaglandin E(2) (PGE(2)) production in human pulmonary artery smooth muscle cells (HPASMC).	Dinoprostone	149-167	kininogen 1	Homo sapiens	125-135
14987993-1	2004	Here we studied the role of phosphoinositide 3-kinase (PI 3-kinase) and mitogen activated protein (MAP) kinase in regulating bradykinin (BK) induced prostaglandin E(2) (PGE(2)) production in human pulmonary artery smooth muscle cells (HPASMC).	Dinoprostone	149-167	kininogen 1	Homo sapiens	137-139
14987993-1	2004	Here we studied the role of phosphoinositide 3-kinase (PI 3-kinase) and mitogen activated protein (MAP) kinase in regulating bradykinin (BK) induced prostaglandin E(2) (PGE(2)) production in human pulmonary artery smooth muscle cells (HPASMC).	Prostaglandins E	169-172	kininogen 1	Homo sapiens	125-135
14987993-1	2004	Here we studied the role of phosphoinositide 3-kinase (PI 3-kinase) and mitogen activated protein (MAP) kinase in regulating bradykinin (BK) induced prostaglandin E(2) (PGE(2)) production in human pulmonary artery smooth muscle cells (HPASMC).	Prostaglandins E	169-172	kininogen 1	Homo sapiens	137-139
14987993-2	2004	BK increased PGE(2) in a three step process involving phospholipase A(2) (PLA(2)), cyclooxygenase (COX) and PGE synthase (PGES).	Prostaglandins E	13-16	kininogen 1	Homo sapiens	0-2
14987993-3	2004	BK stimulated PGE(2) release in cultured HPASMC was inhibited by the PI 3-kinase inhibitor LY294002 and the p38 MAP kinase inhibitor SB202190.	Dinoprostone	14-20	kininogen 1	Homo sapiens	0-2
14987993-3	2004	BK stimulated PGE(2) release in cultured HPASMC was inhibited by the PI 3-kinase inhibitor LY294002 and the p38 MAP kinase inhibitor SB202190.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	91-99	kininogen 1	Homo sapiens	0-2
14987993-3	2004	BK stimulated PGE(2) release in cultured HPASMC was inhibited by the PI 3-kinase inhibitor LY294002 and the p38 MAP kinase inhibitor SB202190.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	133-141	kininogen 1	Homo sapiens	0-2
15134872-3	2004	The key to conversion of bradykinin into an antagonist was replacement of the proline residue at position 7 with a D-aromatic amino acid.	Proline	78-85	kininogen 1	Homo sapiens	25-35
15134872-3	2004	The key to conversion of bradykinin into an antagonist was replacement of the proline residue at position 7 with a D-aromatic amino acid.	d-aromatic amino acid	115-136	kininogen 1	Homo sapiens	25-35
14670842-6	2004	The effect of IL-1beta, BK, and TGF-beta1 on cAMP levels was abrogated by the selective COX-2 inhibitor NS398.	Cyclic AMP	45-49	kininogen 1	Homo sapiens	24-26
14670842-6	2004	The effect of IL-1beta, BK, and TGF-beta1 on cAMP levels was abrogated by the selective COX-2 inhibitor NS398.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	104-109	kininogen 1	Homo sapiens	24-26
14670842-8	2004	Consistent with this, IL-1beta, BK, and TGF-beta1 all induced COX-2 and PGE2 release.	Dinoprostone	72-76	kininogen 1	Homo sapiens	32-34
14670842-9	2004	These results show that BK, IL-1beta, and TGF-beta1 downregulate adenylyl cyclase in human pulmonary artery smooth muscle cells via COX-2 induction and prostanoid release.	Prostaglandins	152-162	kininogen 1	Homo sapiens	24-26
14670842-0	2004	Interleukin-1beta, transforming growth factor-beta1, and bradykinin attenuate cyclic AMP production by human pulmonary artery smooth muscle cells in response to prostacyclin analogues and prostaglandin E2 by cyclooxygenase-2 induction and downregulation of adenylyl cyclase isoforms 1, 2, and 4.	Epoprostenol	161-173	kininogen 1	Homo sapiens	57-67
14670842-0	2004	Interleukin-1beta, transforming growth factor-beta1, and bradykinin attenuate cyclic AMP production by human pulmonary artery smooth muscle cells in response to prostacyclin analogues and prostaglandin E2 by cyclooxygenase-2 induction and downregulation of adenylyl cyclase isoforms 1, 2, and 4.	Dinoprostone	188-204	kininogen 1	Homo sapiens	57-67
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Cyclic AMP	167-171	kininogen 1	Homo sapiens	54-64
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Cyclic AMP	167-171	kininogen 1	Homo sapiens	66-68
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Dinoprostone	273-289	kininogen 1	Homo sapiens	54-64
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Dinoprostone	273-289	kininogen 1	Homo sapiens	66-68
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Dinoprostone	291-295	kininogen 1	Homo sapiens	54-64
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Dinoprostone	291-295	kininogen 1	Homo sapiens	66-68
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Epoprostenol	305-309	kininogen 1	Homo sapiens	54-64
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Epoprostenol	305-309	kininogen 1	Homo sapiens	66-68
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Iloprost	320-328	kininogen 1	Homo sapiens	54-64
14757160-5	2004	The affinities in competing for [3H]-BK binding and in blocking the BK-induced IP production by the non-peptide antagonists LF16-0687 and FR173657 at the wild type and mutant receptors were analysed.	Tritium	33-35	kininogen 1	Homo sapiens	37-39
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	Iloprost	320-328	kininogen 1	Homo sapiens	66-68
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	carboprostacyclin	333-350	kininogen 1	Homo sapiens	54-64
14670842-3	2004	In this study, we show that prolonged incubation with bradykinin (BK), interleukin-1beta (IL-1beta), and transforming growth factor-beta1 (TGF-beta1) markedly impairs cAMP accumulation in human pulmonary artery smooth muscle cells in response to short-term incubation with prostaglandin E2 (PGE2) and the PGI2 analogues iloprost and carbaprostacyclin.	carboprostacyclin	333-350	kininogen 1	Homo sapiens	66-68
15544518-4	2004	In the KKS, bradykinin (BK) and kallidin and their carboxypeptidase metabolites, des-Arg(9)-BK and des-Arg(10)-kallidin, are the effector peptides exerting their actions via BK type 1 (BK-B1) and BK type 2 (BK-B2) receptors.	des-arg	81-88	kininogen 1	Homo sapiens	12-22
14692800-7	2004	In contrast, when in the presence of zwitterionic DPC micelles, the degree of mixed-charge nature of the peptide affects binding (neurokinin A &gt; substance P &gt; Met-enkephalin &gt; bradykinin).	dodecylphosphocholine	50-53	kininogen 1	Homo sapiens	185-195
14692800-9	2004	Diffusion coefficients for the peptides in SDS micelles, when ranked from largest to smallest, follow a trend where increasing net positive charge results in the smallest diffusion coefficient: Met-enkephalin &gt; neurokinin A &gt; bradykinin &gt; substance P.	Sodium Dodecyl Sulfate	43-46	kininogen 1	Homo sapiens	232-242
14692800-10	2004	Diffusion coefficients when in the presence of DPC micelles, when ranked from largest to smallest, follow a trend where the presence of negatively-charged side chains results in the smallest diffusion coefficient: bradykinin &gt; Met-enkephalin &gt; substance P &gt; neurokinin A.	dodecylphosphocholine	47-50	kininogen 1	Homo sapiens	214-224
14977046-0	2004	N-linked glycosylation of the human bradykinin B2 receptor is required for optimal cell-surface expression and coupling.	Nitrogen	0-1	kininogen 1	Homo sapiens	36-46
14691197-2	2004	In the presence of the cyclooxygenase inhibitor indomethacin, bradykinin relaxed preconstricted HCMAs in a concentration-dependent manner.	Indomethacin	48-60	kininogen 1	Homo sapiens	62-72
14691197-2	2004	In the presence of the cyclooxygenase inhibitor indomethacin, bradykinin relaxed preconstricted HCMAs in a concentration-dependent manner.	hcmas	96-101	kininogen 1	Homo sapiens	62-72
14691197-3	2004	N(G)-nitro-L-arginine methyl ester and ODQ (inhibitors of nitric oxide [NO] synthase and guanylyl cyclase, respectively) and the NO scavenger hydroxocobalamin, either alone or in combination, shifted the bradykinin concentration-response curve to the right.	NG-Nitroarginine Methyl Ester	0-34	kininogen 1	Homo sapiens	204-214
14691197-5	2004	In contrast, complete blockade of bradykinin-induced relaxation was obtained when we combined the nonselective BK(Ca) and intermediate-conductance (IK(Ca)) Ca2+-dependent K+ channel blocker charybdotoxin and apamin with hydroxocobalamin.	Charybdotoxin	190-203	kininogen 1	Homo sapiens	34-44
14691197-5	2004	In contrast, complete blockade of bradykinin-induced relaxation was obtained when we combined the nonselective BK(Ca) and intermediate-conductance (IK(Ca)) Ca2+-dependent K+ channel blocker charybdotoxin and apamin with hydroxocobalamin.	Hydroxocobalamin	220-236	kininogen 1	Homo sapiens	34-44
14691197-7	2004	Inhibition of inwardly rectifying K+ channels (K(IR)) and Na+/K+-ATPase (with BaCl2 and ouabain, respectively) shifted the bradykinin concentration-response curve 10-fold to the right but did not exert an additional effect in the presence of hydroxocobalamin.	barium chloride	78-83	kininogen 1	Homo sapiens	123-133
14691197-7	2004	Inhibition of inwardly rectifying K+ channels (K(IR)) and Na+/K+-ATPase (with BaCl2 and ouabain, respectively) shifted the bradykinin concentration-response curve 10-fold to the right but did not exert an additional effect in the presence of hydroxocobalamin.	Hydroxocobalamin	242-258	kininogen 1	Homo sapiens	123-133
14733526-2	2004	This new reagent cleaved the Ser6-Pro7 amide bond in bradykinin at pH 7.	ser6-pro7	29-38	kininogen 1	Homo sapiens	53-63
14733526-2	2004	This new reagent cleaved the Ser6-Pro7 amide bond in bradykinin at pH 7.	Amides	39-44	kininogen 1	Homo sapiens	53-63
14687699-0	2004	PLA2/PGE2 are involved in the inhibitory effect of bradykinin on the angiotensin-(1-7)-stimulated Na(+)-ATPase activity of the proximal tubule.	Dinoprostone	5-9	kininogen 1	Homo sapiens	51-61
15544518-4	2004	In the KKS, bradykinin (BK) and kallidin and their carboxypeptidase metabolites, des-Arg(9)-BK and des-Arg(10)-kallidin, are the effector peptides exerting their actions via BK type 1 (BK-B1) and BK type 2 (BK-B2) receptors.	des-arg	81-88	kininogen 1	Homo sapiens	24-26
15544518-4	2004	In the KKS, bradykinin (BK) and kallidin and their carboxypeptidase metabolites, des-Arg(9)-BK and des-Arg(10)-kallidin, are the effector peptides exerting their actions via BK type 1 (BK-B1) and BK type 2 (BK-B2) receptors.	des-arg	81-88	kininogen 1	Homo sapiens	92-94
15544518-4	2004	In the KKS, bradykinin (BK) and kallidin and their carboxypeptidase metabolites, des-Arg(9)-BK and des-Arg(10)-kallidin, are the effector peptides exerting their actions via BK type 1 (BK-B1) and BK type 2 (BK-B2) receptors.	des-arg	99-106	kininogen 1	Homo sapiens	12-22
15544518-4	2004	In the KKS, bradykinin (BK) and kallidin and their carboxypeptidase metabolites, des-Arg(9)-BK and des-Arg(10)-kallidin, are the effector peptides exerting their actions via BK type 1 (BK-B1) and BK type 2 (BK-B2) receptors.	des-arg	99-106	kininogen 1	Homo sapiens	24-26
14734130-8	2004	Changes in MVO(2) at the highest dose in CHD vs CMP were, respectively: bradykinin, -22 +/- 7% vs: -30 +/- 5% (p &lt; 0.05); ramiprilat, -17 +/- 8% vs -26 +/- 2%, (p &lt; 0.001); and amlodipine, -5 +/- 7% vs -29 +/- 6% (p &lt; 0.001).	mvo(2)	11-17	kininogen 1	Homo sapiens	72-82
14694157-4	2004	Bradykinin, enalaprilat, and amlodipine significantly suppressed cortical oxygen consumption in 4-mo-old rats (bradykinin: -2.5 +/- 0.9% to -21 +/- 1.5%; enalaprilat: -0.7 +/- 0.5% to -26 +/- 1.2%; amlodipine: -1.3 +/- 0.9% to -18 +/- 1.2%; P &lt; 0.05).	Enalaprilat	12-23	kininogen 1	Homo sapiens	111-121
14694157-4	2004	Bradykinin, enalaprilat, and amlodipine significantly suppressed cortical oxygen consumption in 4-mo-old rats (bradykinin: -2.5 +/- 0.9% to -21 +/- 1.5%; enalaprilat: -0.7 +/- 0.5% to -26 +/- 1.2%; amlodipine: -1.3 +/- 0.9% to -18 +/- 1.2%; P &lt; 0.05).	Amlodipine	29-39	kininogen 1	Homo sapiens	111-121
14694157-4	2004	Bradykinin, enalaprilat, and amlodipine significantly suppressed cortical oxygen consumption in 4-mo-old rats (bradykinin: -2.5 +/- 0.9% to -21 +/- 1.5%; enalaprilat: -0.7 +/- 0.5% to -26 +/- 1.2%; amlodipine: -1.3 +/- 0.9% to -18 +/- 1.2%; P &lt; 0.05).	Oxygen	74-80	kininogen 1	Homo sapiens	0-10
14694157-4	2004	Bradykinin, enalaprilat, and amlodipine significantly suppressed cortical oxygen consumption in 4-mo-old rats (bradykinin: -2.5 +/- 0.9% to -21 +/- 1.5%; enalaprilat: -0.7 +/- 0.5% to -26 +/- 1.2%; amlodipine: -1.3 +/- 0.9% to -18 +/- 1.2%; P &lt; 0.05).	Oxygen	74-80	kininogen 1	Homo sapiens	111-121
14694157-4	2004	Bradykinin, enalaprilat, and amlodipine significantly suppressed cortical oxygen consumption in 4-mo-old rats (bradykinin: -2.5 +/- 0.9% to -21 +/- 1.5%; enalaprilat: -0.7 +/- 0.5% to -26 +/- 1.2%; amlodipine: -1.3 +/- 0.9% to -18 +/- 1.2%; P &lt; 0.05).	Enalaprilat	154-165	kininogen 1	Homo sapiens	0-10
14694157-4	2004	Bradykinin, enalaprilat, and amlodipine significantly suppressed cortical oxygen consumption in 4-mo-old rats (bradykinin: -2.5 +/- 0.9% to -21 +/- 1.5%; enalaprilat: -0.7 +/- 0.5% to -26 +/- 1.2%; amlodipine: -1.3 +/- 0.9% to -18 +/- 1.2%; P &lt; 0.05).	Amlodipine	198-208	kininogen 1	Homo sapiens	0-10
14694157-6	2004	However, in 23-mo-old animals, the responses to bradykinin and enalaprilat were attenuated (bradykinin: 0 +/- 0% to -13 +/- 0.9%; enalaprilat: -0.3 +/- 0.3% to -17 +/- 2.1%; P &lt; 0.05), whereas the response to an NO donor was unaffected, suggesting decreased bioavailability of NO.	Enalaprilat	63-74	kininogen 1	Homo sapiens	92-102
14694157-6	2004	However, in 23-mo-old animals, the responses to bradykinin and enalaprilat were attenuated (bradykinin: 0 +/- 0% to -13 +/- 0.9%; enalaprilat: -0.3 +/- 0.3% to -17 +/- 2.1%; P &lt; 0.05), whereas the response to an NO donor was unaffected, suggesting decreased bioavailability of NO.	Enalaprilat	130-141	kininogen 1	Homo sapiens	48-58
14694157-7	2004	Addition of the superoxide radical scavenger tempol restored the ability of bradykinin, enalaprilat, and amlodipine to suppress oxygen consumption in tissue from 23-mo-old animals to levels seen in younger animals, suggesting NO destruction by superoxide as the reason for decreased NO availability.	Superoxides	16-26	kininogen 1	Homo sapiens	76-86
14694157-7	2004	Addition of the superoxide radical scavenger tempol restored the ability of bradykinin, enalaprilat, and amlodipine to suppress oxygen consumption in tissue from 23-mo-old animals to levels seen in younger animals, suggesting NO destruction by superoxide as the reason for decreased NO availability.	tempol	45-51	kininogen 1	Homo sapiens	76-86
14694157-7	2004	Addition of the superoxide radical scavenger tempol restored the ability of bradykinin, enalaprilat, and amlodipine to suppress oxygen consumption in tissue from 23-mo-old animals to levels seen in younger animals, suggesting NO destruction by superoxide as the reason for decreased NO availability.	Oxygen	128-134	kininogen 1	Homo sapiens	76-86
14694157-7	2004	Addition of the superoxide radical scavenger tempol restored the ability of bradykinin, enalaprilat, and amlodipine to suppress oxygen consumption in tissue from 23-mo-old animals to levels seen in younger animals, suggesting NO destruction by superoxide as the reason for decreased NO availability.	Superoxides	244-254	kininogen 1	Homo sapiens	76-86
14734130-9	2004	L-NAME attenuated the effect of bradykinin, ramiprilat and amlodipine in both groups, confirming that the drug effect was secondary to eNOS activation.	NG-Nitroarginine Methyl Ester	0-6	kininogen 1	Homo sapiens	32-42
15325012-7	2004	We concluded that the effects of captopril, an ACE inhibitor, on TAME-esterase induced contractions could thus be due to the degradation of bradykinin by the enzyme kininase being blocked.	Captopril	33-42	kininogen 1	Homo sapiens	140-150
14517215-0	2003	Cyclooxygenase-2 induction by bradykinin in human pulmonary artery smooth muscle cells is mediated by the cyclic AMP response element through a novel autocrine loop involving endogenous prostaglandin E2, E-prostanoid 2 (EP2), and EP4 receptors.	Cyclic AMP	106-116	kininogen 1	Homo sapiens	30-40
14597600-4	2003	In cultured human ASM cells, IL-13 (50 ng ml-1, 24 h) also augmented cytosolic calcium levels to bradykinin, histamine and carbachol by 60, 35 and 26%, respectively.	Calcium	79-86	kininogen 1	Homo sapiens	97-107
14563691-0	2003	Alzheimer"s disease skin fibroblasts selectively express a bradykinin signaling pathway mediating tau protein Ser phosphorylation.	Serine	110-113	kininogen 1	Homo sapiens	59-69
14645533-3	2003	By transfection with various COX-2 promoter reporter constructs, we found that the bp -327-to-+59 promoter region was essential for COX-2 gene transcription by bradykinin and IL-1beta and that the cyclic AMP response element (CRE) was critical in bradykinin-induced transcription, whereas nuclear factor IL-6 and CRE and, to a lesser extent, nuclear factor-kappaB (NF-kappaB) were involved in IL-1beta-induced transcription.	Cyclic AMP	197-207	kininogen 1	Homo sapiens	160-170
14645533-3	2003	By transfection with various COX-2 promoter reporter constructs, we found that the bp -327-to-+59 promoter region was essential for COX-2 gene transcription by bradykinin and IL-1beta and that the cyclic AMP response element (CRE) was critical in bradykinin-induced transcription, whereas nuclear factor IL-6 and CRE and, to a lesser extent, nuclear factor-kappaB (NF-kappaB) were involved in IL-1beta-induced transcription.	Cyclic AMP	197-207	kininogen 1	Homo sapiens	247-257
14645533-6	2003	We also revealed that endogenous prostaglandin E(2) was critical in bradykinin-induced COX-2 transcription initiation and involved in IL-1beta-induced COX-2 transcription at a latter stage.	Dinoprostone	33-51	kininogen 1	Homo sapiens	68-78
14563712-5	2003	Addition of bradykinin (BK) induced significant NOx production that was not inhibited by heparinase pretreatment, demonstrating that the cells were still able to produce abundant NO after heparinase treatment.	nicotine 1-N-oxide	48-51	kininogen 1	Homo sapiens	12-22
14563712-5	2003	Addition of bradykinin (BK) induced significant NOx production that was not inhibited by heparinase pretreatment, demonstrating that the cells were still able to produce abundant NO after heparinase treatment.	nicotine 1-N-oxide	48-51	kininogen 1	Homo sapiens	24-26
14602298-3	2003	The EDHF-mediated relaxation was induced by bradykinin (-10 to approximately -6.5 log M) in the precontraction evoked by U(46619) (10 nmol/L) or U(46619) (1 nmol/L) plus endothelin-1 (6 nmol/L).	edhf	4-8	kininogen 1	Homo sapiens	44-54
14517705-4	2003	As noscapine can act as an antagonist of bradykinin and can effectively reduce brain injury after hypoxic-ischemic insult in neonatal rats, the present work was carried out to investigate its effectiveness in a clinical setting.	Noscapine	3-12	kininogen 1	Homo sapiens	41-51
14557280-8	2003	These results suggest that EDHF contributes substantially to basal forearm vascular resistance, as well as to forearm vasodilatation evoked by substance P and bradykinin in humans in vivo.	edhf	27-31	kininogen 1	Homo sapiens	159-169
12970081-1	2003	Binding affinity at the [3H]-BK binding site and activity as inositol phosphate (IP) production by the peptide bradykinin (BK) and the nonpeptide FR190997 were studied at wild-type or point-mutated human B2 receptors (hB2R) expressed in CHO cells.	Tritium	25-27	kininogen 1	Homo sapiens	29-31
12970081-1	2003	Binding affinity at the [3H]-BK binding site and activity as inositol phosphate (IP) production by the peptide bradykinin (BK) and the nonpeptide FR190997 were studied at wild-type or point-mutated human B2 receptors (hB2R) expressed in CHO cells.	Inositol Phosphates	61-79	kininogen 1	Homo sapiens	111-121
12970081-1	2003	Binding affinity at the [3H]-BK binding site and activity as inositol phosphate (IP) production by the peptide bradykinin (BK) and the nonpeptide FR190997 were studied at wild-type or point-mutated human B2 receptors (hB2R) expressed in CHO cells.	Inositol Phosphates	61-79	kininogen 1	Homo sapiens	29-31
12970081-1	2003	Binding affinity at the [3H]-BK binding site and activity as inositol phosphate (IP) production by the peptide bradykinin (BK) and the nonpeptide FR190997 were studied at wild-type or point-mutated human B2 receptors (hB2R) expressed in CHO cells.	Inositol Phosphates	81-83	kininogen 1	Homo sapiens	111-121
12970081-1	2003	Binding affinity at the [3H]-BK binding site and activity as inositol phosphate (IP) production by the peptide bradykinin (BK) and the nonpeptide FR190997 were studied at wild-type or point-mutated human B2 receptors (hB2R) expressed in CHO cells.	Inositol Phosphates	81-83	kininogen 1	Homo sapiens	29-31
12826020-3	2003	The aim of the present study was to determine the effect of sulphaphenazole on basal and bradykinin-induced NO/PGI2-independent changes in the forearm blood flow (FBF) of healthy subjects.	Sulfaphenazole	60-75	kininogen 1	Homo sapiens	89-99
12826020-3	2003	The aim of the present study was to determine the effect of sulphaphenazole on basal and bradykinin-induced NO/PGI2-independent changes in the forearm blood flow (FBF) of healthy subjects.	Epoprostenol	111-115	kininogen 1	Homo sapiens	89-99
14517215-9	2003	CRE activation occurred by BK inducing cytosolic phospholipase A2-mediated arachidonic acid release and rapid prostaglandin E2 (PGE2) production, thereby increasing cAMP.	Arachidonic Acid	75-91	kininogen 1	Homo sapiens	27-29
14517215-9	2003	CRE activation occurred by BK inducing cytosolic phospholipase A2-mediated arachidonic acid release and rapid prostaglandin E2 (PGE2) production, thereby increasing cAMP.	Dinoprostone	110-126	kininogen 1	Homo sapiens	27-29
14517215-9	2003	CRE activation occurred by BK inducing cytosolic phospholipase A2-mediated arachidonic acid release and rapid prostaglandin E2 (PGE2) production, thereby increasing cAMP.	Dinoprostone	128-132	kininogen 1	Homo sapiens	27-29
14517215-9	2003	CRE activation occurred by BK inducing cytosolic phospholipase A2-mediated arachidonic acid release and rapid prostaglandin E2 (PGE2) production, thereby increasing cAMP.	Cyclic AMP	165-169	kininogen 1	Homo sapiens	27-29
14517215-10	2003	Indomethacin inhibited BK-induced PGE2 production, cAMP accumulation, and CRE/luc reporter and COX-2 promoter luciferase activity.	Indomethacin	0-12	kininogen 1	Homo sapiens	23-25
14517215-10	2003	Indomethacin inhibited BK-induced PGE2 production, cAMP accumulation, and CRE/luc reporter and COX-2 promoter luciferase activity.	Dinoprostone	34-38	kininogen 1	Homo sapiens	23-25
14517215-10	2003	Indomethacin inhibited BK-induced PGE2 production, cAMP accumulation, and CRE/luc reporter and COX-2 promoter luciferase activity.	Cyclic AMP	51-55	kininogen 1	Homo sapiens	23-25
14517215-11	2003	Exogenous PGE2 and EP2 (ONO-AE1 259) and EP4 (ONO-AE1 329) PGE2 receptor agonists mimicked the effect of BK.	Dinoprostone	10-14	kininogen 1	Homo sapiens	105-107
14517215-11	2003	Exogenous PGE2 and EP2 (ONO-AE1 259) and EP4 (ONO-AE1 329) PGE2 receptor agonists mimicked the effect of BK.	ono-ae1	24-31	kininogen 1	Homo sapiens	105-107
14517215-11	2003	Exogenous PGE2 and EP2 (ONO-AE1 259) and EP4 (ONO-AE1 329) PGE2 receptor agonists mimicked the effect of BK.	ono-ae1	46-53	kininogen 1	Homo sapiens	105-107
14517215-12	2003	Collectively these studies indicate that COX-2 induction by BK in human pulmonary artery smooth muscle cells is mediated by the CRE through a novel autocrine loop involving endogenous PGE2.	Dinoprostone	184-188	kininogen 1	Homo sapiens	60-62
14616033-0	2003	Is the C-terminal region of bradykinin the binding site of polyphenols?	Polyphenols	59-70	kininogen 1	Homo sapiens	28-38
14871030-7	2003	Bradykinin B2 receptor antagonist icatibant 100 nmol/l significantly reduced the action of temocaprilat; whereas bradykinin B1 receptor antagonist des-Arg9-Leu8-bradykinin 100 nmol/l had no effect.	temocaprilat	91-103	kininogen 1	Homo sapiens	0-10
14871030-8	2003	These findings suggest that high glucose inhibits human aortic endothelial cell proliferation and that the angiotensin-converting enzyme inhibitor temocaprilat inhibits high glucose-mediated suppression of human aortic endothelial cell proliferation, possibly through suppression of protein kinase C, bradykinin B2 receptors and oxidative stress.	temocaprilat	147-159	kininogen 1	Homo sapiens	301-311
14871030-8	2003	These findings suggest that high glucose inhibits human aortic endothelial cell proliferation and that the angiotensin-converting enzyme inhibitor temocaprilat inhibits high glucose-mediated suppression of human aortic endothelial cell proliferation, possibly through suppression of protein kinase C, bradykinin B2 receptors and oxidative stress.	Glucose	174-181	kininogen 1	Homo sapiens	301-311
15127951-3	2003	On Leu-enkephalin, dynorphin (1-6), dynorphin (1-13), alpha-neoendorphin, and Lys-bradykinin, it showed a preferential aminopeptidase activity by cleaving off hydrophobic or basic amino acids.	Amino Acids, Basic	174-191	kininogen 1	Homo sapiens	82-92
12944405-2	2003	In microtiter plates, biotinylated high molecular weight kininogen (biotin-HK) or biotin-FXI binding to HUVEC monolayers or their matrix proteins, but not fibronectin-coated plastic microtiter plate wells, was specifically blocked by antibodies to each of the receptors of HK, uPAR, gC1qR, or cytokeratin 1.	Biotin	22-28	kininogen 1	Homo sapiens	35-66
12944405-2	2003	In microtiter plates, biotinylated high molecular weight kininogen (biotin-HK) or biotin-FXI binding to HUVEC monolayers or their matrix proteins, but not fibronectin-coated plastic microtiter plate wells, was specifically blocked by antibodies to each of the receptors of HK, uPAR, gC1qR, or cytokeratin 1.	Biotin	68-74	kininogen 1	Homo sapiens	35-66
14627487-5	2003	In the isolated arteries, ADP-ribosyltransferase C3 attenuated the relaxations to bradykinin during contractions with prostaglandin F2alpha in the presence of tween 80 (non ionic detergent), but not in the absence of tween 80.	Dinoprost	118-139	kininogen 1	Homo sapiens	82-92
14517215-0	2003	Cyclooxygenase-2 induction by bradykinin in human pulmonary artery smooth muscle cells is mediated by the cyclic AMP response element through a novel autocrine loop involving endogenous prostaglandin E2, E-prostanoid 2 (EP2), and EP4 receptors.	Dinoprostone	186-202	kininogen 1	Homo sapiens	30-40
14514933-0	2003	Effect of bradykinin on allergen induced increase in exhaled nitric oxide in asthma.	Nitric Oxide	61-73	kininogen 1	Homo sapiens	10-20
14514933-2	2003	In contrast, bradykinin (BK) rapidly reduces FENO.	flubendiamide	45-49	kininogen 1	Homo sapiens	13-23
14514933-2	2003	In contrast, bradykinin (BK) rapidly reduces FENO.	flubendiamide	45-49	kininogen 1	Homo sapiens	25-27
14514933-4	2003	METHODS: Levels of FENO in response to aerosolised BK were studied before (day 3) and 48 hours after (day 10) randomised diluent (diluent/placebo/BK (Dil/P/BK)), allergen (allergen/placebo/BK (All/P/BK), and allergen/L-NMMA/BK (All/L/BK)) challenges (day 8) in 10 atopic, steroid naive, mild asthmatic patients with dual responses to inhaled house dust mite extract.	flubendiamide	19-23	kininogen 1	Homo sapiens	51-53
14514933-8	2003	Despite the long lasting increase in FENO following allergen challenge in the LAR, BK suppressed FENO levels at 48 hours after allergen challenge in the All/P/BK period, lowering the increased FENO (difference from placebo 54.3 ppb (95% CI 23.8 to 84.8); p=0.003) to the baseline level on the pre-allergen day (p=0.51).	flubendiamide	97-101	kininogen 1	Homo sapiens	83-85
14514933-8	2003	Despite the long lasting increase in FENO following allergen challenge in the LAR, BK suppressed FENO levels at 48 hours after allergen challenge in the All/P/BK period, lowering the increased FENO (difference from placebo 54.3 ppb (95% CI 23.8 to 84.8); p=0.003) to the baseline level on the pre-allergen day (p=0.51).	flubendiamide	97-101	kininogen 1	Homo sapiens	83-85
14514933-8	2003	Despite the long lasting increase in FENO following allergen challenge in the LAR, BK suppressed FENO levels at 48 hours after allergen challenge in the All/P/BK period, lowering the increased FENO (difference from placebo 54.3 ppb (95% CI 23.8 to 84.8); p=0.003) to the baseline level on the pre-allergen day (p=0.51).	Polybrominated Biphenyls	228-231	kininogen 1	Homo sapiens	83-85
14514933-9	2003	FENO levels were lower after L-NMMA than after placebo on pre-allergen (difference 10.85 ppb (95% CI 1.3 to 20.4); p=0.03) and post-allergen (difference 36.2 ppb (95% CI 5.5 to 66.9); p=0.03) days in the All/L/BK and All/P/BK periods, respectively.	flubendiamide	0-4	kininogen 1	Homo sapiens	210-212
12754192-4	2003	When we compared results in asthmatic and nonasthmatic muscle cells, both trypsin and bradykinin induced less PGE2 from asthmatic ASM cells, and bradykinin induced significantly less COX-2 mRNA in asthmatic cells.	Dinoprostone	110-114	kininogen 1	Homo sapiens	86-96
14514933-9	2003	FENO levels were lower after L-NMMA than after placebo on pre-allergen (difference 10.85 ppb (95% CI 1.3 to 20.4); p=0.03) and post-allergen (difference 36.2 ppb (95% CI 5.5 to 66.9); p=0.03) days in the All/L/BK and All/P/BK periods, respectively.	omega-N-Methylarginine	29-35	kininogen 1	Homo sapiens	210-212
14650578-5	2003	Moreover, CPA accelerated the Ca2+ influx caused by 5 nM BK and 1mM HIST, but did not alter that caused by 1 microM TG.	cyclopiazonic acid	10-13	kininogen 1	Homo sapiens	57-59
12876216-1	2003	The Ca2+ mobilizing peptide, bradykinin (BK), stimulates endothelial nitric oxide synthase (eNOS)-derived cellular nitric oxide (NO) production in association with altering the subcellular distribution of the enzyme.	Nitric Oxide	69-81	kininogen 1	Homo sapiens	29-39
12876216-1	2003	The Ca2+ mobilizing peptide, bradykinin (BK), stimulates endothelial nitric oxide synthase (eNOS)-derived cellular nitric oxide (NO) production in association with altering the subcellular distribution of the enzyme.	Nitric Oxide	69-81	kininogen 1	Homo sapiens	41-43
12876216-5	2003	Incubation of digitonin-permeabilized ECV304 cells with the non-hydrolyzed GTP analog, GTP-gamma-S, abrogated the BK-mediated internalization of eNOS-GFP as assessed by confocal microscopy.	Digitonin	14-23	kininogen 1	Homo sapiens	114-116
12876216-5	2003	Incubation of digitonin-permeabilized ECV304 cells with the non-hydrolyzed GTP analog, GTP-gamma-S, abrogated the BK-mediated internalization of eNOS-GFP as assessed by confocal microscopy.	Guanosine Triphosphate	75-78	kininogen 1	Homo sapiens	114-116
12876216-5	2003	Incubation of digitonin-permeabilized ECV304 cells with the non-hydrolyzed GTP analog, GTP-gamma-S, abrogated the BK-mediated internalization of eNOS-GFP as assessed by confocal microscopy.	Guanosine 5'-O-(3-Thiotriphosphate)	87-98	kininogen 1	Homo sapiens	114-116
13678152-2	2003	Bradykinin and carbonic anhydrase were labeled with sulfosuccinimidyl-2-(biotinamido) ethyl-1,3-dithiopropionate, a membrane impermeant reagent that is reactive with primary amines.	sulfosuccinimidyl-2-(biotinamido)ethyl-1,3-dithiopropionate	52-112	kininogen 1	Homo sapiens	0-10
13678152-2	2003	Bradykinin and carbonic anhydrase were labeled with sulfosuccinimidyl-2-(biotinamido) ethyl-1,3-dithiopropionate, a membrane impermeant reagent that is reactive with primary amines.	Amines	174-180	kininogen 1	Homo sapiens	0-10
12815179-7	2003	Intra-arterial infusion of 17 beta-oestradiol significantly potentiated bradykinin-induced t-PA release.	Estradiol	27-45	kininogen 1	Homo sapiens	72-82
12928765-3	2003	AC-17 (0.1-1 M) reversed the barrier dysfunction induced by tryptase, thrombin and bradykinin without affecting the endothelial permeability enhanced by Ca(2+) ionophores such as ionomycin and A23187 or phorbol 12-myristate 13-acetate.	carbazochrome	0-5	kininogen 1	Homo sapiens	83-93
12928765-5	2003	On the other hand, AC-17 (0.1-10 M) reduced concentration-dependently the enhancement of [(3)H]inositol triphosphate formation from [(3)H]myo-inositol induced by bradykinin and thrombin.Therefore, it is suggested that AC-17 reduces the vascular hyperpermeability induced by a variety of vasoactive agents through inhibition of agonist-induced phosphoinositide hydrolysis.	carbazochrome	19-24	kininogen 1	Homo sapiens	162-172
12928765-5	2003	On the other hand, AC-17 (0.1-10 M) reduced concentration-dependently the enhancement of [(3)H]inositol triphosphate formation from [(3)H]myo-inositol induced by bradykinin and thrombin.Therefore, it is suggested that AC-17 reduces the vascular hyperpermeability induced by a variety of vasoactive agents through inhibition of agonist-induced phosphoinositide hydrolysis.	[(3)h]inositol triphosphate	89-116	kininogen 1	Homo sapiens	162-172
12928765-5	2003	On the other hand, AC-17 (0.1-10 M) reduced concentration-dependently the enhancement of [(3)H]inositol triphosphate formation from [(3)H]myo-inositol induced by bradykinin and thrombin.Therefore, it is suggested that AC-17 reduces the vascular hyperpermeability induced by a variety of vasoactive agents through inhibition of agonist-induced phosphoinositide hydrolysis.	[(3)h]myo-inositol	132-150	kininogen 1	Homo sapiens	162-172
12900349-8	2003	The reduced response to bradykinin remained significant (P=0.045) after adjusting for the response to glyceryl trinitrate and was independent of conventional risk factors.	Nitroglycerin	102-121	kininogen 1	Homo sapiens	24-34
12748173-0	2003	Transcriptional regulation of interleukin (IL)-8 by bradykinin in human airway smooth muscle cells involves prostanoid-dependent activation of AP-1 and nuclear factor (NF)-IL-6 and prostanoid-independent activation of NF-kappaB.	Prostaglandins	108-118	kininogen 1	Homo sapiens	52-62
12748173-0	2003	Transcriptional regulation of interleukin (IL)-8 by bradykinin in human airway smooth muscle cells involves prostanoid-dependent activation of AP-1 and nuclear factor (NF)-IL-6 and prostanoid-independent activation of NF-kappaB.	Prostaglandins	181-191	kininogen 1	Homo sapiens	52-62
12748173-10	2003	Transcriptional activation of the IL-8 promoter by BK involves the prostanoid-independent activation of NF-kappaB, and prostanoid-dependent activation of AP-1 and NF-IL-6 plays a key role in augmenting the response.	Prostaglandins	67-77	kininogen 1	Homo sapiens	51-53
12748173-11	2003	Endogenous prostanoid generation in response to GPCR ligands such as BK may be an important mechanism whereby GPCRs signal to the nucleus to maximize the transcription of inflammatory response genes.	Prostaglandins	11-21	kininogen 1	Homo sapiens	69-71
12883337-7	2003	The vasodilator response to bradykinin was significantly blunted ( approximately 30%) with l-NMMA.	omega-N-Methylarginine	91-97	kininogen 1	Homo sapiens	28-38
12883337-8	2003	Although there was no effect of l-NMMA on basal t-PA release, acute release of t-PA to bradykinin was higher (P &lt; 0.01) after (from -0.2 +/- 0.5 to 105.2 +/- 9.4 ng.100 mL tissue-1.min-1) versus before (from -0.4 +/- 0.7 to 48.7 +/- 7.3 ng.100 mL tissue-1.min-1) the administration of l-NMMA.	omega-N-Methylarginine	288-294	kininogen 1	Homo sapiens	87-97
12870664-9	2003	SKF 525A also dose-dependently inhibited BK-stimulated production of NO and PGI2, assessed by measuring cGMP and 6-keto-PGF(1alpha) concentration.	Proadifen	0-8	kininogen 1	Homo sapiens	41-43
14650578-1	2003	The effect of cyclopiazonic acid (CPA) on changes in the intracellular free Ca2+ concentration ([Ca2+]i) evoked by bradykinin (BK), histamine (HIST) and thapsigargin (TG) was investigated in human gingival fibroblasts.	cyclopiazonic acid	14-32	kininogen 1	Homo sapiens	115-125
14650578-1	2003	The effect of cyclopiazonic acid (CPA) on changes in the intracellular free Ca2+ concentration ([Ca2+]i) evoked by bradykinin (BK), histamine (HIST) and thapsigargin (TG) was investigated in human gingival fibroblasts.	cyclopiazonic acid	34-37	kininogen 1	Homo sapiens	115-125
14650578-3	2003	Pretreatment with CPA (&lt; 5 microM) enhanced the [Ca2+]i responses evoked by 5 nM BK and 1 mM HIST.	cyclopiazonic acid	18-21	kininogen 1	Homo sapiens	84-86
12749889-0	2003	Design and synthesis of novel pyrrolidine-containing bradykinin antagonists.	pyrrolidine	30-41	kininogen 1	Homo sapiens	53-63
12749889-1	2003	The design and synthesis of novel pyrrolidine-containing bradykinin antagonists, II, are described.	pyrrolidine	34-45	kininogen 1	Homo sapiens	57-67
17021482-2	2003	The most effective treatment for the deleterious cardiovascular and pulmonary effects of serotonin and bradykinin is octreotide, a somatostatin analogue.	Octreotide	117-127	kininogen 1	Homo sapiens	103-113
12766083-1	2003	PURPOSE: It has been shown that bradykinin (BK) protects retinal neurons against glutamate excitotoxicity, but it was not clear how BK inhibits glutamate excitotoxicity.	Glutamic Acid	81-90	kininogen 1	Homo sapiens	32-42
12766083-1	2003	PURPOSE: It has been shown that bradykinin (BK) protects retinal neurons against glutamate excitotoxicity, but it was not clear how BK inhibits glutamate excitotoxicity.	Glutamic Acid	81-90	kininogen 1	Homo sapiens	44-46
12766083-2	2003	The purpose of this study was to investigate the effect of opening the mitochondrial adenosine triphosphate (ATP)-sensitive potassium (Mit K (ATP)) channel on glutamate excitotoxicity and the protective effect of BK using cultured retinal neurons.	Adenosine Triphosphate	109-112	kininogen 1	Homo sapiens	213-215
12766083-8	2003	BK and diazoxide protected retinal neurons against glutamate excitotoxicity and inhibited glutamate-induced mitochondrial depolarization.	Glutamic Acid	51-60	kininogen 1	Homo sapiens	0-2
12766083-8	2003	BK and diazoxide protected retinal neurons against glutamate excitotoxicity and inhibited glutamate-induced mitochondrial depolarization.	Glutamic Acid	90-99	kininogen 1	Homo sapiens	0-2
12766083-9	2003	These actions of BK and diazoxide were inhibited by the coapplication of 5HD and glibenclamide.	5-(2-Hydroxyethyl)nonane-1,9-Diol	73-76	kininogen 1	Homo sapiens	17-19
12766083-9	2003	These actions of BK and diazoxide were inhibited by the coapplication of 5HD and glibenclamide.	Glyburide	81-94	kininogen 1	Homo sapiens	17-19
12766083-11	2003	CONCLUSIONS: These results suggest that BK and diazoxide protect retinal neurons against glutamate excitotoxicity by opening the Mit K (ATP) channel.	Glutamic Acid	89-98	kininogen 1	Homo sapiens	40-42
12756290-5	2003	Upon stimulation of NO production by bradykinin, however, recycling is co-stimulated to the extent that more than 80% of the citrulline produced is recycled to arginine.	Citrulline	125-135	kininogen 1	Homo sapiens	37-47
12756290-5	2003	Upon stimulation of NO production by bradykinin, however, recycling is co-stimulated to the extent that more than 80% of the citrulline produced is recycled to arginine.	Arginine	160-168	kininogen 1	Homo sapiens	37-47
12626646-6	2003	8-iso-PGE2 was able to completely relax tissues that had been denuded of endothelium (as indicated by loss of responsiveness to bradykinin).	8-isoprostaglandin E2	0-10	kininogen 1	Homo sapiens	128-138
12763764-3	2003	METHODS AND RESULTS: Isometric tension and membrane-potential recordings demonstrated that bradykinin and substance P caused EDHF-mediated relaxations and hyperpolarizations of porcine coronary microvessels in the presence of indomethacin and Nomega-nitro-L-arginine.	Indomethacin	226-238	kininogen 1	Homo sapiens	91-101
12763764-3	2003	METHODS AND RESULTS: Isometric tension and membrane-potential recordings demonstrated that bradykinin and substance P caused EDHF-mediated relaxations and hyperpolarizations of porcine coronary microvessels in the presence of indomethacin and Nomega-nitro-L-arginine.	Nitroarginine	243-266	kininogen 1	Homo sapiens	91-101
12763764-5	2003	Endothelial production of H2O2 was quantified in bradykinin- or substance P-stimulated intact blood vessels by ESR spectroscopy.	Hydrogen Peroxide	26-30	kininogen 1	Homo sapiens	49-59
12763764-6	2003	Tiron, a superoxide scavenger that facilitates H2O2 formation, enhanced bradykinin-induced production of H2O2, as well as the EDHF-mediated relaxations and hyperpolarizations.	1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt	0-5	kininogen 1	Homo sapiens	72-82
12763764-6	2003	Tiron, a superoxide scavenger that facilitates H2O2 formation, enhanced bradykinin-induced production of H2O2, as well as the EDHF-mediated relaxations and hyperpolarizations.	Superoxides	9-19	kininogen 1	Homo sapiens	72-82
12763764-6	2003	Tiron, a superoxide scavenger that facilitates H2O2 formation, enhanced bradykinin-induced production of H2O2, as well as the EDHF-mediated relaxations and hyperpolarizations.	Hydrogen Peroxide	105-109	kininogen 1	Homo sapiens	72-82
12829196-2	2003	This is despite the fact that ACE inhibition also inhibits the enzyme kininase II and leads to accumulation of bradykinin which increases prostaglandins.	Prostaglandins	138-152	kininogen 1	Homo sapiens	111-121
12855973-7	2003	RESULTS: Incubation with indomethacin (n=6), in the presence of L-NAME, significantly reduced (P&lt;0.01) maximum BK-induced relaxation (-103.5+/-8.8%) compared to paired rings in the presence of L-NAME alone (-130.8+/-8.8%).	Indomethacin	25-37	kininogen 1	Homo sapiens	114-116
12855973-7	2003	RESULTS: Incubation with indomethacin (n=6), in the presence of L-NAME, significantly reduced (P&lt;0.01) maximum BK-induced relaxation (-103.5+/-8.8%) compared to paired rings in the presence of L-NAME alone (-130.8+/-8.8%).	NG-Nitroarginine Methyl Ester	64-70	kininogen 1	Homo sapiens	114-116
12855973-7	2003	RESULTS: Incubation with indomethacin (n=6), in the presence of L-NAME, significantly reduced (P&lt;0.01) maximum BK-induced relaxation (-103.5+/-8.8%) compared to paired rings in the presence of L-NAME alone (-130.8+/-8.8%).	NG-Nitroarginine Methyl Ester	196-202	kininogen 1	Homo sapiens	114-116
12767053-6	2003	One mechanism involves the action of bradykinin, acting through bradykinin B(2) receptors, to increase nitric oxide (NO) production and ultimately enhance glucose transport.	Nitric Oxide	103-115	kininogen 1	Homo sapiens	37-47
12767053-6	2003	One mechanism involves the action of bradykinin, acting through bradykinin B(2) receptors, to increase nitric oxide (NO) production and ultimately enhance glucose transport.	Nitric Oxide	103-115	kininogen 1	Homo sapiens	64-74
12767053-6	2003	One mechanism involves the action of bradykinin, acting through bradykinin B(2) receptors, to increase nitric oxide (NO) production and ultimately enhance glucose transport.	Glucose	155-162	kininogen 1	Homo sapiens	37-47
12767053-6	2003	One mechanism involves the action of bradykinin, acting through bradykinin B(2) receptors, to increase nitric oxide (NO) production and ultimately enhance glucose transport.	Glucose	155-162	kininogen 1	Homo sapiens	64-74
12767053-10	2003	These data support the concept that ACE inhibitors can beneficially modulate glucose control in insulin-resistant states, possibly through a NO-dependent effect of bradykinin and/or antagonism of ATII action on skeletal muscle.	Glucose	77-84	kininogen 1	Homo sapiens	164-174
12787410-10	2003	In isolated porcine renal arteries, bradykinin-induced vasodilation was significantly reduced by either iberiotoxin or H2O2.	iberiotoxin	104-115	kininogen 1	Homo sapiens	36-46
12787410-10	2003	In isolated porcine renal arteries, bradykinin-induced vasodilation was significantly reduced by either iberiotoxin or H2O2.	Hydrogen Peroxide	119-123	kininogen 1	Homo sapiens	36-46
12870664-9	2003	SKF 525A also dose-dependently inhibited BK-stimulated production of NO and PGI2, assessed by measuring cGMP and 6-keto-PGF(1alpha) concentration.	Epoprostenol	76-80	kininogen 1	Homo sapiens	41-43
12870664-9	2003	SKF 525A also dose-dependently inhibited BK-stimulated production of NO and PGI2, assessed by measuring cGMP and 6-keto-PGF(1alpha) concentration.	Cyclic GMP	104-108	kininogen 1	Homo sapiens	41-43
12870664-9	2003	SKF 525A also dose-dependently inhibited BK-stimulated production of NO and PGI2, assessed by measuring cGMP and 6-keto-PGF(1alpha) concentration.	6-keto-pgf	113-123	kininogen 1	Homo sapiens	41-43
12578561-3	2003	Serine and arginine are also the residues at positions P"(1) and P"(2) in human kininogen, from which hK1 releases Lys-bradykinin.	Serine	0-6	kininogen 1	Homo sapiens	119-129
12578561-3	2003	Serine and arginine are also the residues at positions P"(1) and P"(2) in human kininogen, from which hK1 releases Lys-bradykinin.	Arginine	11-19	kininogen 1	Homo sapiens	119-129
12732401-10	2003	Fenofibrate plus CoQ significantly improved (P&lt;0.05) the AUC for ACh, BK and SNP without significantly altering basal responses to L-NMMA.	Fenofibrate	0-11	kininogen 1	Homo sapiens	73-75
12732401-10	2003	Fenofibrate plus CoQ significantly improved (P&lt;0.05) the AUC for ACh, BK and SNP without significantly altering basal responses to L-NMMA.	coenzyme Q10	17-20	kininogen 1	Homo sapiens	73-75
12654707-9	2003	This effect is inhibited by either icatibant and or L-NMMA, suggesting that both bradykinin and NO contribute to the vascular effects of AT1-receptor antagonists in this patient population.	omega-N-Methylarginine	52-58	kininogen 1	Homo sapiens	81-91
12623947-2	2003	We compared intravenously administered ACE inhibitors, perindoprilat and enalaprilat, for myocardial drug uptake and effects on angiotensin and bradykinin peptides versus hemodynamic effects in 25 patients with stable angina and well-preserved left ventricular systolic function.	Enalaprilat	73-84	kininogen 1	Homo sapiens	144-154
12841944-3	2003	Ritanserin caused a rightward shift of serotonin-induced relaxation without decreasing maximum response at 10(-9) and 10(-8)M, but it inhibited the maximum relaxation response at 10(-7)M. The study showed that AT-1015 and ritanserin had no inhibitory effect on bradykinin-induced relaxation in porcine coronary artery with endothelium.	Ritanserin	0-10	kininogen 1	Homo sapiens	261-271
12841944-3	2003	Ritanserin caused a rightward shift of serotonin-induced relaxation without decreasing maximum response at 10(-9) and 10(-8)M, but it inhibited the maximum relaxation response at 10(-7)M. The study showed that AT-1015 and ritanserin had no inhibitory effect on bradykinin-induced relaxation in porcine coronary artery with endothelium.	N-(2-(4-(5H-dibenzo(a,d)cyclohepten-5-yliden)piperidino)ethyl)-1-formyl-4-piperidinecarboxamide	210-217	kininogen 1	Homo sapiens	261-271
12611975-7	2003	CMi(His+) units were most responsive to histamine and to PGE(2) and less to serotonin, ACh, bradykinin, and capsaicin.	Histidine	4-7	kininogen 1	Homo sapiens	92-102
12716436-6	2003	Pretreatment of cells with the maximal effective concentration of UDP reduced the subsequent carbachol- or bradykinin-induced [Ca2+]i rise without inhibition of IP3 generation.	Uridine Diphosphate	66-69	kininogen 1	Homo sapiens	107-117
12594217-0	2003	Differential tyrosine phosphorylation of plasma membrane Ca2+-ATPase and regulation of calcium pump activity by carbachol and bradykinin.	Tyrosine	13-21	kininogen 1	Homo sapiens	126-136
12594217-2	2003	After depletion of Ca(2+) stores by either TG, BK, or CCh, the addition of Ca(2+) gave a much larger rise in Ca(2+) levels in CCh-treated and TG-treated cells than in cells treated with BK.	Carbachol	126-129	kininogen 1	Homo sapiens	186-188
12594217-2	2003	After depletion of Ca(2+) stores by either TG, BK, or CCh, the addition of Ca(2+) gave a much larger rise in Ca(2+) levels in CCh-treated and TG-treated cells than in cells treated with BK.	Thapsigargin	142-144	kininogen 1	Homo sapiens	186-188
12594217-9	2003	An investigation of tyrosine phosphorylation levels of the plasma membrane Ca(2+)-ATPase (PMCA) demonstrated that CCh stimulates an increase in tyrosine phosphorylation levels, which has been reported to inhibit Ca(2+) pump activity, whereas in contrast, BK stimulates a reduction of PMCA tyrosine phosphorylation levels.	Carbachol	114-117	kininogen 1	Homo sapiens	255-257
12594217-9	2003	An investigation of tyrosine phosphorylation levels of the plasma membrane Ca(2+)-ATPase (PMCA) demonstrated that CCh stimulates an increase in tyrosine phosphorylation levels, which has been reported to inhibit Ca(2+) pump activity, whereas in contrast, BK stimulates a reduction of PMCA tyrosine phosphorylation levels.	Tyrosine	144-152	kininogen 1	Homo sapiens	255-257
12594217-9	2003	An investigation of tyrosine phosphorylation levels of the plasma membrane Ca(2+)-ATPase (PMCA) demonstrated that CCh stimulates an increase in tyrosine phosphorylation levels, which has been reported to inhibit Ca(2+) pump activity, whereas in contrast, BK stimulates a reduction of PMCA tyrosine phosphorylation levels.	Tyrosine	144-152	kininogen 1	Homo sapiens	255-257
12594217-10	2003	Thus, BK and CCh have a differential effect both on Ca(2+) pump activity and on tyrosine phosphorylation levels of the PMCA.	Tyrosine	80-88	kininogen 1	Homo sapiens	6-8
12684036-4	2003	Association of cPGES with Hsp90 was increased in cells stimulated with A23187 or bradykinin, accompanied by concomitant increases in cPGES activity and PGE(2) production.	Prostaglandins E	16-19	kininogen 1	Homo sapiens	81-91
12706934-8	2003	The increases in CBF induced by BK in the perindopril and losartan groups were significantly greater than those in the control group.	Perindopril	42-53	kininogen 1	Homo sapiens	32-34
12706934-8	2003	The increases in CBF induced by BK in the perindopril and losartan groups were significantly greater than those in the control group.	Losartan	58-66	kininogen 1	Homo sapiens	32-34
12706934-11	2003	CONCLUSIONS: Perindopril and losartan similarly augment BK-induced coronary vasodilation.	Perindopril	13-24	kininogen 1	Homo sapiens	56-58
12706934-11	2003	CONCLUSIONS: Perindopril and losartan similarly augment BK-induced coronary vasodilation.	Losartan	29-37	kininogen 1	Homo sapiens	56-58
12706934-12	2003	Perindopril may have a greater potential to enhance the BK-induced coronary release of t-PA than losartan.	Perindopril	0-11	kininogen 1	Homo sapiens	56-58
12706934-12	2003	Perindopril may have a greater potential to enhance the BK-induced coronary release of t-PA than losartan.	Losartan	97-105	kininogen 1	Homo sapiens	56-58
12657278-1	2003	The synthesis and structure-activity relationships of a novel series of aroylpyrrole alkylamides as potent selective bradykinin B(2) receptor antagonists are described.	aroylpyrrole alkylamides	72-96	kininogen 1	Homo sapiens	117-127
12620893-7	2003	We demonstrate 1) that optical recordings allow precise multisite measurements of voltage changes evoked by the extracellular signaling molecules ATP and bradykinin and 2) that responsiveness to ATP differs in various layers of cultured keratinocytes.	Adenosine Triphosphate	195-198	kininogen 1	Homo sapiens	154-170
12644415-10	2003	CONCLUSIONS: Iontophoresed acetylcholine and bradykinin significantly increase the flow-flux and impair THR in forearm skin, further validating the concept that THR represents true vasodilatation during arterial occlusion.	Threonine	104-107	kininogen 1	Homo sapiens	45-55
12644415-10	2003	CONCLUSIONS: Iontophoresed acetylcholine and bradykinin significantly increase the flow-flux and impair THR in forearm skin, further validating the concept that THR represents true vasodilatation during arterial occlusion.	Threonine	161-164	kininogen 1	Homo sapiens	45-55
12642509-5	2003	In controls, vasodilation to bradykinin was inhibited by L-NMMA and remained unchanged by ouabain or vitamin C.	omega-N-Methylarginine	57-63	kininogen 1	Homo sapiens	29-39
12642509-6	2003	In hypertensive patients, vasodilation to bradykinin was blunted and resistant to L-NMMA but sensitive to ouabain.	omega-N-Methylarginine	82-88	kininogen 1	Homo sapiens	42-52
12642509-6	2003	In hypertensive patients, vasodilation to bradykinin was blunted and resistant to L-NMMA but sensitive to ouabain.	Ouabain	106-113	kininogen 1	Homo sapiens	42-52
12642509-7	2003	Vitamin C increased the response to bradykinin and restored the inhibiting effect of L-NMMA while preventing the effect of ouabain.	Ascorbic Acid	0-9	kininogen 1	Homo sapiens	36-46
12642509-10	2003	Moreover, lercanidipine increased the vasodilation to bradykinin and restored the inhibiting effect of L-NMMA on bradykinin-induced vasodilation while preventing the effect of ouabain.	lercanidipine	10-23	kininogen 1	Homo sapiens	54-64
12642509-10	2003	Moreover, lercanidipine increased the vasodilation to bradykinin and restored the inhibiting effect of L-NMMA on bradykinin-induced vasodilation while preventing the effect of ouabain.	lercanidipine	10-23	kininogen 1	Homo sapiens	113-123
12642509-10	2003	Moreover, lercanidipine increased the vasodilation to bradykinin and restored the inhibiting effect of L-NMMA on bradykinin-induced vasodilation while preventing the effect of ouabain.	omega-N-Methylarginine	103-109	kininogen 1	Homo sapiens	113-123
12645517-3	2003	In addition, TAFIa has been shown to be capable of removing the carboxyl-terminal arginine residues from the anaphylatoxins and bradykinin, thus implying a role for the TAFI pathway in the vascular responses to inflammation.	Arginine	82-90	kininogen 1	Homo sapiens	128-138
12424093-2	2003	ANG II partially reversed the increase in [Ca(2+)](i) generated by cyclopiazonic acid (CPA; 10(-5) M), acetylcholine (ACh; 10(-5) M), or bradykinin (BK; 10(-7) M).	Acetylcholine	118-121	kininogen 1	Homo sapiens	137-147
12594059-0	2003	Bradykinin induces interleukin-6 production in human airway smooth muscle cells: modulation by Th2 cytokines and dexamethasone.	Dexamethasone	113-126	kininogen 1	Homo sapiens	0-10
12594059-6	2003	In contrast, BK-induced IL-6 secretion was enhanced by exogenous prostaglandin E(2) and salmeterol.	Dinoprostone	65-83	kininogen 1	Homo sapiens	13-15
12594059-6	2003	In contrast, BK-induced IL-6 secretion was enhanced by exogenous prostaglandin E(2) and salmeterol.	Salmeterol Xinafoate	88-98	kininogen 1	Homo sapiens	13-15
12594059-8	2003	Blocking ERK1/2 with PD98059 or p38 MAPK with SB203580 reduced BK-induced IL-6 expression.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	21-28	kininogen 1	Homo sapiens	63-65
12594059-8	2003	Blocking ERK1/2 with PD98059 or p38 MAPK with SB203580 reduced BK-induced IL-6 expression.	SB 203580	46-54	kininogen 1	Homo sapiens	63-65
12594059-10	2003	BK-induced, AP-1-dependent transcription was inhibited by indomethacin and dexamethasone.	Indomethacin	58-70	kininogen 1	Homo sapiens	0-2
12594059-10	2003	BK-induced, AP-1-dependent transcription was inhibited by indomethacin and dexamethasone.	Dexamethasone	75-88	kininogen 1	Homo sapiens	0-2
12594059-11	2003	Curcumin, an inhibitor of AP-1, also reduced BK-induced IL-6 expression.	Curcumin	0-8	kininogen 1	Homo sapiens	45-47
12675336-8	2003	The reversible labeling of Tyr-containing peptide was demonstrated with [Tyr8]-bradykinin as a model for high-molecular-mass peptides and proteins.	Tyrosine	27-30	kininogen 1	Homo sapiens	79-89
12607129-1	2003	OBJECTIVE: Although it has been shown recently that acetylcholine (ACh)-induced vasodilation of forearm resistance vessels is predominantly mediated by nitric oxide, direct biochemical evidence for eNOS stimulation by bradykinin (BK) in the human arterial circulation is still lacking.	Acetylcholine	52-65	kininogen 1	Homo sapiens	218-228
12607129-1	2003	OBJECTIVE: Although it has been shown recently that acetylcholine (ACh)-induced vasodilation of forearm resistance vessels is predominantly mediated by nitric oxide, direct biochemical evidence for eNOS stimulation by bradykinin (BK) in the human arterial circulation is still lacking.	Acetylcholine	67-70	kininogen 1	Homo sapiens	218-228
12717806-0	2003	Rapid optimization of the post-column fluorogenic ninhydrin reaction for the HPLC-based determination of bradykinin and related fragments.	Ninhydrin	50-59	kininogen 1	Homo sapiens	105-115
12623967-6	2003	Tissue kallikrein competed for [3H]bradykinin binding to B2R-GFP only at 1 micromol/L.	Tritium	32-34	kininogen 1	Homo sapiens	35-45
12639806-6	2003	BK is a vasoactive peptide that increases calcium levels inside the cells indirectly stimulating PKC.	Calcium	42-49	kininogen 1	Homo sapiens	0-2
12724039-0	2003	Thiorphan enhances bradykinin-induced vascular relaxation in hypoxic/hyperkalaemic porcine coronary artery.	Thiorphan	0-9	kininogen 1	Homo sapiens	19-29
12724039-5	2003	Experiments were performed to study the effects of 30 min pre-treatment with the NEP-inhibitor, thiorphan (10 microM), both at physiological and at low pO(2)s. Hypoxia inhibited the bradykinin-induced relaxation in porcine epicardial coronary arteries.	Thiorphan	96-105	kininogen 1	Homo sapiens	182-192
12724039-6	2003	In normoxia, thiorphan significantly enhanced the decrease of coronary tone produced by bradykinin (1-10 nM) when U46619 was used as contractile agent.	Thiorphan	13-22	kininogen 1	Homo sapiens	88-98
12724039-7	2003	Under hypoxic conditions, in U46619 contracture, thiorphan did not influence, but in KCl contracture it enhanced the magnitude of relaxations induced by bradykinin.	Thiorphan	49-58	kininogen 1	Homo sapiens	153-163
12724039-7	2003	Under hypoxic conditions, in U46619 contracture, thiorphan did not influence, but in KCl contracture it enhanced the magnitude of relaxations induced by bradykinin.	Potassium Chloride	85-88	kininogen 1	Homo sapiens	153-163
12535846-6	2003	Bradykinin (10(-6) M) stimulated a marked increase in the production of 6-keto-PGF(1alpha), PGE(2), and PGF(2alpha) and a small increase of PGD(2) by ECs.	6-keto-pgf	72-82	kininogen 1	Homo sapiens	0-10
12535846-6	2003	Bradykinin (10(-6) M) stimulated a marked increase in the production of 6-keto-PGF(1alpha), PGE(2), and PGF(2alpha) and a small increase of PGD(2) by ECs.	Prostaglandins E	92-95	kininogen 1	Homo sapiens	0-10
12535846-6	2003	Bradykinin (10(-6) M) stimulated a marked increase in the production of 6-keto-PGF(1alpha), PGE(2), and PGF(2alpha) and a small increase of PGD(2) by ECs.	Prostaglandins F	79-82	kininogen 1	Homo sapiens	0-10
12592377-6	2003	Bradykinin promotes phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis by PLC and translocation of various PKC isoforms from the cytosolic fraction to the particulate fraction.	Phosphatidylinositol 4,5-Diphosphate	20-57	kininogen 1	Homo sapiens	0-10
12592377-6	2003	Bradykinin promotes phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis by PLC and translocation of various PKC isoforms from the cytosolic fraction to the particulate fraction.	Phosphatidylinositol 4,5-Diphosphate	59-63	kininogen 1	Homo sapiens	0-10
12573493-6	2003	Cerivastatin and fluvastatin increase CYP 2C mRNA and protein in native and cultured endothelial cells, and enhance the bradykinin-induced NO/PGI(2)-independent relaxation of arterial segments as well as the generation of reactive oxygen species.	cerivastatin	0-12	kininogen 1	Homo sapiens	120-130
12573493-6	2003	Cerivastatin and fluvastatin increase CYP 2C mRNA and protein in native and cultured endothelial cells, and enhance the bradykinin-induced NO/PGI(2)-independent relaxation of arterial segments as well as the generation of reactive oxygen species.	Fluvastatin	17-28	kininogen 1	Homo sapiens	120-130
12573493-6	2003	Cerivastatin and fluvastatin increase CYP 2C mRNA and protein in native and cultured endothelial cells, and enhance the bradykinin-induced NO/PGI(2)-independent relaxation of arterial segments as well as the generation of reactive oxygen species.	Epoprostenol	142-148	kininogen 1	Homo sapiens	120-130
12573493-6	2003	Cerivastatin and fluvastatin increase CYP 2C mRNA and protein in native and cultured endothelial cells, and enhance the bradykinin-induced NO/PGI(2)-independent relaxation of arterial segments as well as the generation of reactive oxygen species.	Reactive Oxygen Species	222-245	kininogen 1	Homo sapiens	120-130
12568624-9	2003	At longer delay times, parent ions depletion is mainly determined by a slow decay rate and fragmentation efficiency curves for des-Arg(1) and des-Arg(9)-bradykinin diverge.	des-arg	142-149	kininogen 1	Homo sapiens	153-163
12568624-10	2003	Dissociation thresholds of 1.17 and 1.09 eV and activation entropies of -22.2 and -23.3 cal/(mol K) were obtained for des-Arg(1) and des-Arg(9)-bradykinin from RRKM modeling of time-resolved data.	des-arg	118-125	kininogen 1	Homo sapiens	144-154
12568624-10	2003	Dissociation thresholds of 1.17 and 1.09 eV and activation entropies of -22.2 and -23.3 cal/(mol K) were obtained for des-Arg(1) and des-Arg(9)-bradykinin from RRKM modeling of time-resolved data.	des-arg	133-140	kininogen 1	Homo sapiens	144-154
12568624-11	2003	Dissociation parameters for des-Arg(1)-bradykinin are in good agreement with parameters derived from thermal experiments.	des-arg	28-35	kininogen 1	Homo sapiens	39-49
12568624-12	2003	However, there is a significant discrepancy between the thermal data and dissociation parameters for des-Arg(9)-bradykinin obtained in this study.	des-arg	101-108	kininogen 1	Homo sapiens	112-122
12566370-8	2003	Enalaprilat increased the effect of exogenous bradykinin on FBF 60% (from 17.5+/-2.5 to 28.1+/-4.0 mL.	Enalaprilat	0-11	kininogen 1	Homo sapiens	46-56
12566370-10	2003	Enalaprilat increased the t-PA response to bradykinin to a greater extent than the FBF response, shifting the relationship between net t-PA release and FBF (P=0.005).	Enalaprilat	0-11	kininogen 1	Homo sapiens	43-53
12575983-6	2003	The increase in intracellular concentration of O2.- was followed by a dose-dependent reduction in basal and bradykinin-induced intracellular NO concentration (p from &lt;0.01 to &lt;0.001).	Superoxides	47-49	kininogen 1	Homo sapiens	108-118
12424096-6	2003	In isolated and pressurized small coronary arteries, N-vanillylnonanamide, apocynin, or uric acid, a peroxynitrite scavenger, largely restored the inhibitory effects of ceramide on bradykinin- and A-23187-induced vasorelaxation.	vanillyl-N-nonylamide	53-73	kininogen 1	Homo sapiens	181-191
12424096-6	2003	In isolated and pressurized small coronary arteries, N-vanillylnonanamide, apocynin, or uric acid, a peroxynitrite scavenger, largely restored the inhibitory effects of ceramide on bradykinin- and A-23187-induced vasorelaxation.	acetovanillone	75-83	kininogen 1	Homo sapiens	181-191
12424096-6	2003	In isolated and pressurized small coronary arteries, N-vanillylnonanamide, apocynin, or uric acid, a peroxynitrite scavenger, largely restored the inhibitory effects of ceramide on bradykinin- and A-23187-induced vasorelaxation.	Uric Acid	88-97	kininogen 1	Homo sapiens	181-191
12424096-6	2003	In isolated and pressurized small coronary arteries, N-vanillylnonanamide, apocynin, or uric acid, a peroxynitrite scavenger, largely restored the inhibitory effects of ceramide on bradykinin- and A-23187-induced vasorelaxation.	Ceramides	169-177	kininogen 1	Homo sapiens	181-191
12559981-3	2003	Based on the individual kinetic parameters calculated here, bradykinin is classified as a weak competitive inhibitor against hydrolysis of S-2238 and of a PAR4-like peptide.	S 2238	139-145	kininogen 1	Homo sapiens	60-70
12498258-4	2002	The combination of ampholyte 9-11 with pharmalyte 3-10 surprisingly provides baseline resolution between bradykinin (pI 12) and cytochrome c (pI 10.3).	ampholyte 9-11	19-33	kininogen 1	Homo sapiens	105-115
12733493-8	2003	In prevention of HSR associated with bradykinin in addition to elimination of a combination of a negatively charged dialysis membrane and ACEI treatment a part is played also by rinsing of the dialyzer before haemodialysis with a bicarbonate solution and the modification of the membrane surface (implemented by the manufacturer) which reduces its negative charge.	Bicarbonates	230-241	kininogen 1	Homo sapiens	37-47
12525155-3	2003	BK and S1P each elicited a sustained increase in phosphatidic acid content through a rapid and transient activation of PLD.	Phosphatidic Acids	49-66	kininogen 1	Homo sapiens	0-2
12525155-6	2003	In membranes, inhibition of PKCdelta by rottlerin enhanced BK activation of PLD but inhibited that by S1P.	rottlerin	40-49	kininogen 1	Homo sapiens	59-61
12525155-7	2003	Rottlerin inhibited activation of PLD in nuclei by both BK and S1P.	rottlerin	0-9	kininogen 1	Homo sapiens	56-58
12527416-8	2003	However, similar concentrations of KMV induce the release of cytochrome c from mitochondria into the cytosol, reduce basal [Ca(2+)](i) by 23% (P<0.005), and diminish the bradykinin (BK)-induced calcium release from the endoplasmic reticulum (ER) by 46% (P<0.005).	alpha-keto-beta-methylvaleric acid	35-38	kininogen 1	Homo sapiens	170-180
12531198-2	2003	Using des-Arg bradykinin as a template, we designed a series of intramolecularly quenched fluorogenic peptide substrates for ACE2.	des-arg	6-13	kininogen 1	Homo sapiens	14-24
12527738-11	2003	Finally, both bradykinin and NO donor released adenosine from superfused endothelial cells in vitro; L-NAME attenuated only the former response.	Adenosine	47-56	kininogen 1	Homo sapiens	14-24
12867160-1	2003	Bradykinin (1 microM) and histamine (100 microM) evoked an initial transient increase and a subsequent sustained increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) in fura-2-loaded human gingival fibroblasts, which may be attributed to Ca(2+) release from intracellular stores and Ca(2+) entry from extracellular sites, respectively.	Fura-2	177-183	kininogen 1	Homo sapiens	0-10
12867160-2	2003	In fibroblasts pretreated with tyrosine kinase inhibitors such as herbimycin A (1 microM) and tyrphostin 47 (20 microM), the sustained level of [Ca(2+)](i) induced by bradykinin and histamine increased, but not the initial peak level.	herbimycin	66-78	kininogen 1	Homo sapiens	167-177
12867160-2	2003	In fibroblasts pretreated with tyrosine kinase inhibitors such as herbimycin A (1 microM) and tyrphostin 47 (20 microM), the sustained level of [Ca(2+)](i) induced by bradykinin and histamine increased, but not the initial peak level.	Tyrphostins	94-104	kininogen 1	Homo sapiens	167-177
12867160-2	2003	In fibroblasts pretreated with tyrosine kinase inhibitors such as herbimycin A (1 microM) and tyrphostin 47 (20 microM), the sustained level of [Ca(2+)](i) induced by bradykinin and histamine increased, but not the initial peak level.	Histamine	182-191	kininogen 1	Homo sapiens	167-177
12867160-4	2003	Thapsigargin, an inhibitor of Ca(2+)-ATPase in inositol 1,4,5-trisphosphate-sensitive Ca(2+) stores, mimicked the effect of bradykinin and histamine.	Thapsigargin	0-12	kininogen 1	Homo sapiens	124-134
12867160-4	2003	Thapsigargin, an inhibitor of Ca(2+)-ATPase in inositol 1,4,5-trisphosphate-sensitive Ca(2+) stores, mimicked the effect of bradykinin and histamine.	Inositol 1,4,5-Trisphosphate	47-75	kininogen 1	Homo sapiens	124-134
12867160-5	2003	In the fibroblasts pretreated with tyrosine kinase inhibitors, the bradykinin-, histamine- and thapsigargin-induced Ca(2+) entry was clearly enhanced, but not the transient [Ca(2+)](i) increase.	Thapsigargin	95-107	kininogen 1	Homo sapiens	67-77
12501072-1	2002	OBJECTIVE: The purpose of this study was to evaluate whether a 3-hour incubation with 17beta-estradiol will enhance blood flow- and bradykinin-mediated dilatation and alter pressure-induced basal tone in myometrial resistance arteries from women with preeclampsia and to evaluate the role of nitric oxide in the responses that were observed.	Estradiol	86-102	kininogen 1	Homo sapiens	132-142
12466245-14	2002	Substance P, bradykinin (100 nM) and 1-EBIO evoked charybdotoxin-sensitive, iberiotoxin-insensitive whole-cell perforated-patch currents.	Charybdotoxin	51-64	kininogen 1	Homo sapiens	13-23
12466245-14	2002	Substance P, bradykinin (100 nM) and 1-EBIO evoked charybdotoxin-sensitive, iberiotoxin-insensitive whole-cell perforated-patch currents.	iberiotoxin	76-87	kininogen 1	Homo sapiens	13-23
14561183-6	2002	Precisely, bradykinin, and PGI(2) among the prostanoids, are major mediators for exudation and pain perception of the initial acute phase of inflammation; both mediators collaborate to enhance these effects.	Prostaglandins	44-55	kininogen 1	Homo sapiens	11-21
12553669-8	2002	We report that p70 S6 kinase (S6K)1 participates in this IF rearrangement since the inhibitor rapamycin or a dominant inhibitory S6K could reduce the Cdc42V12 or bradykinin-induced vimentin collapse.	Sirolimus	94-103	kininogen 1	Homo sapiens	162-172
12489800-3	2002	BK generation may be influenced by several agents, and the aim of this work was to investigate the effect of glycosaminoglycans (GAGs) on human high-molecular-weight kininogen (HK) hydrolysis by huPK and on inflammation.	Glycosaminoglycans	109-127	kininogen 1	Homo sapiens	144-175
12489802-2	2002	Cleaved HK (HKa) and its cell-binding domain 5 (D5), kininostatin, are potent antiangiogenic polypeptides.	kininostatin	53-65	kininogen 1	Homo sapiens	8-10
12444153-5	2002	Pretreatment of airway epithelial cells with BK or IL-1beta enhanced SDF-1alpha induced phospho-extracellular signal-regulated kinase and calcium mobilization, in addition to increasing the level of CXCR4 protein.	Calcium	138-145	kininogen 1	Homo sapiens	45-47
12505055-9	2002	Ang 1-9 and 1-7 augmented arachidonic acid and NO release by bradykinin.	Arachidonic Acid	26-42	kininogen 1	Homo sapiens	61-71
12512702-5	2002	Beta-AP (1-41) maximally stimulated phagocytosis at 0.1 microg/ml, BK--at 1.0 microg/ml, and fCTP--at 2.0 microg/ml.	beta-ap	0-7	kininogen 1	Homo sapiens	67-69
12456494-5	2002	Dilation to 10(-8) mol/L bradykinin (BK) was abolished in vessels exposed to ONOO- (-2.5+/-8%; P&lt;0.05) but not DC-ONOO- (65+/-8%).	onoo	77-81	kininogen 1	Homo sapiens	25-35
12456494-5	2002	Dilation to 10(-8) mol/L bradykinin (BK) was abolished in vessels exposed to ONOO- (-2.5+/-8%; P&lt;0.05) but not DC-ONOO- (65+/-8%).	onoo	77-81	kininogen 1	Homo sapiens	37-39
12433966-6	2002	Diclofenac significantly attenuated the bradykinin-induced relaxation only for the normotensive pregnant group (31 % inhibition, P &lt; 0.001).	Diclofenac	0-10	kininogen 1	Homo sapiens	40-50
12433966-7	2002	The bradykinin-induced membrane hyperpolarization consisted of diclofenac-sensitive and -insensitive components.	Diclofenac	63-73	kininogen 1	Homo sapiens	4-14
12433966-9	2002	The concentrations of 6-keto-PGF(1alpha) (a stable metabolite of prostacyclin) in these arteries were significantly lower in pre-eclampsia in both the absence and presence of bradykinin (about 0.2-0.4 times the normotensive pregnant value in each case, P &lt; 0.01).	6-keto-pgf	22-32	kininogen 1	Homo sapiens	175-185
12433966-9	2002	The concentrations of 6-keto-PGF(1alpha) (a stable metabolite of prostacyclin) in these arteries were significantly lower in pre-eclampsia in both the absence and presence of bradykinin (about 0.2-0.4 times the normotensive pregnant value in each case, P &lt; 0.01).	Epoprostenol	65-77	kininogen 1	Homo sapiens	175-185
12421548-6	2002	The basolateral OA/alpha-ketoglutarate exchange process now appears to be physiologically regulated by several factors in mammalian tubules, including peptide hormones (e.g., bradykinin) and the autonomic nervous system acting via protein kinase C (PKC) pathways and epidermal growth factor (EGF) working via the mitogen-activated protein kinase (MAPK) pathway.	Ketoglutaric Acids	19-38	kininogen 1	Homo sapiens	175-185
12376356-4	2002	Our results suggest that chronic exposure to fenoterol induces proinflammatory effects mediated by nuclear factor-kappaB and pathways involving leukotrienes, prostanoids, bradykinin, tachykinins, protein kinase C, and p38(MAPK), leading to the regulation of smooth muscle contraction to ET-1 and ACh.	Fenoterol	45-54	kininogen 1	Homo sapiens	171-181
12381678-2	2002	Bradykinin-induced changes in isometric force or smooth muscle membrane potential were assessed in rings of porcine renal interlobar artery preconstricted with the thromboxane analogue U46619 in the continuous presence of N(omega)-nitro-L-arginine and diclofenac to inhibit NO synthases and cyclo-oxygenases.	Thromboxanes	164-175	kininogen 1	Homo sapiens	0-10
12381678-2	2002	Bradykinin-induced changes in isometric force or smooth muscle membrane potential were assessed in rings of porcine renal interlobar artery preconstricted with the thromboxane analogue U46619 in the continuous presence of N(omega)-nitro-L-arginine and diclofenac to inhibit NO synthases and cyclo-oxygenases.	Nitroarginine	222-247	kininogen 1	Homo sapiens	0-10
12381678-2	2002	Bradykinin-induced changes in isometric force or smooth muscle membrane potential were assessed in rings of porcine renal interlobar artery preconstricted with the thromboxane analogue U46619 in the continuous presence of N(omega)-nitro-L-arginine and diclofenac to inhibit NO synthases and cyclo-oxygenases.	Diclofenac	252-262	kininogen 1	Homo sapiens	0-10
12381678-3	2002	3 Inhibition of NO- and PGI2-production induced a rightward shift in the concentration-relaxation curve to bradykinin without affecting maximal relaxation.	Epoprostenol	24-28	kininogen 1	Homo sapiens	107-117
12381678-5	2002	Charybdotoxin and apamin also reduced the bradykinin-induced, EDHF-mediated hyperpolarization of smooth muscle cells from 13.7+/-1.3 mV to 5.7+/-1.2 mV.	Charybdotoxin	0-13	kininogen 1	Homo sapiens	42-52
12381678-5	2002	Charybdotoxin and apamin also reduced the bradykinin-induced, EDHF-mediated hyperpolarization of smooth muscle cells from 13.7+/-1.3 mV to 5.7+/-1.2 mV.	edhf	62-66	kininogen 1	Homo sapiens	42-52
12381678-7	2002	A low concentration of ouabain (100 nM) abolished the EDHF-mediated relaxation and reduced the bradykinin-induced hyperpolarization of smooth muscle cells (13.6+/-2.8 mV versus 5.20+/-1.39 mV in the absence and presence of ouabain).	Ouabain	23-30	kininogen 1	Homo sapiens	95-105
12381678-7	2002	A low concentration of ouabain (100 nM) abolished the EDHF-mediated relaxation and reduced the bradykinin-induced hyperpolarization of smooth muscle cells (13.6+/-2.8 mV versus 5.20+/-1.39 mV in the absence and presence of ouabain).	Ouabain	223-230	kininogen 1	Homo sapiens	95-105
12643465-5	2002	Ligation of adrenergic, adenosine, bradykinin or opioid receptors involves signaling via both tyrosine and calcium-dependent protein kinases (PKC), which activate mitochondrial ATP-dependent potassium channels.	Adenosine	24-33	kininogen 1	Homo sapiens	35-45
12487427-0	2002	Investigation of bradykinin metabolism in human and rat plasma in the presence of the dual ACE/NEP inhibitors GW660511X and omapatrilat.	GW660511X	110-119	kininogen 1	Homo sapiens	17-27
12487427-0	2002	Investigation of bradykinin metabolism in human and rat plasma in the presence of the dual ACE/NEP inhibitors GW660511X and omapatrilat.	omapatrilat	124-135	kininogen 1	Homo sapiens	17-27
12372901-6	2002	A low concentration (6 micromol/l) of riluzole selectively potentiated the bradykinin (but not ATP and histamine)-induced increase in [Ca(2+)](i).	Riluzole	38-46	kininogen 1	Homo sapiens	75-85
12372905-4	2002	Pretreatment of the neutrophils with the B(2) receptor antagonist HOE-140 (icatibant) inhibited the bradykinin-induced migration but not that induced by B(1) receptor agonists, whereas the B(1 )receptor antagonist des-Arg(10)HOE-140 abolished the migration elicited by des-Arg(9)-bradykinin or des-Arg(10)-kallidin but not that evoked by bradykinin.	des-arg	269-276	kininogen 1	Homo sapiens	100-110
12372905-5	2002	Pretreatment of the neutrophils with the leukotriene B(4) (LTB(4)) antagonist ZK158252 inhibited the LTB(4)-induced chemotaxis as well as the chemotaxis produced by bradykinin and des-Arg(10)-kallidin.	Leukotriene B4	41-54	kininogen 1	Homo sapiens	165-175
12372905-5	2002	Pretreatment of the neutrophils with the leukotriene B(4) (LTB(4)) antagonist ZK158252 inhibited the LTB(4)-induced chemotaxis as well as the chemotaxis produced by bradykinin and des-Arg(10)-kallidin.	ZK-158252	78-86	kininogen 1	Homo sapiens	165-175
12372905-5	2002	Pretreatment of the neutrophils with the leukotriene B(4) (LTB(4)) antagonist ZK158252 inhibited the LTB(4)-induced chemotaxis as well as the chemotaxis produced by bradykinin and des-Arg(10)-kallidin.	Leukotriene B4	59-62	kininogen 1	Homo sapiens	165-175
12384249-0	2002	Bradykinin increases permeability by calcium and 5-lipoxygenase in the ECV304/C6 cell culture model of the blood-brain barrier.	Calcium	37-44	kininogen 1	Homo sapiens	0-10
12384249-2	2002	The inflammatory mediator bradykinin (1 microM) was studied and found to induce a fall in TEER; the link between this change and intracellular free calcium concentration ([Ca(2+)](i)) was then examined.	Calcium	148-155	kininogen 1	Homo sapiens	26-36
12384249-8	2002	The putative phospholipase C inhibitors, U73122 (20 microM) and ETH-18-OCH(3) (100 microM), unexpectedly increased [Ca(2+)](i); after their application, bradykinin was ineffective.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	41-47	kininogen 1	Homo sapiens	153-163
12384249-8	2002	The putative phospholipase C inhibitors, U73122 (20 microM) and ETH-18-OCH(3) (100 microM), unexpectedly increased [Ca(2+)](i); after their application, bradykinin was ineffective.	eth-18-och	64-74	kininogen 1	Homo sapiens	153-163
12384249-10	2002	The fall in TEER from bradykinin was blocked by HOE 140, U73122 and thapsigargin combined with La(3+), and also by aristolochic acid and NDGA, but not indomethacin, calphostin C or L-NAME.	4-hydroxy-2-octenal	48-51	kininogen 1	Homo sapiens	22-32
12384249-10	2002	The fall in TEER from bradykinin was blocked by HOE 140, U73122 and thapsigargin combined with La(3+), and also by aristolochic acid and NDGA, but not indomethacin, calphostin C or L-NAME.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	57-63	kininogen 1	Homo sapiens	22-32
12384249-10	2002	The fall in TEER from bradykinin was blocked by HOE 140, U73122 and thapsigargin combined with La(3+), and also by aristolochic acid and NDGA, but not indomethacin, calphostin C or L-NAME.	Thapsigargin	68-80	kininogen 1	Homo sapiens	22-32
12384249-10	2002	The fall in TEER from bradykinin was blocked by HOE 140, U73122 and thapsigargin combined with La(3+), and also by aristolochic acid and NDGA, but not indomethacin, calphostin C or L-NAME.	lanthanum(3+)	95-101	kininogen 1	Homo sapiens	22-32
12384249-10	2002	The fall in TEER from bradykinin was blocked by HOE 140, U73122 and thapsigargin combined with La(3+), and also by aristolochic acid and NDGA, but not indomethacin, calphostin C or L-NAME.	aristolochic acid I	115-132	kininogen 1	Homo sapiens	22-32
12384249-10	2002	The fall in TEER from bradykinin was blocked by HOE 140, U73122 and thapsigargin combined with La(3+), and also by aristolochic acid and NDGA, but not indomethacin, calphostin C or L-NAME.	Masoprocol	137-141	kininogen 1	Homo sapiens	22-32
12384249-10	2002	The fall in TEER from bradykinin was blocked by HOE 140, U73122 and thapsigargin combined with La(3+), and also by aristolochic acid and NDGA, but not indomethacin, calphostin C or L-NAME.	calphostin C	165-177	kininogen 1	Homo sapiens	22-32
12384249-10	2002	The fall in TEER from bradykinin was blocked by HOE 140, U73122 and thapsigargin combined with La(3+), and also by aristolochic acid and NDGA, but not indomethacin, calphostin C or L-NAME.	NG-Nitroarginine Methyl Ester	181-187	kininogen 1	Homo sapiens	22-32
12384249-12	2002	Thus bradykinin reduced TEER through B(2) receptor-linked release of Ca(2+) from thapsigargin-sensitive stores, leading to activation of PLA(2) and metabolism of arachidonic acid by 5-lipoxygenase.	Thapsigargin	81-93	kininogen 1	Homo sapiens	5-15
12384249-12	2002	Thus bradykinin reduced TEER through B(2) receptor-linked release of Ca(2+) from thapsigargin-sensitive stores, leading to activation of PLA(2) and metabolism of arachidonic acid by 5-lipoxygenase.	Arachidonic Acid	162-178	kininogen 1	Homo sapiens	5-15
12392844-4	2002	Nitric oxide (NO) bioactivity was represented by both basal and bradykinin-stimulated cellular cyclic guanosine monophosphate accumulation and L-citrulline conversion from L-arginine.	Nitric Oxide	0-12	kininogen 1	Homo sapiens	64-74
12392844-4	2002	Nitric oxide (NO) bioactivity was represented by both basal and bradykinin-stimulated cellular cyclic guanosine monophosphate accumulation and L-citrulline conversion from L-arginine.	Cyclic GMP	95-125	kininogen 1	Homo sapiens	64-74
12392844-4	2002	Nitric oxide (NO) bioactivity was represented by both basal and bradykinin-stimulated cellular cyclic guanosine monophosphate accumulation and L-citrulline conversion from L-arginine.	Citrulline	143-155	kininogen 1	Homo sapiens	64-74
12392844-4	2002	Nitric oxide (NO) bioactivity was represented by both basal and bradykinin-stimulated cellular cyclic guanosine monophosphate accumulation and L-citrulline conversion from L-arginine.	Arginine	172-182	kininogen 1	Homo sapiens	64-74
12225948-3	2002	Bradykinin, transforming growth factor-beta1 (TGF-beta1), and interleukin-1beta (IL-1beta) increased inducible COX-2 expression and prostaglandin E(2) (PGE(2)) release.	Prostaglandins E	132-147	kininogen 1	Homo sapiens	0-10
12225948-3	2002	Bradykinin, transforming growth factor-beta1 (TGF-beta1), and interleukin-1beta (IL-1beta) increased inducible COX-2 expression and prostaglandin E(2) (PGE(2)) release.	Prostaglandins E	152-155	kininogen 1	Homo sapiens	0-10
12452440-0	2002	The hyaluronan-binding serine protease from human plasma cleaves HMW and LMW kininogen and releases bradykinin.	Hyaluronic Acid	4-14	kininogen 1	Homo sapiens	100-110
12352318-0	2002	Calcium antagonist clevidipine reduces myocardial reperfusion injury by a mechanism related to bradykinin and nitric oxide.	Calcium	0-7	kininogen 1	Homo sapiens	95-105
12352318-0	2002	Calcium antagonist clevidipine reduces myocardial reperfusion injury by a mechanism related to bradykinin and nitric oxide.	clevidipine	19-30	kininogen 1	Homo sapiens	95-105
12352318-1	2002	Certain calcium antagonists, in addition to their classic actions, can increase blood flow during ischemia via bradykinin- and nitric oxide (NO)-dependent mechanisms and protect the ischemic myocardium against reperfusion injury by enhancing NO bioavailability.	Calcium	8-15	kininogen 1	Homo sapiens	111-121
12352318-2	2002	The current study aimed to investigate the possible involvement of bradykinin and NO in the cardioprotective action of the short-acting calcium antagonist clevidipine during late ischemia and reperfusion.	clevidipine	155-166	kininogen 1	Homo sapiens	67-77
12352318-10	2002	The results suggest that the cardioprotective effect of clevidipine during late ischemia and early reperfusion is mediated via bradykinin- and NO-related mechanisms.	clevidipine	56-67	kininogen 1	Homo sapiens	127-145
12235256-0	2002	Angiotensin-converting enzyme inhibitor-associated angioedema is characterized by a slower degradation of des-arginine(9)-bradykinin.	des-arginine	106-118	kininogen 1	Homo sapiens	122-132
12460556-4	2002	The elevation of Erk1/2 phosphorylation occurred immediately after BK stimulation and required an IP3-sensitive Ca(2+) release as well as activation of PKC and c-src as upstream events.	Inositol 1,4,5-Trisphosphate	98-101	kininogen 1	Homo sapiens	67-69
12460556-5	2002	Treatment of cells with the PI-3 kinase blocker LY924002 partially inhibited the BK-stimulated Erk1/2 phosphorylation in AC, but had no effect in AD cells, suggesting that the BK-induced Erk1/2 phosphorylation in AD cells is independent of PI-3 kinase.	ly924002	48-56	kininogen 1	Homo sapiens	81-83
12460556-5	2002	Treatment of cells with the PI-3 kinase blocker LY924002 partially inhibited the BK-stimulated Erk1/2 phosphorylation in AC, but had no effect in AD cells, suggesting that the BK-induced Erk1/2 phosphorylation in AD cells is independent of PI-3 kinase.	ly924002	48-56	kininogen 1	Homo sapiens	176-178
12460556-6	2002	Activation of the cAMP-responsive element binding protein (CREB) monitored as an increase in phosphorylation at Ser-133 was also observed after BK stimulation.	Serine	112-115	kininogen 1	Homo sapiens	144-146
12395949-3	2002	Thus, a two-step isocratic SDC protocol was developed and applied to the purification of important biologically active peptides, i.e. bradykinin antagonists of 10 and 11 residues.	S-[2-(Aminosulfonyl)ethyl]-D-Cysteine	27-30	kininogen 1	Homo sapiens	134-144
12190800-5	2002	RESULTS: PGE1 concentration-dependently (&gt;3 ng/ml) inhibited aggregation: the incubation buffer from PAE cells stimulated by bradykinin also inhibited aggregation.	Alprostadil	9-13	kininogen 1	Homo sapiens	128-138
12190800-7	2002	The half-maximum effective concentration of bradykinin to inhibit aggregation (95.4+/-22.3 nM) was significantly decreased to 10.3+/-2.5 nM by 0.1 ng/ml PGE1 and to 0.9+/-0.5 nM by 1 ng/ml PGE1, respectively.	Alprostadil	153-157	kininogen 1	Homo sapiens	44-54
12190800-7	2002	The half-maximum effective concentration of bradykinin to inhibit aggregation (95.4+/-22.3 nM) was significantly decreased to 10.3+/-2.5 nM by 0.1 ng/ml PGE1 and to 0.9+/-0.5 nM by 1 ng/ml PGE1, respectively.	Alprostadil	189-193	kininogen 1	Homo sapiens	44-54
12169581-0	2002	Bradykinin increases IL-8 generation in airway epithelial cells via COX-2-derived prostanoids.	Prostaglandins	82-93	kininogen 1	Homo sapiens	0-10
12169581-2	2002	Here we tested the hypothesis that bradykinin, an inflammatory mediator and chloride secretagogue, would increase IL-8 generation in airway epithelial cells through autocrine generation of endogenous prostanoids.	Chlorides	76-84	kininogen 1	Homo sapiens	35-45
12169581-2	2002	Here we tested the hypothesis that bradykinin, an inflammatory mediator and chloride secretagogue, would increase IL-8 generation in airway epithelial cells through autocrine generation of endogenous prostanoids.	Prostaglandins	200-211	kininogen 1	Homo sapiens	35-45
12169581-3	2002	Bradykinin increased IL-8 generation in both a non-cystic fibrosis (A549) and cystic fibrosis epithelial cell line (CFTE29) that was inhibited by the nonselective cyclooxygenase (COX) inhibitor indomethacin and the COX-2 selective inhibitor NS-398.	Indomethacin	194-206	kininogen 1	Homo sapiens	0-10
12169581-3	2002	Bradykinin increased IL-8 generation in both a non-cystic fibrosis (A549) and cystic fibrosis epithelial cell line (CFTE29) that was inhibited by the nonselective cyclooxygenase (COX) inhibitor indomethacin and the COX-2 selective inhibitor NS-398.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	241-247	kininogen 1	Homo sapiens	0-10
12181110-5	2002	Indomethacin (Indo; 10(-5) M) alone had no effect on dilation to BK in any groups, but Indo and N(omega)-nitro-L-arginine methyl ester (L-NAME; 10(-4) M) reduced dilation to BK in Pre-W more than in Y-M. L-NAME increased dilation to BK in subcutaneous fat from Y-M but had no effect in Post-W and O-M. Indo- and L-NAME-resistant dilation in all vessels was markedly reduced by 30 mM KCl.	NG-Nitroarginine Methyl Ester	96-134	kininogen 1	Homo sapiens	174-176
12181110-5	2002	Indomethacin (Indo; 10(-5) M) alone had no effect on dilation to BK in any groups, but Indo and N(omega)-nitro-L-arginine methyl ester (L-NAME; 10(-4) M) reduced dilation to BK in Pre-W more than in Y-M. L-NAME increased dilation to BK in subcutaneous fat from Y-M but had no effect in Post-W and O-M. Indo- and L-NAME-resistant dilation in all vessels was markedly reduced by 30 mM KCl.	NG-Nitroarginine Methyl Ester	96-134	kininogen 1	Homo sapiens	174-176
12181155-3	2002	With the use of fluorescence microscopic imaging analysis, a calcium ionophore, A-23187 (2 microM), and bradykinin (2 microM) were found to increase endothelial [NO](i) in freshly dissected lumen-opened small renal arteries loaded with 4,5-diaminofluorescein diacetate (DAF-2DA; 10 microM).	4,5-diaminofluorescein diacetate	236-268	kininogen 1	Homo sapiens	104-114
12181155-3	2002	With the use of fluorescence microscopic imaging analysis, a calcium ionophore, A-23187 (2 microM), and bradykinin (2 microM) were found to increase endothelial [NO](i) in freshly dissected lumen-opened small renal arteries loaded with 4,5-diaminofluorescein diacetate (DAF-2DA; 10 microM).	4,5-diaminofluorescein diacetate	270-277	kininogen 1	Homo sapiens	104-114
12372905-4	2002	Pretreatment of the neutrophils with the B(2) receptor antagonist HOE-140 (icatibant) inhibited the bradykinin-induced migration but not that induced by B(1) receptor agonists, whereas the B(1 )receptor antagonist des-Arg(10)HOE-140 abolished the migration elicited by des-Arg(9)-bradykinin or des-Arg(10)-kallidin but not that evoked by bradykinin.	des-arg	214-221	kininogen 1	Homo sapiens	100-110
12372905-4	2002	Pretreatment of the neutrophils with the B(2) receptor antagonist HOE-140 (icatibant) inhibited the bradykinin-induced migration but not that induced by B(1) receptor agonists, whereas the B(1 )receptor antagonist des-Arg(10)HOE-140 abolished the migration elicited by des-Arg(9)-bradykinin or des-Arg(10)-kallidin but not that evoked by bradykinin.	des-arg	269-276	kininogen 1	Homo sapiens	100-110
12231370-6	2002	RESULTS: Exposure to cyclosporine and mycophenolate mofetil was associated with a dose-dependent decrease in endothelium-dependent relaxations to serotonin (an agonist that binds to 5-HT1D receptors coupled to Gi-protein) but no impairment of relaxations to bradykinin (an agonist that binds to B2 receptors coupled to Gq-proteins).	Cyclosporine	21-33	kininogen 1	Homo sapiens	258-268
12630551-5	2002	The EDHF-mediated relaxation was induced by bradykinin (BK, -10 approximately -6.5 log M) after U46619 (-8 log M, in group I) or K+-precontraction (in group II) in the presence of indomethacin (7 microM), NG-nitro-L-arginine (300 microM), and hemoglobin (20 microM).	edhf	4-8	kininogen 1	Homo sapiens	44-54
12630551-5	2002	The EDHF-mediated relaxation was induced by bradykinin (BK, -10 approximately -6.5 log M) after U46619 (-8 log M, in group I) or K+-precontraction (in group II) in the presence of indomethacin (7 microM), NG-nitro-L-arginine (300 microM), and hemoglobin (20 microM).	edhf	4-8	kininogen 1	Homo sapiens	56-58
12630551-8	2002	Procaine decreased the BK-induced hyperpolarization from -72.3 +/- 0.7 mV to -68.8 +/- 0.8 mV (-6.5 log M, p &lt; 0.01).	Procaine	0-8	kininogen 1	Homo sapiens	23-25
12231370-6	2002	RESULTS: Exposure to cyclosporine and mycophenolate mofetil was associated with a dose-dependent decrease in endothelium-dependent relaxations to serotonin (an agonist that binds to 5-HT1D receptors coupled to Gi-protein) but no impairment of relaxations to bradykinin (an agonist that binds to B2 receptors coupled to Gq-proteins).	Mycophenolic Acid	38-59	kininogen 1	Homo sapiens	258-268
12231370-6	2002	RESULTS: Exposure to cyclosporine and mycophenolate mofetil was associated with a dose-dependent decrease in endothelium-dependent relaxations to serotonin (an agonist that binds to 5-HT1D receptors coupled to Gi-protein) but no impairment of relaxations to bradykinin (an agonist that binds to B2 receptors coupled to Gq-proteins).	Serotonin	146-155	kininogen 1	Homo sapiens	258-268
12231370-7	2002	Exposure to tacrolimus and rapamycin caused severe impairment of relaxations to serotonin and a lesser one to bradykinin.	Tacrolimus	12-22	kininogen 1	Homo sapiens	110-120
12231370-7	2002	Exposure to tacrolimus and rapamycin caused severe impairment of relaxations to serotonin and a lesser one to bradykinin.	Sirolimus	27-36	kininogen 1	Homo sapiens	110-120
12222553-3	2002	An increase in bradykinin levels results in continued prostaglandin E2 synthesis, vasodilation, increased vascular permeability, and increased interstitial fluid.	Dinoprostone	54-70	kininogen 1	Homo sapiens	15-25
12215601-7	2002	Maximum relaxation to bradykinin (1 micromol/L, an endothelium-dependent agonist) was 77+/-11% (mean+/-SE) after AdBglII and 31+/-22% (P&lt;0.05) after AdiNOS.	adbglii	113-120	kininogen 1	Homo sapiens	22-32
12215601-7	2002	Maximum relaxation to bradykinin (1 micromol/L, an endothelium-dependent agonist) was 77+/-11% (mean+/-SE) after AdBglII and 31+/-22% (P&lt;0.05) after AdiNOS.	adinos	152-158	kininogen 1	Homo sapiens	22-32
12215601-9	2002	Responses to both nitroprusside and bradykinin were improved by aminoguanidine (300 micromol/L), an inhibitor of iNOS.	pimagedine	64-78	kininogen 1	Homo sapiens	36-46
12011093-4	2002	Assays using human plasma showed that hamadarin dose-dependently inhibits activation of the plasma contact system and subsequent release of bradykinin, a primary mediator of inflammatory reactions.	hamadarin	38-47	kininogen 1	Homo sapiens	140-150
12011093-8	2002	We propose that hamadarin may attenuate the host"s acute inflammatory responses to the mosquito"s bites by inhibition of bradykinin release and thus enable mosquitoes to take a blood meal efficiently and safely.	hamadarin	16-25	kininogen 1	Homo sapiens	121-131
12163339-5	2002	Responses to bradykinin were attenuated in the presence of the gap junction inhibitors 18-alpha-glycyrrhetinic acid (18-alpha GA, 100 micro M), carbenoxolone (100 micro M) and palmitoleic acid (50 micro M).	18alpha-glycyrrhetinic acid	87-115	kininogen 1	Homo sapiens	13-23
12163339-5	2002	Responses to bradykinin were attenuated in the presence of the gap junction inhibitors 18-alpha-glycyrrhetinic acid (18-alpha GA, 100 micro M), carbenoxolone (100 micro M) and palmitoleic acid (50 micro M).	Carbenoxolone	144-157	kininogen 1	Homo sapiens	13-23
12163339-5	2002	Responses to bradykinin were attenuated in the presence of the gap junction inhibitors 18-alpha-glycyrrhetinic acid (18-alpha GA, 100 micro M), carbenoxolone (100 micro M) and palmitoleic acid (50 micro M).	palmitoleic acid	176-192	kininogen 1	Homo sapiens	13-23
12163339-6	2002	SR141716A, the CB(1) receptor antagonist attenuated responses to bradykinin, but only at high concentrations (10 micro M).	Rimonabant	0-9	kininogen 1	Homo sapiens	65-75
12163339-7	2002	These results suggest that gap junctional communication is involved in the nitric oxide (NO)- and prostanoid-independent vasodilator responses to bradykinin in myometrial small arteries in normal pregnancy.	Nitric Oxide	75-87	kininogen 1	Homo sapiens	146-156
12163339-7	2002	These results suggest that gap junctional communication is involved in the nitric oxide (NO)- and prostanoid-independent vasodilator responses to bradykinin in myometrial small arteries in normal pregnancy.	Prostaglandins	98-108	kininogen 1	Homo sapiens	146-156
12163354-0	2002	Charybdotoxin-sensitive small conductance K(Ca) channel activated by bradykinin and substance P in endothelial cells.	Charybdotoxin	0-13	kininogen 1	Homo sapiens	69-79
12163354-9	2002	Charybdotoxin inhibited by 75% the bradykinin-induced current and by 80% the substance P-induced current.	Charybdotoxin	0-13	kininogen 1	Homo sapiens	35-45
12163354-10	2002	Charybdotoxin plus iberiotoxin (50 nM each) inhibited by 97% the bradykinin-response.	Charybdotoxin	0-13	kininogen 1	Homo sapiens	65-75
12163354-10	2002	Charybdotoxin plus iberiotoxin (50 nM each) inhibited by 97% the bradykinin-response.	iberiotoxin	19-30	kininogen 1	Homo sapiens	65-75
12190655-3	2002	OBJECTIVE: The study aimed to determine if airways hyper-responsiveness to bradykinin provides a more sensitive index of glucocorticoid responsiveness in asthmatic subjects than does hyper-responsiveness to methacholine.	Methacholine Chloride	207-219	kininogen 1	Homo sapiens	75-85
12190655-8	2002	Fluticasone treatment significantly reduced responsiveness to bradykinin (P &lt; 0.001 by Friedman anova) and methacholine (P = 0.02), but changes in responsiveness to bradykinin were significantly greater than those in methacholine responsiveness (P = 0.002).	Fluticasone	0-11	kininogen 1	Homo sapiens	62-72
12190655-8	2002	Fluticasone treatment significantly reduced responsiveness to bradykinin (P &lt; 0.001 by Friedman anova) and methacholine (P = 0.02), but changes in responsiveness to bradykinin were significantly greater than those in methacholine responsiveness (P = 0.002).	Fluticasone	0-11	kininogen 1	Homo sapiens	168-178
12190655-11	2002	By contrast, DeltaLog PD20 for bradykinin was significantly greater in patients receiving fluticasone compared to those on placebo at all but the 16-week treatment time.	Fluticasone	90-101	kininogen 1	Homo sapiens	31-41
12190655-12	2002	Ten of 13 subjects receiving fluticasone failed, on at least one post-treatment visit, to show a 20% fall in forced expiratory volume (FEV1), even at the highest dose of bradykinin.	Fluticasone	29-40	kininogen 1	Homo sapiens	170-180
12210201-3	2002	Limits of detection of 3 and 18 fmoles (at a signal-to-noise ratio equal to 3) were achieved for fluorescamine-derivatized bradykinin and lysine, respectively.	Fluorescamine	97-110	kininogen 1	Homo sapiens	123-133
12154194-1	2002	Bradykinin is known to cause vasodilatation in resistance vessels and may, together with adenosine, be an important regulator of tissue blood flow during exercise.	Adenosine	89-98	kininogen 1	Homo sapiens	0-10
12110002-8	2002	The inhibitory effect of BK on IGF-I-induced activation of Erk 1 and 2 was completely abolished by addition of a B2 antagonist, by chelation of intracellular calcium and by tyrosine phosphatase inhibition.	Calcium	158-165	kininogen 1	Homo sapiens	25-27
12167797-6	2002	RESULTS: In group I, 20-mmol/L potassium ion greatly reduced the bradykinin-induced relaxation (35.0% +/- 4.9% vs 86.0% +/- 5.3%, P &lt;.001), which was significantly restored by magnesium ion (51.9% +/- 4.0%, P =.017).	Potassium	31-40	kininogen 1	Homo sapiens	65-75
12167797-6	2002	RESULTS: In group I, 20-mmol/L potassium ion greatly reduced the bradykinin-induced relaxation (35.0% +/- 4.9% vs 86.0% +/- 5.3%, P &lt;.001), which was significantly restored by magnesium ion (51.9% +/- 4.0%, P =.017).	Magnesium	179-188	kininogen 1	Homo sapiens	65-75
12167797-8	2002	In group IV, potassium ion depolarized the smooth muscle and decreased the bradykinin-induced hyperpolarization (-72.0 +/- 1.5 vs -61.7 +/- 0.7 mV, n = 7, P &lt;.001), which was significantly restored by magnesium ion (-68.0 +/- 2.5 mV vs -72.5 +/- 1.5 mV, n = 6, P =.029).	Potassium	13-22	kininogen 1	Homo sapiens	75-85
12167797-8	2002	In group IV, potassium ion depolarized the smooth muscle and decreased the bradykinin-induced hyperpolarization (-72.0 +/- 1.5 vs -61.7 +/- 0.7 mV, n = 7, P &lt;.001), which was significantly restored by magnesium ion (-68.0 +/- 2.5 mV vs -72.5 +/- 1.5 mV, n = 6, P =.029).	Magnesium	204-213	kininogen 1	Homo sapiens	75-85
12372699-5	2002	This effect of BK(1-9) (10(-6) M) was mimicked by the B2 agonist [Phe(8)(CH(2)NH)Arg(9)]-bradykinin (10(-5) M) and blocked by the selective B2-receptor antagonist HOE140 (10(-5) M).	Phenylalanine	66-69	kininogen 1	Homo sapiens	89-99
12372699-5	2002	This effect of BK(1-9) (10(-6) M) was mimicked by the B2 agonist [Phe(8)(CH(2)NH)Arg(9)]-bradykinin (10(-5) M) and blocked by the selective B2-receptor antagonist HOE140 (10(-5) M).	Arginine	81-84	kininogen 1	Homo sapiens	89-99
12174832-3	2002	Quercetin pre-treatment (88.7 micromol/kg p.o., 45 min; 14.7 micromol/kg i.v., 5 min) significantly potentiated the hypotensive effect of bradykinin (10 nmol/kg i.v.).	Quercetin	0-9	kininogen 1	Homo sapiens	138-148
12097645-3	2002	This study demonstrates that bradykinin, acting at B2 bradykinin receptors, excites sensory nerve endings by activating capsaicin receptors via production of 12-lipoxygenase metabolites of arachidonic acid.	Arachidonic Acid	189-205	kininogen 1	Homo sapiens	29-39
12097645-3	2002	This study demonstrates that bradykinin, acting at B2 bradykinin receptors, excites sensory nerve endings by activating capsaicin receptors via production of 12-lipoxygenase metabolites of arachidonic acid.	Arachidonic Acid	189-205	kininogen 1	Homo sapiens	54-64
12063315-0	2002	Hydrogen peroxide acts as an EDHF in the piglet pial vasculature in response to bradykinin.	Hydrogen Peroxide	0-17	kininogen 1	Homo sapiens	80-90
12063315-2	2002	Topically applied BK (3 micromol/l) induced vasodilation (62 +/- 12%) after the administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) and indomethacin, which was inhibited by endothelial impairment or by the BK(2) receptor antagonist HOE-140 (0.3 micromol/l).	NG-Nitroarginine Methyl Ester	98-136	kininogen 1	Homo sapiens	18-20
12063315-2	2002	Topically applied BK (3 micromol/l) induced vasodilation (62 +/- 12%) after the administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) and indomethacin, which was inhibited by endothelial impairment or by the BK(2) receptor antagonist HOE-140 (0.3 micromol/l).	NG-Nitroarginine Methyl Ester	138-144	kininogen 1	Homo sapiens	18-20
12063315-2	2002	Topically applied BK (3 micromol/l) induced vasodilation (62 +/- 12%) after the administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) and indomethacin, which was inhibited by endothelial impairment or by the BK(2) receptor antagonist HOE-140 (0.3 micromol/l).	Indomethacin	150-162	kininogen 1	Homo sapiens	18-20
12063315-8	2002	We conclude that H(2)O(2) mediates the non-nitric oxide-, non-prostanoid-dependent vasorelaxation to BK in the piglet pial vasculature.	Hydrogen Peroxide	17-25	kininogen 1	Homo sapiens	101-103
12063315-8	2002	We conclude that H(2)O(2) mediates the non-nitric oxide-, non-prostanoid-dependent vasorelaxation to BK in the piglet pial vasculature.	Nitric Oxide	43-55	kininogen 1	Homo sapiens	101-103
12063315-8	2002	We conclude that H(2)O(2) mediates the non-nitric oxide-, non-prostanoid-dependent vasorelaxation to BK in the piglet pial vasculature.	Prostaglandins	62-72	kininogen 1	Homo sapiens	101-103
12118747-4	2002	The endothelium-derived hyperpolarizing factor-mediated relaxation to bradykinin was studied in the rings precontracted with U46619 in the presence of N(omega)-nitro-L-arginine and indomethacin.	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	125-131	kininogen 1	Homo sapiens	70-80
12086980-10	2002	Delta(9)-THC prevented both the bradykinin-induced hyperpolarization and the nitric oxide and prostacyclin-independent relaxation of pre-contracted rings of porcine coronary artery.	Dronabinol	0-12	kininogen 1	Homo sapiens	32-42
12086980-13	2002	In the absence of Delta(9)-THC, neither PD98059 nor U0126 affected the NO-mediated relaxation of coronary artery rings but both substances induced a leftward shift in the concentration - relaxation curve to bradykinin when diclofenac and N(omega)nitro-L-arginine were present.	Diclofenac	223-233	kininogen 1	Homo sapiens	207-217
12086980-13	2002	In the absence of Delta(9)-THC, neither PD98059 nor U0126 affected the NO-mediated relaxation of coronary artery rings but both substances induced a leftward shift in the concentration - relaxation curve to bradykinin when diclofenac and N(omega)nitro-L-arginine were present.	Nitroarginine	238-262	kininogen 1	Homo sapiens	207-217
12086980-14	2002	Moreover, PD98059 and U0126 prolonged the bradykinin-induced hyperpolarization of porcine coronary arteries, without affecting the magnitude of the response.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	10-17	kininogen 1	Homo sapiens	42-52
12086980-14	2002	Moreover, PD98059 and U0126 prolonged the bradykinin-induced hyperpolarization of porcine coronary arteries, without affecting the magnitude of the response.	U 0126	22-27	kininogen 1	Homo sapiens	42-52
12086980-17	2002	Moreover, the activation of ERK1/2 by endothelial cell agonists such as bradykinin, appears to exert a negative feedback inhibition on EDHF-mediated responses.	edhf	135-139	kininogen 1	Homo sapiens	72-82
12095405-5	2002	The nitric oxide synthase (NOS) inhibitor, N-nitro-l-arginine methyl ester, significantly attenuated the responses to bradykinin in arteries from non-pregnant women and almost abolished responses in arteries from women with pre-eclampsia.	n-nitro-l-arginine methyl ester	43-74	kininogen 1	Homo sapiens	118-128
12095405-8	2002	These results support the suggestion that, in the absence of NO, an EDHF can mediate vasodilator responses to bradykinin during normal pregnancy, an effect not apparent in arteries from non-pregnant women or women with pre-eclampsia.	edhf	68-72	kininogen 1	Homo sapiens	110-120
12107246-3	2002	The aim of our study was to identify genetic variants that influence the phenotype of patients with PA. We hypothesized that genetic variants potentially affecting aldosterone production (aldosterone synthase, CYP11B2), renal proximal tubule reabsorption (alpha-adducin), or the mechanisms of counterbalance leading to vasodilatation and sodium excretion (bradykinin B(2)-receptor, B(2)R) could influence the clinical and biochemical characteristics of patients with PA. We studied three polymorphisms of these genes (C-344T of CYP11B2, G460W of alpha-adducin, and C-58T of B(2)R) in 167 primary aldosteronism patients (56 with aldosterone-producing adenoma and 111 with idiopathic hyperaldosteronism).	Aldosterone	164-175	kininogen 1	Homo sapiens	356-366
12133028-1	2002	PURPOSE: To determine whether the prostacyclin-inhibiting properties of aspirin counteracts the bradykinin-induced prostacyclin-stimulating effects of angiotensin-converting enzyme (ACE) inhibitors, thereby attenuating the beneficial effects of ACE inhibitors in heart failure patients.	Aspirin	72-79	kininogen 1	Homo sapiens	96-106
12133028-1	2002	PURPOSE: To determine whether the prostacyclin-inhibiting properties of aspirin counteracts the bradykinin-induced prostacyclin-stimulating effects of angiotensin-converting enzyme (ACE) inhibitors, thereby attenuating the beneficial effects of ACE inhibitors in heart failure patients.	Epoprostenol	115-127	kininogen 1	Homo sapiens	96-106
12133028-7	2002	Bradykinin, a potent vasodilator, acts by stimulating formation of vasodilatory prostaglandins such as prostacyclin, whereas aspirin or acetyl salicylic acid inhibits the enzyme cyclooxygenase, which in turn decreases the production of the prostaglandins.	Prostaglandins	80-94	kininogen 1	Homo sapiens	0-10
12133028-7	2002	Bradykinin, a potent vasodilator, acts by stimulating formation of vasodilatory prostaglandins such as prostacyclin, whereas aspirin or acetyl salicylic acid inhibits the enzyme cyclooxygenase, which in turn decreases the production of the prostaglandins.	Epoprostenol	103-115	kininogen 1	Homo sapiens	0-10
12133028-7	2002	Bradykinin, a potent vasodilator, acts by stimulating formation of vasodilatory prostaglandins such as prostacyclin, whereas aspirin or acetyl salicylic acid inhibits the enzyme cyclooxygenase, which in turn decreases the production of the prostaglandins.	Prostaglandins	240-254	kininogen 1	Homo sapiens	0-10
12546079-5	2002	BK- (10(-7) M) induced EDHF-mediated hyperpolarization (-10.9 +/- 1.5 mV, n = 7) in the IMA was significantly greater than that in RA (-5.8 +/- 0.9 mV, n = 6, p = 0.04) and SV (-5.1 +/- 0.5 mV, n = 8, p &lt; 0.01).	edhf	23-27	kininogen 1	Homo sapiens	0-2
12546079-3	2002	NO-sensitive electrode or intracellular glass microelectrode was used to study NO or EDHF in response to acetylcholine (ACh) and bradykinin (BK).	edhf	85-89	kininogen 1	Homo sapiens	129-139
12546079-3	2002	NO-sensitive electrode or intracellular glass microelectrode was used to study NO or EDHF in response to acetylcholine (ACh) and bradykinin (BK).	edhf	85-89	kininogen 1	Homo sapiens	141-143
12091579-2	2002	It has been suggested that the capsaicin receptor (VR1), a nociceptor-specific cation channel sensitive to noxious heat, protons, and capsaicin, is a channel that is modified by BK in these effects.	Capsaicin	31-40	kininogen 1	Homo sapiens	178-180
12091579-6	2002	We also demonstrated that in capsaicin-sensitive dorsal root ganglion (DRG) neurons the activation threshold of heat-induced current, which is considered to be VR-1 mediated, was lowered by BK and that this effect was also mediated by PKC.	Capsaicin	29-38	kininogen 1	Homo sapiens	190-192
12088864-0	2002	Mechanisms of bradykinin-induced glucagon release in clonal alpha-cells In-R1-G9: involvement of Ca(2+)-dependent and -independent pathways.	Glucagon	33-41	kininogen 1	Homo sapiens	14-24
12088864-1	2002	The mechanisms by which bradykinin (BK) increases glucagon release were investigated.	Glucagon	50-58	kininogen 1	Homo sapiens	24-34
12088864-1	2002	The mechanisms by which bradykinin (BK) increases glucagon release were investigated.	Glucagon	50-58	kininogen 1	Homo sapiens	36-38
12088864-2	2002	BK (0.1-10 microM) increased [Ca(2+)](i) and glucagon release in clonal alpha-cells In-R1-G9.	Glucagon	45-53	kininogen 1	Homo sapiens	0-2
12088864-3	2002	BK-induced glucagon release was lower in the absence than in the presence of extracellular Ca(2+), but it still increased glucagon release while [Ca(2+)](i) was stringently deprived.	Glucagon	11-19	kininogen 1	Homo sapiens	0-2
12088864-3	2002	BK-induced glucagon release was lower in the absence than in the presence of extracellular Ca(2+), but it still increased glucagon release while [Ca(2+)](i) was stringently deprived.	Glucagon	122-130	kininogen 1	Homo sapiens	0-2
12088864-4	2002	Depletion of intracellular Ca(2+) store with thapsigargin abolished both the BK-induced Ca(2+) peak and sustained plateau.	Thapsigargin	45-57	kininogen 1	Homo sapiens	77-79
12088864-5	2002	Microinjection of heparin abolished BK-induced Ca(2+) release.	Heparin	18-25	kininogen 1	Homo sapiens	36-38
12088864-7	2002	U-73122 (8 microM), a phospholipase C (PLC) inhibitor, abolished BK-induced increases in [Ca(2+)](i), but only reduced BK-induced glucagon release by 40%.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	0-7	kininogen 1	Homo sapiens	65-67
12088864-7	2002	U-73122 (8 microM), a phospholipase C (PLC) inhibitor, abolished BK-induced increases in [Ca(2+)](i), but only reduced BK-induced glucagon release by 40%.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	0-7	kininogen 1	Homo sapiens	119-121
12088864-7	2002	U-73122 (8 microM), a phospholipase C (PLC) inhibitor, abolished BK-induced increases in [Ca(2+)](i), but only reduced BK-induced glucagon release by 40%.	Glucagon	130-138	kininogen 1	Homo sapiens	119-121
12088864-8	2002	A phospholipase D (PLD) inhibitor zLYCK reduced BK-induced glucagon release by 60%.	Glucagon	59-67	kininogen 1	Homo sapiens	48-50
12088864-10	2002	Both SK&amp;F 96365, a receptor-operated Ca(2+) channel (ROC) blocker and nimodipine, an L-type Ca(2+) channel blocker, reduced BK-induced [Ca(2+)](i) increase and glucagon release.	amicloral	5-11	kininogen 1	Homo sapiens	128-130
12088864-10	2002	Both SK&amp;F 96365, a receptor-operated Ca(2+) channel (ROC) blocker and nimodipine, an L-type Ca(2+) channel blocker, reduced BK-induced [Ca(2+)](i) increase and glucagon release.	Nimodipine	74-84	kininogen 1	Homo sapiens	128-130
12088864-10	2002	Both SK&amp;F 96365, a receptor-operated Ca(2+) channel (ROC) blocker and nimodipine, an L-type Ca(2+) channel blocker, reduced BK-induced [Ca(2+)](i) increase and glucagon release.	Glucagon	164-172	kininogen 1	Homo sapiens	128-130
12049646-8	2002	The B1-selective analogue [Arg0,Trp5,Leu8,des-Arg9]-BK was inactive at nanomolar concentrations.	des-arg9	42-50	kininogen 1	Homo sapiens	52-54
12049652-3	2002	To investigate the molecular mechanisms underlying the rapid deactivation of eNOS after stimulation with receptor agonists, we measured the time courses of eNOS activation and intracellular free Ca2+ concentration ([Ca2+]i) in response to bradykinin (BK) and ATP.	Adenosine Triphosphate	259-262	kininogen 1	Homo sapiens	239-249
12049652-4	2002	Incubation of porcine aortic endothelial cells with BK (1 microM) in the presence of 3 mM extracellular Ca2+ increased [Ca2+]i from 110 to 350 nM and enhanced the rate of l-[3H]citrulline formation from 0.1 to 5 fmol/min.	l-[3h]citrulline	171-187	kininogen 1	Homo sapiens	52-54
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	14-17	kininogen 1	Homo sapiens	31-33
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	14-17	kininogen 1	Homo sapiens	67-69
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	14-17	kininogen 1	Homo sapiens	67-69
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	73-76	kininogen 1	Homo sapiens	67-69
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	73-76	kininogen 1	Homo sapiens	67-69
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	73-76	kininogen 1	Homo sapiens	67-69
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	73-76	kininogen 1	Homo sapiens	67-69
12052484-3	2002	Endothelial nitric oxide production was quantified as the forearm blood flow response to intra-brachial infusion of bradykinin and N(G) monomethyl-L-arginine (L-NMMA).	Nitric Oxide	12-24	kininogen 1	Homo sapiens	116-126
12049789-4	2002	To investigate the interaction, an NMR study was carried out on the binding of a representative polyphenol, penta-O-galloyl-D-glucopyranose, to a nonapeptide hormone, bradykinin (BDK), where proline accounts for 30% of residues.	Polyphenols	96-106	kininogen 1	Homo sapiens	167-177
12049789-4	2002	To investigate the interaction, an NMR study was carried out on the binding of a representative polyphenol, penta-O-galloyl-D-glucopyranose, to a nonapeptide hormone, bradykinin (BDK), where proline accounts for 30% of residues.	Polyphenols	96-106	kininogen 1	Homo sapiens	179-182
12049789-4	2002	To investigate the interaction, an NMR study was carried out on the binding of a representative polyphenol, penta-O-galloyl-D-glucopyranose, to a nonapeptide hormone, bradykinin (BDK), where proline accounts for 30% of residues.	penta-o-galloyl-d-glucopyranose	108-139	kininogen 1	Homo sapiens	167-177
12049789-4	2002	To investigate the interaction, an NMR study was carried out on the binding of a representative polyphenol, penta-O-galloyl-D-glucopyranose, to a nonapeptide hormone, bradykinin (BDK), where proline accounts for 30% of residues.	penta-o-galloyl-d-glucopyranose	108-139	kininogen 1	Homo sapiens	179-182
12049789-4	2002	To investigate the interaction, an NMR study was carried out on the binding of a representative polyphenol, penta-O-galloyl-D-glucopyranose, to a nonapeptide hormone, bradykinin (BDK), where proline accounts for 30% of residues.	Proline	191-198	kininogen 1	Homo sapiens	167-177
12031713-3	2002	RESULTS: Bradykinin-induced NO-mediated relaxation of KCl-constricted arterial rings was slightly attenuated following exposure to cortisol.	Potassium Chloride	54-57	kininogen 1	Homo sapiens	9-19
12031713-3	2002	RESULTS: Bradykinin-induced NO-mediated relaxation of KCl-constricted arterial rings was slightly attenuated following exposure to cortisol.	Hydrocortisone	131-139	kininogen 1	Homo sapiens	9-19
11880373-3	2002	We found that enalaprilat and other ACE inhibitors in nanomolar concentrations activate human bradykinin B(1) receptors directly in the absence of ACE and the B(1) agonist des-Arg(10)-Lys(1)-bradykinin.	Enalaprilat	14-25	kininogen 1	Homo sapiens	94-104
12227494-4	2002	The [Ca2+]i response of BK (100 nM) was inhibited by 10 micro M of the BKB2 antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7]-BK, and HIST (1 mM) was completely inhibited by 100 nM of the H1 antagonist, (+)-chlorpheniramine, in the presence and absence of extracellular Ca2+ (1.5 mM).	D-Arginine	88-93	kininogen 1	Homo sapiens	24-26
12227494-4	2002	The [Ca2+]i response of BK (100 nM) was inhibited by 10 micro M of the BKB2 antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7]-BK, and HIST (1 mM) was completely inhibited by 100 nM of the H1 antagonist, (+)-chlorpheniramine, in the presence and absence of extracellular Ca2+ (1.5 mM).	[hyp3	94-99	kininogen 1	Homo sapiens	24-26
12227494-4	2002	The [Ca2+]i response of BK (100 nM) was inhibited by 10 micro M of the BKB2 antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7]-BK, and HIST (1 mM) was completely inhibited by 100 nM of the H1 antagonist, (+)-chlorpheniramine, in the presence and absence of extracellular Ca2+ (1.5 mM).	Histamine	125-129	kininogen 1	Homo sapiens	24-26
12227494-4	2002	The [Ca2+]i response of BK (100 nM) was inhibited by 10 micro M of the BKB2 antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7]-BK, and HIST (1 mM) was completely inhibited by 100 nM of the H1 antagonist, (+)-chlorpheniramine, in the presence and absence of extracellular Ca2+ (1.5 mM).	Chlorpheniramine	194-214	kininogen 1	Homo sapiens	24-26
11830581-10	2002	Angiotensin II (IC(50) = 2 microm) or bradykinin (IC(50) = 100 microm), but not angiotensin II-(1-7) or bradykinin(1-5), and the prolyl oligopeptidase inhibitor Fmoc-Ala-Pyr-CN (IC(50) = 50 nm) also blocked purified PKA activation of PK.	fmoc-ala-pyr-cn	161-176	kininogen 1	Homo sapiens	38-48
11880373-3	2002	We found that enalaprilat and other ACE inhibitors in nanomolar concentrations activate human bradykinin B(1) receptors directly in the absence of ACE and the B(1) agonist des-Arg(10)-Lys(1)-bradykinin.	Enalaprilat	14-25	kininogen 1	Homo sapiens	191-201
11880373-3	2002	We found that enalaprilat and other ACE inhibitors in nanomolar concentrations activate human bradykinin B(1) receptors directly in the absence of ACE and the B(1) agonist des-Arg(10)-Lys(1)-bradykinin.	Lysine	184-187	kininogen 1	Homo sapiens	94-104
12022543-7	2002	RESULTS: Quinapril-treated animals required less cardioversions for ventricular arrhythmias (1.58 +/- 0.40 vs 2.77 +/- 0.22; p &lt; 0.05), had higher wall motion scores assessed by two-dimensional echocardiography (4 = normal to -1 = dyskinesia; 2.11 +/- 0.10 vs 1.50 +/- 0.07; p &lt; 0.05), more complete coronary artery endothelial relaxation to bradykinin (45% +/- 3% vs 7% +/- 4%; p &lt; 0.005), and lower infarct size (24.0% +/- 3.0% vs 40.0% +/- 1.7%; p &lt; 0.0001).	Quinapril	9-18	kininogen 1	Homo sapiens	348-358
12063092-5	2002	Functionally, the bradykinin B(2) receptor ligand, bradykinin, but not the B(1) ligand, des-Arg(10)-kallidin, produced a marked increase in prostaglandin E(2) release when administered following interleukin-1 beta treatment.	Prostaglandins E	140-155	kininogen 1	Homo sapiens	18-28
12006549-0	2002	Bradykinin antagonist dimer, CU201, inhibits the growth of human lung cancer cell lines in vitro and in vivo and produces synergistic growth inhibition in combination with other antitumor agents.	CU201	29-34	kininogen 1	Homo sapiens	0-10
12019279-11	2002	Ang 1-9 and Ang 1-7 potentiated bradykinin action on the B(2) receptor by raising arachidonic acid and NO release at much lower concentrations than their 50% inhibition concentrations (IC(50)s) with ACE.	Arachidonic Acid	82-98	kininogen 1	Homo sapiens	32-42
11933166-4	2002	The enzyme activity was drastically enhanced by the presence of chloride ion, and strongly inhibited by captopril and bradykinin potentiator B.	Chlorides	64-72	kininogen 1	Homo sapiens	118-128
11815627-9	2002	ACE2 also efficiently hydrolyzes des-Arg(9)-bradykinin (k(cat)/K(m) = 1.3 x 10(5) m(-1) s(-1)), but it does not hydrolyze bradykinin.	des-arg	33-40	kininogen 1	Homo sapiens	44-54
12063092-5	2002	Functionally, the bradykinin B(2) receptor ligand, bradykinin, but not the B(1) ligand, des-Arg(10)-kallidin, produced a marked increase in prostaglandin E(2) release when administered following interleukin-1 beta treatment.	Prostaglandins E	140-155	kininogen 1	Homo sapiens	51-61
12063092-6	2002	Arachidonic acid release in response to bradykinin was markedly enhanced by prior incubation with interleukin-1 beta and this was prevented by the prior addition of dexamethasone.	Arachidonic Acid	0-16	kininogen 1	Homo sapiens	40-50
12063092-6	2002	Arachidonic acid release in response to bradykinin was markedly enhanced by prior incubation with interleukin-1 beta and this was prevented by the prior addition of dexamethasone.	Dexamethasone	165-178	kininogen 1	Homo sapiens	40-50
11930011-0	2002	Bradykinin antagonist dimer, CU201, inhibits the growth of human lung cancer cell lines by a "biased agonist" mechanism.	CU201	29-34	kininogen 1	Homo sapiens	0-10
11893577-8	2002	Endothelial stunning by intracarotid injection of phorbol 12,13-dibutyrate did not affect NMDA-induced vasodilation but attenuated vascular responses to hypercapnia and BK by approximately 70% (n = 7).	Phorbol 12,13-Dibutyrate	50-74	kininogen 1	Homo sapiens	169-171
11992135-3	2002	ACE inhibitors reduce angiotensin II and, by blocking the metabolism of bradykinin, ACE inhibitors upregulate nitric oxide and prostacycline.	Nitric Oxide	110-122	kininogen 1	Homo sapiens	72-82
11992135-3	2002	ACE inhibitors reduce angiotensin II and, by blocking the metabolism of bradykinin, ACE inhibitors upregulate nitric oxide and prostacycline.	Epoprostenol (TN)	127-140	kininogen 1	Homo sapiens	72-82
11986905-10	2002	This proposal is supported by different clinical trials that have shown that the ACE inhibitors with higher affinity by the tissular ACE, such as quinapril, are the most effective in reversing ED principally by accumulating bradykinin.	Quinapril	146-155	kininogen 1	Homo sapiens	224-234
11897760-0	2002	Smoking impairs bradykinin-stimulated t-PA release.	t-pa	38-42	kininogen 1	Homo sapiens	16-26
11882619-8	2002	Arachidonic acid release by bradykinin from CHO/NEP-B(2) cells was also augmented by 100 nmol/L phosphoramidon or omapatrilat about 3-fold, and again, the inhibitors resensitized the desensitized B(2) receptor.	Arachidonic Acid	0-16	kininogen 1	Homo sapiens	28-38
11854434-6	2002	Addition of Lys-des-Arg(9)-BK (1-100 nM) rapidly concentrated the receptor-associated fluorescence into multiple aggregates that remained associated with the plasma membrane (no significant internalization) and colocalized with caveolin-1.	lys-des-arg	12-23	kininogen 1	Homo sapiens	27-29
12423422-2	2002	Bradykinin (BK) is a nine amino acid peptide (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) formed from the plasma precursor kininogen during inflammation and tissue injury.	amino acid peptide	26-44	kininogen 1	Homo sapiens	0-10
12423422-2	2002	Bradykinin (BK) is a nine amino acid peptide (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) formed from the plasma precursor kininogen during inflammation and tissue injury.	amino acid peptide	26-44	kininogen 1	Homo sapiens	12-14
12423422-8	2002	BK acts mainly indirectly, primarily through airway nerve activation, but also by the release of prostanoids, thromboxanes and nitric oxide (NO).	Prostaglandins	97-108	kininogen 1	Homo sapiens	0-2
12423422-8	2002	BK acts mainly indirectly, primarily through airway nerve activation, but also by the release of prostanoids, thromboxanes and nitric oxide (NO).	Thromboxanes	110-122	kininogen 1	Homo sapiens	0-2
12423422-8	2002	BK acts mainly indirectly, primarily through airway nerve activation, but also by the release of prostanoids, thromboxanes and nitric oxide (NO).	Nitric Oxide	127-139	kininogen 1	Homo sapiens	0-2
11882619-8	2002	Arachidonic acid release by bradykinin from CHO/NEP-B(2) cells was also augmented by 100 nmol/L phosphoramidon or omapatrilat about 3-fold, and again, the inhibitors resensitized the desensitized B(2) receptor.	phosphoramidon	96-110	kininogen 1	Homo sapiens	28-38
11882619-8	2002	Arachidonic acid release by bradykinin from CHO/NEP-B(2) cells was also augmented by 100 nmol/L phosphoramidon or omapatrilat about 3-fold, and again, the inhibitors resensitized the desensitized B(2) receptor.	omapatrilat	114-125	kininogen 1	Homo sapiens	28-38
11882619-11	2002	Consequently, omapatrilat could augment bradykinin effects on B(2), when either ACE or NEP is expressed close to receptor on cell membrane.	omapatrilat	14-25	kininogen 1	Homo sapiens	40-50
11791011-0	2002	Bradykinin inhibits serum-depletion-induced apoptosis of human vascular endothelial cells by inducing nitric oxide via calcium ion kinetics.	Nitric Oxide	102-114	kininogen 1	Homo sapiens	0-10
11791011-0	2002	Bradykinin inhibits serum-depletion-induced apoptosis of human vascular endothelial cells by inducing nitric oxide via calcium ion kinetics.	Calcium	119-126	kininogen 1	Homo sapiens	0-10
11842287-1	2002	Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells.	Silicates	148-157	kininogen 1	Homo sapiens	0-10
11791011-4	2002	The apoptosis inhibited by bradykinin was reduced by nitric oxide inhibitor N(G)-monomethyl-L-arginine (L-NMMA) and consequently restored by combined treatment with L-NMMA and L-arginine.	Nitric Oxide	53-65	kininogen 1	Homo sapiens	27-37
11842287-1	2002	Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells.	Silicates	148-157	kininogen 1	Homo sapiens	74-105
11842287-1	2002	Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells.	Uric Acid	159-164	kininogen 1	Homo sapiens	0-10
11842287-1	2002	Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells.	Uric Acid	159-164	kininogen 1	Homo sapiens	74-105
11842287-1	2002	Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells.	diphosphoric acid	170-183	kininogen 1	Homo sapiens	0-10
11842287-1	2002	Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells.	diphosphoric acid	170-183	kininogen 1	Homo sapiens	74-105
11842287-1	2002	Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells.	Heparin	221-228	kininogen 1	Homo sapiens	0-10
11842287-1	2002	Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells.	Glycosaminoglycans	236-255	kininogen 1	Homo sapiens	0-10
11842287-1	2002	Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells.	Sulfoglycosphingolipids	261-271	kininogen 1	Homo sapiens	0-10
11842287-1	2002	Bradykinin is formed by the interaction of factor XII, prekallikrein, and high-molecular-weight kininogen on negatively charged inorganic surfaces (silicates, urate, and pyrophosphate) or macromolecular organic surfaces (heparin, other mucopolysaccharides, and sulfatides) or on assembly along the surface of cells.	Sulfoglycosphingolipids	261-271	kininogen 1	Homo sapiens	74-105
11791011-4	2002	The apoptosis inhibited by bradykinin was reduced by nitric oxide inhibitor N(G)-monomethyl-L-arginine (L-NMMA) and consequently restored by combined treatment with L-NMMA and L-arginine.	omega-N-Methylarginine	76-102	kininogen 1	Homo sapiens	27-37
11791011-4	2002	The apoptosis inhibited by bradykinin was reduced by nitric oxide inhibitor N(G)-monomethyl-L-arginine (L-NMMA) and consequently restored by combined treatment with L-NMMA and L-arginine.	omega-N-Methylarginine	104-110	kininogen 1	Homo sapiens	27-37
11791011-4	2002	The apoptosis inhibited by bradykinin was reduced by nitric oxide inhibitor N(G)-monomethyl-L-arginine (L-NMMA) and consequently restored by combined treatment with L-NMMA and L-arginine.	omega-N-Methylarginine	165-171	kininogen 1	Homo sapiens	27-37
11791011-4	2002	The apoptosis inhibited by bradykinin was reduced by nitric oxide inhibitor N(G)-monomethyl-L-arginine (L-NMMA) and consequently restored by combined treatment with L-NMMA and L-arginine.	Arginine	92-102	kininogen 1	Homo sapiens	27-37
11791011-5	2002	Bradykinin increased influx of extracellular Ca2+, generation of inositol 1,4,5-trisphosphate, and release of Ca2+ from intracellular storage sites, thus increasing the total intracellular Ca2+ concentration ([Ca2+]i).	Inositol 1,4,5-Trisphosphate	65-93	kininogen 1	Homo sapiens	0-10
11791011-6	2002	Bradykinin increased nitric oxide production, which was inhibited by L-NMMA and restored by combined treatment with L-NMMA and L-arginine.	Nitric Oxide	21-33	kininogen 1	Homo sapiens	0-10
11791011-6	2002	Bradykinin increased nitric oxide production, which was inhibited by L-NMMA and restored by combined treatment with L-NMMA and L-arginine.	omega-N-Methylarginine	69-75	kininogen 1	Homo sapiens	0-10
11791011-6	2002	Bradykinin increased nitric oxide production, which was inhibited by L-NMMA and restored by combined treatment with L-NMMA and L-arginine.	omega-N-Methylarginine	116-122	kininogen 1	Homo sapiens	0-10
11791011-6	2002	Bradykinin increased nitric oxide production, which was inhibited by L-NMMA and restored by combined treatment with L-NMMA and L-arginine.	Arginine	127-137	kininogen 1	Homo sapiens	0-10
11791011-8	2002	Caspase-3 inhibitor, acetyl-Asp-Met-Gln-Asp-aldehyde, enhanced bradykinin-induced inhibition of apoptosis but did not effect bradykinin-induced nitric oxide production.	acetyl-aspartyl-methionyl-glutaminyl-aspartyl-aldehyde	21-52	kininogen 1	Homo sapiens	63-73
11791011-9	2002	These findings suggest that bradykinin inhibits serum-depletion-induced apoptosis in HUVECs by enhancing nitric oxide production via an increase in [Ca2+]i.	Nitric Oxide	105-117	kininogen 1	Homo sapiens	28-38
12152253-2	2002	Bradykinin promotes generation by endothelium such substances as endothelium-derived hyperpolarizing factor, prostacyclin and nitric oxide.	Epoprostenol	109-121	kininogen 1	Homo sapiens	0-10
12503625-8	2002	A series of BODIPY TMR labeled peptides have been prepared that bind to a range of GPCRs including melanin concentrating hormone, bradykinin, and melanocortin receptors.	tmr	19-22	kininogen 1	Homo sapiens	130-140
11883711-8	2002	Incubation with triethyltin at a concentration that did not increase [Ca2+]i (1 microM) in Ca2+-containing medium for 3 min potentiated ATP (10 microM)- or bradykinin (1 microLM)-induced [Ca2+]i increases by 41 +/- 3% and 51 +/- 2%, respectively.	triethyltin	16-27	kininogen 1	Homo sapiens	156-166
11798159-4	2002	Bradykinin elicited endothelium-dependent relaxations and hyperpolarizations in the presence of indomethacin and N(omega)-nitro-l-arginine, which thus were attributed to EDHF, in human mesenteric arteries.	Indomethacin	96-108	kininogen 1	Homo sapiens	0-10
11798159-4	2002	Bradykinin elicited endothelium-dependent relaxations and hyperpolarizations in the presence of indomethacin and N(omega)-nitro-l-arginine, which thus were attributed to EDHF, in human mesenteric arteries.	Nitroarginine	113-138	kininogen 1	Homo sapiens	0-10
11798159-4	2002	Bradykinin elicited endothelium-dependent relaxations and hyperpolarizations in the presence of indomethacin and N(omega)-nitro-l-arginine, which thus were attributed to EDHF, in human mesenteric arteries.	edhf	170-174	kininogen 1	Homo sapiens	0-10
11711543-4	2002	At the same time, BK produced the tyrosine phosphorylation and internalization of KDR/Flk-1 as did VEGF itself.	Tyrosine	34-42	kininogen 1	Homo sapiens	18-20
11738247-1	2002	Bradykinin receptor subtypes linked to prostaglandin release have been assessed in a human osteosarcoma cell line with osteoblastic phenotype (MG-63).	Prostaglandins	39-52	kininogen 1	Homo sapiens	0-10
11738247-2	2002	Bradykinin (BK; 1 micromol/l) caused a burst of prostaglandin E(2) release that was maximal at 10 min.	prostaglandin e(2) release	48-74	kininogen 1	Homo sapiens	0-10
11761163-6	2002	This study showed significant differences in adsorption patterns among the heparin-coated and the uncoated surfaces, notably for fibronectin, fibrinogen, C3 and high molecular weight kininogen (HMWK).	Heparin	75-82	kininogen 1	Homo sapiens	161-192
11761163-6	2002	This study showed significant differences in adsorption patterns among the heparin-coated and the uncoated surfaces, notably for fibronectin, fibrinogen, C3 and high molecular weight kininogen (HMWK).	Heparin	75-82	kininogen 1	Homo sapiens	194-198
11849193-0	2002	Effect of aspirin on vasodilation to bradykinin and substance P in patients with heart failure treated with ACE inhibitor.	Aspirin	10-17	kininogen 1	Homo sapiens	37-47
11855668-7	2002	The extent of reduction of left ventricular wall motion score by perindopril was closely correlated with that of inhibition of serum ACE activities (P&lt;0.01) and with that of increase in plasma bradykinin concentrations (P&lt;0.05).	Perindopril	65-76	kininogen 1	Homo sapiens	196-206
11814619-0	2002	Synthesis and pharmacological properties of TOAC-labeled angiotensin and bradykinin analogs.	2,2,6,6-tetramethylpiperidine-N-oxide-4-amino-4-carboxylic acid	44-48	kininogen 1	Homo sapiens	73-83
11814619-1	2002	Angiotensin II (AngII) and bradykinin (BK) derivatives containing the TOAC (2,2,6,6-tetramethylpiperidine-N-oxyl-4-amino-4-carboxylic acid) spin label were synthesized by solid phase methodology.	toac (2,2,6,6-tetramethylpiperidine-n-oxyl-4-amino-4-carboxylic acid)	70-139	kininogen 1	Homo sapiens	27-37
11814619-1	2002	Angiotensin II (AngII) and bradykinin (BK) derivatives containing the TOAC (2,2,6,6-tetramethylpiperidine-N-oxyl-4-amino-4-carboxylic acid) spin label were synthesized by solid phase methodology.	toac (2,2,6,6-tetramethylpiperidine-n-oxyl-4-amino-4-carboxylic acid)	70-139	kininogen 1	Homo sapiens	39-41
12152253-2	2002	Bradykinin promotes generation by endothelium such substances as endothelium-derived hyperpolarizing factor, prostacyclin and nitric oxide.	Nitric Oxide	126-138	kininogen 1	Homo sapiens	0-10
11730978-6	2001	Incubation with growth factors generally decreased the BK-stimulated GLU release, an effect most pronounced for bFGF, which completely blocked BK-stimulated release.	Glutamic Acid	69-72	kininogen 1	Homo sapiens	55-57
11741551-7	2001	Enalaprilat induced a 70% reduction of ACE activity and a significant increase of bradykinin in pulmonary arterial blood.	Enalaprilat	0-11	kininogen 1	Homo sapiens	82-92
11789779-8	2001	RESULTS: After exposure to hyperkalemia, the EDHF-mediated maximal relaxation by bradykinin (72.5% +/- 7.8% versus 41.6% +/- 10.6%; p &lt; 0.05), but not by EET(11,12) (18.4% +/- 3.3% versus 25.1% +/- 4.9%; p &gt; 0.05) was significantly reduced.	edhf	45-49	kininogen 1	Homo sapiens	81-91
11730978-2	2001	BK (0.5 and 1 microM) induced a dramatic and significant increase in glutamate release.	Glutamic Acid	69-78	kininogen 1	Homo sapiens	0-2
11730978-4	2001	The BK-evoked release of GLU was almost completely blocked by HOE 140, a selective BK2-receptor antagonist at high doses.	Glutamic Acid	25-28	kininogen 1	Homo sapiens	4-6
11789779-8	2001	RESULTS: After exposure to hyperkalemia, the EDHF-mediated maximal relaxation by bradykinin (72.5% +/- 7.8% versus 41.6% +/- 10.6%; p &lt; 0.05), but not by EET(11,12) (18.4% +/- 3.3% versus 25.1% +/- 4.9%; p &gt; 0.05) was significantly reduced.	EET	157-160	kininogen 1	Homo sapiens	81-91
11843770-5	2001	There were positive correlations between MAP reduction and BK concentration at 3 (BK3; r = 0.58, p &lt; 0.01) and 6 (BK6; r = 0.67, p &lt; 0.001) min with PAN but not with PS.	polysulfone P 1700	172-174	kininogen 1	Homo sapiens	59-61
11716803-0	2001	Omapatrilat: a new tool for understanding metabolism of bradykinin at the endothelium level.	omapatrilat	0-11	kininogen 1	Homo sapiens	56-66
11738279-6	2001	RESULTS: Lower ACh and BK responses were associated with a higher body mass index (BMI), a higher total cholesterol to high-density lipoprotein (HDL) cholesterol ratio, lower HDL cholesterol and a cigarette smoking habit (all p &lt; 0.05).	Cholesterol	104-115	kininogen 1	Homo sapiens	23-25
11741551-11	2001	Effective cardiac ACE inhibition can be achieved by low-dose intracoronary enalaprilat, which primarily causes a potentiation of bradykinin.	Enalaprilat	75-86	kininogen 1	Homo sapiens	129-139
11738279-6	2001	RESULTS: Lower ACh and BK responses were associated with a higher body mass index (BMI), a higher total cholesterol to high-density lipoprotein (HDL) cholesterol ratio, lower HDL cholesterol and a cigarette smoking habit (all p &lt; 0.05).	Cholesterol	150-161	kininogen 1	Homo sapiens	23-25
11738279-6	2001	RESULTS: Lower ACh and BK responses were associated with a higher body mass index (BMI), a higher total cholesterol to high-density lipoprotein (HDL) cholesterol ratio, lower HDL cholesterol and a cigarette smoking habit (all p &lt; 0.05).	Cholesterol	150-161	kininogen 1	Homo sapiens	23-25
11738279-7	2001	Higher low-density lipoprotein (LDL) cholesterol was also associated with a lower BK response (p = 0.001).	Cholesterol	37-48	kininogen 1	Homo sapiens	82-84
11691515-6	2001	Although sodium nitroprusside did not affect plasma t-PA concentrations, they were increased dose-dependently in the infused forearm by substance P and bradykinin infusion (ANOVA, p &lt; 0.001 for both).	Nitroprusside	9-29	kininogen 1	Homo sapiens	152-162
11707692-9	2001	Bradykinin (1, 10, 100, 1,000 n M ) and cyclopiazonic acid (10 microM) significantly relaxed porcine coronary artery rings precontracted with histamine (1 microM).	Histamine	142-151	kininogen 1	Homo sapiens	0-10
11744416-5	2001	RESULTS: The relaxation to bradykinin (0.1 to 300 nmol/liter) after U46619 (30 to 300 nmol/liter) pre-contraction was similar with both KHS and UWS pre-incubation; however, it was reduced after KCl pre-contraction (15 to 20 mmol/liter), this reduction being greater after UWS incubation.	Potassium Chloride	194-197	kininogen 1	Homo sapiens	27-37
11744416-6	2001	The inhibitory effect of N(G)-nitro-L-arginine methylester (0.1 mmol/liter) on bradykinin-induced relaxation was lower in UWS- than KHS-incubated segments after U46619 pre-contraction, but similar after KCl pre-contraction; however, the inhibitory effect of 0.5 mmol/liter ouabain was unaffected.	n(g)-nitro	25-35	kininogen 1	Homo sapiens	79-89
11744416-6	2001	The inhibitory effect of N(G)-nitro-L-arginine methylester (0.1 mmol/liter) on bradykinin-induced relaxation was lower in UWS- than KHS-incubated segments after U46619 pre-contraction, but similar after KCl pre-contraction; however, the inhibitory effect of 0.5 mmol/liter ouabain was unaffected.	Arginine	36-46	kininogen 1	Homo sapiens	79-89
11744416-6	2001	The inhibitory effect of N(G)-nitro-L-arginine methylester (0.1 mmol/liter) on bradykinin-induced relaxation was lower in UWS- than KHS-incubated segments after U46619 pre-contraction, but similar after KCl pre-contraction; however, the inhibitory effect of 0.5 mmol/liter ouabain was unaffected.	Potassium Chloride	203-206	kininogen 1	Homo sapiens	79-89
11744416-7	2001	Tetraethylammonium (5 mmol/liter) reduced the response to bradykinin more strongly after UWS pre-incubation.	Tetraethylammonium	0-18	kininogen 1	Homo sapiens	58-68
11767997-3	2001	The changes in dilatation of the left coronary artery in response to bradykinin at doses of 0.2, 0.6 and 2.0 microg/min in the CSA group were significantly greater than those in the other 2 groups.	Cyclosporine	127-130	kininogen 1	Homo sapiens	69-79
11767997-5	2001	Bradykinin caused a similar increase in coronary blood flow in the control group and CSA group, but had less of an effect in the CSA+CAD group.	Cyclosporine	85-88	kininogen 1	Homo sapiens	0-10
11767997-6	2001	In conclusion, the vasorelaxing effect of BK was preserved not only in epicardial spasm coronary arteries induced by ACh, but also in resistance coronary arteries distal to the spasm arteries in patients with CSA.	Acetylcholine	117-120	kininogen 1	Homo sapiens	42-44
11793144-20	2001	In animals and humans, the responses to injections of BK can be increased by 5-HT or PG E2.	Dinoprostone	85-90	kininogen 1	Homo sapiens	54-56
11689473-0	2001	Human airway smooth muscle cells secrete vascular endothelial growth factor: up-regulation by bradykinin via a protein kinase C and prostanoid-dependent mechanism.	Prostaglandins	132-142	kininogen 1	Homo sapiens	94-104
11689473-4	2001	Bradykinin-induced VEGF secretion was dependent on the B2 bradykinin receptor, activation of protein kinase C, and generation of endogenous prostanoids.	Prostaglandins	140-151	kininogen 1	Homo sapiens	0-10
11691515-7	2001	Bradykinin-induced release of active t-PA was more than doubled during treatment with quinapril in comparison to placebo or losartan (two-way ANOVA: p &lt; 0.003 for treatment group, p &lt; 0.001 for t-PA response and p = ns for interaction), whereas the substance P response was unaffected.	Quinapril	86-95	kininogen 1	Homo sapiens	0-10
11472709-10	2001	Methionine-induced impairment of resistance vessel dilatation to acetylcholine and bradykinin (p &lt;0.05 vs placebo) was prevented by administration of vitamin E (acetylcholine, p = 0.004; bradykinin, p = 0.004; both vs methionine alone).	Methionine	0-10	kininogen 1	Homo sapiens	83-93
11712858-2	2001	We also reported that certain antiphosphatidylethanolamine antibodies (aPE) are not specific for phosphatidylethanolamine (PE) per se, but are directed to PE-binding plasma proteins, high molecular weight kininogen (HK), and low molecular weight kininogen (LK).	phosphatidylethanolamine	34-58	kininogen 1	Homo sapiens	183-214
11712858-2	2001	We also reported that certain antiphosphatidylethanolamine antibodies (aPE) are not specific for phosphatidylethanolamine (PE) per se, but are directed to PE-binding plasma proteins, high molecular weight kininogen (HK), and low molecular weight kininogen (LK).	phosphatidylethanolamine	72-74	kininogen 1	Homo sapiens	183-214
11677365-9	2001	CONCLUSIONS: Ang(1-7) potentiates the vasodilating effect of bradykinin, possibly through a mechanism(s) involving nitric oxide release, in human forearm resistance vessels.	Nitric Oxide	115-127	kininogen 1	Homo sapiens	61-71
11587919-3	2001	In addition, nitric oxide mediates a number of vasodilator responses in ocular vessels to agonists such as acetylcholine, bradykinin, histamine, substance P and insulin.	Nitric Oxide	13-25	kininogen 1	Homo sapiens	122-132
11591608-6	2001	A K(ir) channel blocker, BaCl(2) (30 micromol/L), inhibited vasodilatory responses to KCl and bradykinin but not to adenosine, pinacidil, or nitroprusside.	barium chloride	25-32	kininogen 1	Homo sapiens	94-104
11591608-9	2001	In the presence of Ba(2+), adenosine still dilated the local site, but the local dilations to bradykinin and KCl and the remote dilations to adenosine, bradykinin, and KCl were inhibited.	Barium	19-21	kininogen 1	Homo sapiens	94-104
11591608-9	2001	In the presence of Ba(2+), adenosine still dilated the local site, but the local dilations to bradykinin and KCl and the remote dilations to adenosine, bradykinin, and KCl were inhibited.	Barium	19-21	kininogen 1	Homo sapiens	152-162
11557555-5	2001	Treatment with [Hyp(3),Tyr(Me)(8)]bradykinin, a B(2) receptor agonist, stimulated thymidine incorporation by 146%, whereas B(1)-selective Lys-des-Arg(9)-bradykinin had no effect.	Tyrosine	23-26	kininogen 1	Homo sapiens	34-44
11557555-5	2001	Treatment with [Hyp(3),Tyr(Me)(8)]bradykinin, a B(2) receptor agonist, stimulated thymidine incorporation by 146%, whereas B(1)-selective Lys-des-Arg(9)-bradykinin had no effect.	Thymidine	82-91	kininogen 1	Homo sapiens	34-44
11557555-5	2001	Treatment with [Hyp(3),Tyr(Me)(8)]bradykinin, a B(2) receptor agonist, stimulated thymidine incorporation by 146%, whereas B(1)-selective Lys-des-Arg(9)-bradykinin had no effect.	lys-des-arg	138-149	kininogen 1	Homo sapiens	153-163
11606206-7	2001	The recombinant W03G9.4 removed the N-terminal amino acid from bradykinin (RPPGFSPFR), a Caenorhabditis elegans neuropeptide (KPSFVRFamide) and Lem Trp 1 (APSGFLGVRamide), but did not display activity towards angiotensin I (NRVYIHPFHL), des-Arg bradykinin and AF1 (KNEFIRFamide).	apsgflgvramide	155-169	kininogen 1	Homo sapiens	63-73
11606206-7	2001	The recombinant W03G9.4 removed the N-terminal amino acid from bradykinin (RPPGFSPFR), a Caenorhabditis elegans neuropeptide (KPSFVRFamide) and Lem Trp 1 (APSGFLGVRamide), but did not display activity towards angiotensin I (NRVYIHPFHL), des-Arg bradykinin and AF1 (KNEFIRFamide).	des-arg	237-244	kininogen 1	Homo sapiens	63-73
11606206-8	2001	The activity towards bradykinin was inhibited by EDTA and 1, 10 phenanthroline, as expected for a metalloenzyme, and also by apstatin (IC50, 1 microM), a selective inhibitor of mammalian AP-P. A Km of 45 microM and an optimum pH of 7-8 was observed with bradykinin as the substrate.	Edetic Acid	49-53	kininogen 1	Homo sapiens	21-31
11606206-8	2001	The activity towards bradykinin was inhibited by EDTA and 1, 10 phenanthroline, as expected for a metalloenzyme, and also by apstatin (IC50, 1 microM), a selective inhibitor of mammalian AP-P. A Km of 45 microM and an optimum pH of 7-8 was observed with bradykinin as the substrate.	Edetic Acid	49-53	kininogen 1	Homo sapiens	254-264
11606206-8	2001	The activity towards bradykinin was inhibited by EDTA and 1, 10 phenanthroline, as expected for a metalloenzyme, and also by apstatin (IC50, 1 microM), a selective inhibitor of mammalian AP-P. A Km of 45 microM and an optimum pH of 7-8 was observed with bradykinin as the substrate.	1,10-phenanthroline	58-78	kininogen 1	Homo sapiens	21-31
11606206-8	2001	The activity towards bradykinin was inhibited by EDTA and 1, 10 phenanthroline, as expected for a metalloenzyme, and also by apstatin (IC50, 1 microM), a selective inhibitor of mammalian AP-P. A Km of 45 microM and an optimum pH of 7-8 was observed with bradykinin as the substrate.	1,10-phenanthroline	58-78	kininogen 1	Homo sapiens	254-264
11606206-8	2001	The activity towards bradykinin was inhibited by EDTA and 1, 10 phenanthroline, as expected for a metalloenzyme, and also by apstatin (IC50, 1 microM), a selective inhibitor of mammalian AP-P. A Km of 45 microM and an optimum pH of 7-8 was observed with bradykinin as the substrate.	apstatin	125-133	kininogen 1	Homo sapiens	21-31
11606206-8	2001	The activity towards bradykinin was inhibited by EDTA and 1, 10 phenanthroline, as expected for a metalloenzyme, and also by apstatin (IC50, 1 microM), a selective inhibitor of mammalian AP-P. A Km of 45 microM and an optimum pH of 7-8 was observed with bradykinin as the substrate.	apstatin	125-133	kininogen 1	Homo sapiens	254-264
11606206-9	2001	The activity of the nematode AP-P, like its mammalian counterparts, was strongly influenced by metal ions, with Co2+, Mn2+ and Zn2+ all inhibiting the hydrolysis of bradykinin.	Metals	95-100	kininogen 1	Homo sapiens	165-175
11606206-9	2001	The activity of the nematode AP-P, like its mammalian counterparts, was strongly influenced by metal ions, with Co2+, Mn2+ and Zn2+ all inhibiting the hydrolysis of bradykinin.	Cobalt(2+)	112-116	kininogen 1	Homo sapiens	165-175
11606206-9	2001	The activity of the nematode AP-P, like its mammalian counterparts, was strongly influenced by metal ions, with Co2+, Mn2+ and Zn2+ all inhibiting the hydrolysis of bradykinin.	Manganese(2+)	118-122	kininogen 1	Homo sapiens	165-175
11606206-9	2001	The activity of the nematode AP-P, like its mammalian counterparts, was strongly influenced by metal ions, with Co2+, Mn2+ and Zn2+ all inhibiting the hydrolysis of bradykinin.	Zinc	127-131	kininogen 1	Homo sapiens	165-175
11641302-5	2001	EC cGMP increased 300% in response to bradykinin and A23187 and 200% in response to ADP.	Cyclic GMP	3-7	kininogen 1	Homo sapiens	38-48
11641302-6	2001	Exposure of ECs to H(2)O(2) (50 micromol/L) for 30 minutes significantly impaired cGMP levels in response to ADP, bradykinin, and the receptor-independent NO agonist A23187.	Hydrogen Peroxide	19-27	kininogen 1	Homo sapiens	114-124
11641302-6	2001	Exposure of ECs to H(2)O(2) (50 micromol/L) for 30 minutes significantly impaired cGMP levels in response to ADP, bradykinin, and the receptor-independent NO agonist A23187.	Cyclic GMP	82-86	kininogen 1	Homo sapiens	114-124
11641302-7	2001	In contrast, preincubation with HOCl (50 micromol/L) impaired cGMP production only in response to ADP and bradykinin but not A23187.	Hypochlorous Acid	32-36	kininogen 1	Homo sapiens	106-116
11641302-7	2001	In contrast, preincubation with HOCl (50 micromol/L) impaired cGMP production only in response to ADP and bradykinin but not A23187.	Cyclic GMP	62-66	kininogen 1	Homo sapiens	106-116
11907639-6	2001	Following acute infusion of the ACEI, BK levels in the CHF state increased from baseline (57% +/- 22; P &lt; 0.05).	acei	32-36	kininogen 1	Homo sapiens	38-40
11568080-4	2001	An NO-sensitive electrode (to directly measure NO release) or intracellular glass microelectrode (to measure membrane potential) was used to study NO or EDHF in response to acetylcholine (ACh) and bradykinin (BK) before and after incubation with indomethacin (a cyclooxygenase inhibitor), N(G)-nitro-L-arginine (an NO synthase inhibitor), and oxyhemoglobin (an NO scavenger).	edhf	153-157	kininogen 1	Homo sapiens	197-207
11568080-6	2001	BK-induced EDHF-mediated hyperpolarization in the IMA was significantly greater than that in RA (BK 10(-)(7) mol/L: -10.9+/-1.5 [n=7] versus -5.8+/-0.9 [n=6] mV, P=0.04).	edhf	11-15	kininogen 1	Homo sapiens	0-2
11522609-0	2001	Inhibitory effects of brefeldin A, a membrane transport blocker, on the bradykinin-induced hyperpolarization-mediated relaxation in the porcine coronary artery.	Brefeldin A	22-33	kininogen 1	Homo sapiens	72-82
11522609-5	2001	In the presence of 10 microM indomethacin and 30 microM N(G)-nitro-L-arginine (L-NOARG), both bradykinin and substance P induced a transient decrease in [Ca(2+)]i and tension in arterial strips contracted with 100 nM U46619 (thromboxane A2 analogue).	Indomethacin	29-41	kininogen 1	Homo sapiens	94-104
11522609-5	2001	In the presence of 10 microM indomethacin and 30 microM N(G)-nitro-L-arginine (L-NOARG), both bradykinin and substance P induced a transient decrease in [Ca(2+)]i and tension in arterial strips contracted with 100 nM U46619 (thromboxane A2 analogue).	Nitroarginine	56-77	kininogen 1	Homo sapiens	94-104
11522609-5	2001	In the presence of 10 microM indomethacin and 30 microM N(G)-nitro-L-arginine (L-NOARG), both bradykinin and substance P induced a transient decrease in [Ca(2+)]i and tension in arterial strips contracted with 100 nM U46619 (thromboxane A2 analogue).	Nitroarginine	79-86	kininogen 1	Homo sapiens	94-104
11522609-5	2001	In the presence of 10 microM indomethacin and 30 microM N(G)-nitro-L-arginine (L-NOARG), both bradykinin and substance P induced a transient decrease in [Ca(2+)]i and tension in arterial strips contracted with 100 nM U46619 (thromboxane A2 analogue).	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	217-223	kininogen 1	Homo sapiens	94-104
11522609-5	2001	In the presence of 10 microM indomethacin and 30 microM N(G)-nitro-L-arginine (L-NOARG), both bradykinin and substance P induced a transient decrease in [Ca(2+)]i and tension in arterial strips contracted with 100 nM U46619 (thromboxane A2 analogue).	Thromboxanes	225-236	kininogen 1	Homo sapiens	94-104
11522609-6	2001	A 6 h pre-treatment with 20 microg ml(-1) brefeldin A abolished the bradykinin-induced relaxation, while it had no effect on the substance P-induced relaxation.	Brefeldin A	42-53	kininogen 1	Homo sapiens	68-78
11522609-10	2001	The indomethacin/L-NOARG-resistant relaxation induced by bradykinin was completely inhibited by 3 mM tetrabutylammonium (non-specific Ca(2+)-activated K(+) channel blocker), while that induced by substance P was not inhibited by 3 mM tetrabutylammonium or 1 mM 4-aminopyridine (voltage-dependent K(+) channels blocker) alone, but completely inhibited by their combination.	Indomethacin	4-16	kininogen 1	Homo sapiens	57-67
11522609-10	2001	The indomethacin/L-NOARG-resistant relaxation induced by bradykinin was completely inhibited by 3 mM tetrabutylammonium (non-specific Ca(2+)-activated K(+) channel blocker), while that induced by substance P was not inhibited by 3 mM tetrabutylammonium or 1 mM 4-aminopyridine (voltage-dependent K(+) channels blocker) alone, but completely inhibited by their combination.	Nitroarginine	17-24	kininogen 1	Homo sapiens	57-67
11522609-10	2001	The indomethacin/L-NOARG-resistant relaxation induced by bradykinin was completely inhibited by 3 mM tetrabutylammonium (non-specific Ca(2+)-activated K(+) channel blocker), while that induced by substance P was not inhibited by 3 mM tetrabutylammonium or 1 mM 4-aminopyridine (voltage-dependent K(+) channels blocker) alone, but completely inhibited by their combination.	tetrabutylammonium	101-119	kininogen 1	Homo sapiens	57-67
11522609-10	2001	The indomethacin/L-NOARG-resistant relaxation induced by bradykinin was completely inhibited by 3 mM tetrabutylammonium (non-specific Ca(2+)-activated K(+) channel blocker), while that induced by substance P was not inhibited by 3 mM tetrabutylammonium or 1 mM 4-aminopyridine (voltage-dependent K(+) channels blocker) alone, but completely inhibited by their combination.	tetrabutylammonium	234-252	kininogen 1	Homo sapiens	57-67
11522609-10	2001	The indomethacin/L-NOARG-resistant relaxation induced by bradykinin was completely inhibited by 3 mM tetrabutylammonium (non-specific Ca(2+)-activated K(+) channel blocker), while that induced by substance P was not inhibited by 3 mM tetrabutylammonium or 1 mM 4-aminopyridine (voltage-dependent K(+) channels blocker) alone, but completely inhibited by their combination.	4-Aminopyridine	261-276	kininogen 1	Homo sapiens	57-67
11522609-14	2001	In conclusion, bradykinin produce EDHF in a brefeldin A-sensitive mechanism in the porcine coronary artery.	edhf	34-38	kininogen 1	Homo sapiens	15-25
11522609-14	2001	In conclusion, bradykinin produce EDHF in a brefeldin A-sensitive mechanism in the porcine coronary artery.	Brefeldin A	44-55	kininogen 1	Homo sapiens	15-25
11566939-4	2001	In the present study, we provide evidence that des-Arg(9)-bradykinin (dABK) (10(-8) M), acting through B1KR, stimulates the phosphorylation of mitogen-activated protein kinase (MAPK) (p42(mapk) and p44(mapk)).	des-arg	47-54	kininogen 1	Homo sapiens	58-68
11675956-5	2001	Although angiotensin II and bradykinin plasma levels during LDL apheresis were significantly greater with losartan than without, blood pressure reduction by losartan was mild and unpleasant symptoms were not induced.	Losartan	106-114	kininogen 1	Homo sapiens	28-38
11675956-7	2001	The greater rise in bradykinin levels during apheresis with losartan might be ascribable to angiotensin type 2-receptor stimulation.	Losartan	60-68	kininogen 1	Homo sapiens	20-30
11588409-4	2001	Like conventional ACE inhibitors, omapatrilat causes extracellular volume reduction and vasodilatation; moreover, it increases levels of atrial and brain natriuretic peptides and bradykinin.	omapatrilat	34-45	kininogen 1	Homo sapiens	179-189
11704557-5	2001	8-Bromoguanosine 3",5"-cyclic monophosphate abolished acetylcholine- or bradykinin-induced oscillations.	8-bromocyclic GMP	0-43	kininogen 1	Homo sapiens	72-82
11551775-3	2001	Bradykinin, a nonapeptide formed by enzymatic cleavage of a plasma protein precursor, activates eNOS by an independent pathway that does not require serine phosphorylation, suggesting a complex interplay of signals in the control of endothelial formation of nitric oxide.	Nitric Oxide	258-270	kininogen 1	Homo sapiens	0-10
11500030-6	2001	The sequence of bombinakinin M is preceded by a single basic residue (arginine), which represents the site of cleavage for releasing of mature bombinakinin M. This is the first cDNA cloning of bradykinin-related peptides from amphibian skin.	Arginine	70-78	kininogen 1	Homo sapiens	193-203
11472709-10	2001	Methionine-induced impairment of resistance vessel dilatation to acetylcholine and bradykinin (p &lt;0.05 vs placebo) was prevented by administration of vitamin E (acetylcholine, p = 0.004; bradykinin, p = 0.004; both vs methionine alone).	Methionine	0-10	kininogen 1	Homo sapiens	190-200
11472709-10	2001	Methionine-induced impairment of resistance vessel dilatation to acetylcholine and bradykinin (p &lt;0.05 vs placebo) was prevented by administration of vitamin E (acetylcholine, p = 0.004; bradykinin, p = 0.004; both vs methionine alone).	Vitamin E	153-162	kininogen 1	Homo sapiens	83-93
11472709-10	2001	Methionine-induced impairment of resistance vessel dilatation to acetylcholine and bradykinin (p &lt;0.05 vs placebo) was prevented by administration of vitamin E (acetylcholine, p = 0.004; bradykinin, p = 0.004; both vs methionine alone).	Vitamin E	153-162	kininogen 1	Homo sapiens	190-200
11472709-10	2001	Methionine-induced impairment of resistance vessel dilatation to acetylcholine and bradykinin (p &lt;0.05 vs placebo) was prevented by administration of vitamin E (acetylcholine, p = 0.004; bradykinin, p = 0.004; both vs methionine alone).	Acetylcholine	164-177	kininogen 1	Homo sapiens	83-93
11487526-2	2001	In the presence of 300 microM L-nitroarginine and 10 microM indomethacin, iloprost-induced hyperpolarizations were partially inhibited by 10 microM glibenclamide whereas those to NOR-1, substance P and bradykinin were unaffected.	H-Arg(NO2)-OH	30-45	kininogen 1	Homo sapiens	202-212
11487526-2	2001	In the presence of 300 microM L-nitroarginine and 10 microM indomethacin, iloprost-induced hyperpolarizations were partially inhibited by 10 microM glibenclamide whereas those to NOR-1, substance P and bradykinin were unaffected.	Indomethacin	60-72	kininogen 1	Homo sapiens	202-212
11487526-2	2001	In the presence of 300 microM L-nitroarginine and 10 microM indomethacin, iloprost-induced hyperpolarizations were partially inhibited by 10 microM glibenclamide whereas those to NOR-1, substance P and bradykinin were unaffected.	Iloprost	74-82	kininogen 1	Homo sapiens	202-212
11487526-2	2001	In the presence of 300 microM L-nitroarginine and 10 microM indomethacin, iloprost-induced hyperpolarizations were partially inhibited by 10 microM glibenclamide whereas those to NOR-1, substance P and bradykinin were unaffected.	Glyburide	148-161	kininogen 1	Homo sapiens	202-212
11487526-6	2001	In contrast, after incubation for this period of time in HEPES-buffered Tyrode solution or Krebs containing 10 mM HEPES the EDHF response to substance P was abolished and that to bradykinin was markedly reduced.	HEPES	57-62	kininogen 1	Homo sapiens	179-189
11487526-6	2001	In contrast, after incubation for this period of time in HEPES-buffered Tyrode solution or Krebs containing 10 mM HEPES the EDHF response to substance P was abolished and that to bradykinin was markedly reduced.	tyrode	72-78	kininogen 1	Homo sapiens	179-189
11487526-6	2001	In contrast, after incubation for this period of time in HEPES-buffered Tyrode solution or Krebs containing 10 mM HEPES the EDHF response to substance P was abolished and that to bradykinin was markedly reduced.	krebs	91-96	kininogen 1	Homo sapiens	179-189
11487526-6	2001	In contrast, after incubation for this period of time in HEPES-buffered Tyrode solution or Krebs containing 10 mM HEPES the EDHF response to substance P was abolished and that to bradykinin was markedly reduced.	HEPES	114-119	kininogen 1	Homo sapiens	179-189
11487526-7	2001	The residual bradykinin-induced hyperpolarization following incubation in Tyrode solution was inhibited by iberiotoxin and by 10 microM 17-octadecynoic acid.	tyrode	74-80	kininogen 1	Homo sapiens	13-23
11487526-7	2001	The residual bradykinin-induced hyperpolarization following incubation in Tyrode solution was inhibited by iberiotoxin and by 10 microM 17-octadecynoic acid.	iberiotoxin	107-118	kininogen 1	Homo sapiens	13-23
11487526-7	2001	The residual bradykinin-induced hyperpolarization following incubation in Tyrode solution was inhibited by iberiotoxin and by 10 microM 17-octadecynoic acid.	17-octadecynoic acid	136-156	kininogen 1	Homo sapiens	13-23
11496234-1	2001	BACKGROUND: Endogenous nitric oxide protects against airway hyperresponsiveness (AHR) to bradykinin in mild asthma, whereas AHR to bradykinin is enhanced by inhaled allergens.	Nitric Oxide	23-35	kininogen 1	Homo sapiens	89-99
11496234-10	2001	CONCLUSIONS: These data indicate that allergen exposure in asthma induces increased airway hyperresponsiveness to bradykinin through impaired release of bronchoprotective nitric oxide associated with downregulation of ecNOS.	Nitric Oxide	171-183	kininogen 1	Homo sapiens	114-124
11518845-4	2001	RESULTS: In controls, vasodilation to acetylcholine and bradykinin was inhibited by L-NMMA.	omega-N-Methylarginine	84-90	kininogen 1	Homo sapiens	56-66
11518845-5	2001	In hypertensive patients, vasodilation to acetylcholine and bradykinin, but not to sodium nitroprusside, was blunted and resistant to L-NMMA.	omega-N-Methylarginine	134-140	kininogen 1	Homo sapiens	60-70
11518845-7	2001	Lacidipine but not atenolol increased the vasodilation to acetylcholine and bradykinin and restored the inhibiting effect of L-NMMA on endothelium-dependent vasodilation, without affecting the response to sodium nitroprusside.	lacidipine	0-10	kininogen 1	Homo sapiens	76-86
11523086-0	2001	Gas-phase basicities for ions from bradykinin and its des-arginine analogues.	des-arginine	54-66	kininogen 1	Homo sapiens	35-45
11523086-1	2001	Apparent gas-phase basicities (GB(app)s) for [M + H]+ of bradykinin, des-Arg1-bradykinin and des-Arg9-bradykinin have been assigned by deprotonation reactions of [M + 2H]2+ in a Fourier transform ion cyclotron resonance mass spectrometer.	Deuterium	167-169	kininogen 1	Homo sapiens	57-67
11523086-1	2001	Apparent gas-phase basicities (GB(app)s) for [M + H]+ of bradykinin, des-Arg1-bradykinin and des-Arg9-bradykinin have been assigned by deprotonation reactions of [M + 2H]2+ in a Fourier transform ion cyclotron resonance mass spectrometer.	Deuterium	167-169	kininogen 1	Homo sapiens	78-88
11523086-1	2001	Apparent gas-phase basicities (GB(app)s) for [M + H]+ of bradykinin, des-Arg1-bradykinin and des-Arg9-bradykinin have been assigned by deprotonation reactions of [M + 2H]2+ in a Fourier transform ion cyclotron resonance mass spectrometer.	Deuterium	167-169	kininogen 1	Homo sapiens	78-88
11523086-10	2001	The presence of two highly basic arginine residues on bradykinin results in its high GB(app), while the basicity of des-Arg1-bradykinin ions is increased by the presence of two proline residues at the N-terminus.	Arginine	33-41	kininogen 1	Homo sapiens	54-64
11523086-10	2001	The presence of two highly basic arginine residues on bradykinin results in its high GB(app), while the basicity of des-Arg1-bradykinin ions is increased by the presence of two proline residues at the N-terminus.	Proline	177-184	kininogen 1	Homo sapiens	54-64
11523086-10	2001	The presence of two highly basic arginine residues on bradykinin results in its high GB(app), while the basicity of des-Arg1-bradykinin ions is increased by the presence of two proline residues at the N-terminus.	Proline	177-184	kininogen 1	Homo sapiens	125-135
11483701-2	2001	To determine the mechanism of bradykinin-induced production of endothelium-derived contracting factors, we monitored the changes in cytosolic Ca(2+) concentration ([Ca(2+)](i)) in in situ endothelial cells in porcine aortic valvular strips and the changes in [Ca(2+)](i) of smooth muscle cells and force in porcine interlobar renal arterial strips using front-surface fluorometry of fura-2.	Fura-2	383-389	kininogen 1	Homo sapiens	30-40
11483701-4	2001	In the presence of N(omega)-nitro-L-arginine methyl ester, bradykinin caused an endothelium-dependent transient elevation of [Ca(2+)](i) and contraction in smooth muscle in the interlobar renal artery.	NG-Nitroarginine Methyl Ester	19-57	kininogen 1	Homo sapiens	59-69
11483701-10	2001	Pretreatment with either 10(-5) M 1-(beta-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenethyl)-1H-imidazole hydrochloride (SKF96365) or 0.2 mM Ni(2+) abolished the contraction induced by bradykinin in the presence of extracellular Ca(2+).	1-(beta-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenethyl)-1h-imidazole hydrochloride	34-117	kininogen 1	Homo sapiens	183-193
11483701-12	2001	Treatment with 10(-5) M indomethacin completely inhibited the contractile response induced by Ca(2+) replenishment, regardless of the timing of its application, before or after the application of bradykinin.	Indomethacin	24-36	kininogen 1	Homo sapiens	196-206
11483711-5	2001	Bradykinin, which activates PKC, also enhanced the response to capsaicin in DRG neurones.	Capsaicin	63-72	kininogen 1	Homo sapiens	0-10
11404259-6	2001	Coincubation with phosphoramidon augmented the effect of 10(-9) and 10(-8) M bradykinin.	phosphoramidon	18-32	kininogen 1	Homo sapiens	77-87
11487526-9	2001	Incubation in HEPES-buffered Tyrode solution abolishes the EDHF responses to substance P and bradykinin to reveal an additional hyperpolarizing mechanism, associated with the opening of K(+) channels, activated only by bradykinin.	HEPES	14-19	kininogen 1	Homo sapiens	93-103
11487526-9	2001	Incubation in HEPES-buffered Tyrode solution abolishes the EDHF responses to substance P and bradykinin to reveal an additional hyperpolarizing mechanism, associated with the opening of K(+) channels, activated only by bradykinin.	HEPES	14-19	kininogen 1	Homo sapiens	219-229
11487526-9	2001	Incubation in HEPES-buffered Tyrode solution abolishes the EDHF responses to substance P and bradykinin to reveal an additional hyperpolarizing mechanism, associated with the opening of K(+) channels, activated only by bradykinin.	tyrode	29-35	kininogen 1	Homo sapiens	93-103
11487526-9	2001	Incubation in HEPES-buffered Tyrode solution abolishes the EDHF responses to substance P and bradykinin to reveal an additional hyperpolarizing mechanism, associated with the opening of K(+) channels, activated only by bradykinin.	tyrode	29-35	kininogen 1	Homo sapiens	219-229
11487526-9	2001	Incubation in HEPES-buffered Tyrode solution abolishes the EDHF responses to substance P and bradykinin to reveal an additional hyperpolarizing mechanism, associated with the opening of K(+) channels, activated only by bradykinin.	edhf	59-63	kininogen 1	Homo sapiens	93-103
11406494-0	2001	Bradykinin and des-Arg(9)-bradykinin metabolic pathways and kinetics of activation of human plasma.	des-arg	15-22	kininogen 1	Homo sapiens	26-36
11406494-2	2001	The potentiating effect of an angiotensin-converting enzyme (ACE) inhibitor was, however, more extensive for BK (9.0-fold) than for des-Arg(9)-BK (2.2- fold).	des-arg	132-139	kininogen 1	Homo sapiens	143-145
11406494-5	2001	For des-Arg(9)-BK, the active metabolite of BK, the rate of degradation was higher in women compared with men, correlating significantly with serum APP activity (r(2) = 0.6485, P &lt; 0.001).	des-arg	4-11	kininogen 1	Homo sapiens	15-17
11406494-5	2001	For des-Arg(9)-BK, the active metabolite of BK, the rate of degradation was higher in women compared with men, correlating significantly with serum APP activity (r(2) = 0.6485, P &lt; 0.001).	des-arg	4-11	kininogen 1	Homo sapiens	44-46
11406499-4	2001	The NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (0.1 mM) reversed the BK-stimulated NO generation as measured with either DAF-2 or by the oxidation of Fe(2+) hemoglobin.	NG-Nitroarginine Methyl Ester	26-64	kininogen 1	Homo sapiens	87-89
11406499-4	2001	The NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (0.1 mM) reversed the BK-stimulated NO generation as measured with either DAF-2 or by the oxidation of Fe(2+) hemoglobin.	4,5-diaminofluorescein	139-144	kininogen 1	Homo sapiens	87-89
11406499-8	2001	We conclude that NO generation by isolated OMDVR can be increased by L-arginine, that the endothelium-dependent vasodilator BK enhances NO production, and that NO consumption by superoxide plays a role in the determination of cellular NO concentrations.	Superoxides	178-188	kininogen 1	Homo sapiens	124-126
11410114-12	2001	The mechanism could be either that lisinopril limits the angiotensin II-induced production of superoxide radicals which would normally inactivate NO, or that lisinopril may increase bradykinin-mediated NO release.	Lisinopril	158-168	kininogen 1	Homo sapiens	182-192
11444496-2	2001	In cultured porcine aortic endothelial cells, the sustained increases in the intracellular Ca2+ concentration ([Ca2+]i) elicited by bradykinin and cyclopiazonic acid, which were strongly dependent on the presence of extracellular Ca2+, were suppressed by the NSCC blockers, SK&amp;F 96365 and mefenamic acid.	amicloral	274-280	kininogen 1	Homo sapiens	132-142
11444496-2	2001	In cultured porcine aortic endothelial cells, the sustained increases in the intracellular Ca2+ concentration ([Ca2+]i) elicited by bradykinin and cyclopiazonic acid, which were strongly dependent on the presence of extracellular Ca2+, were suppressed by the NSCC blockers, SK&amp;F 96365 and mefenamic acid.	Mefenamic Acid	293-307	kininogen 1	Homo sapiens	132-142
11444496-4	2001	In the presence of SK&amp;F 96365 or mefenamic acid, the peak amplitude was severely reduced and the decay phase of hyperpolarization to bradykinin was greatly accelerated, which was apparently similar to the response obtained in Ca2+-free medium.	amicloral	19-25	kininogen 1	Homo sapiens	137-147
11444496-4	2001	In the presence of SK&amp;F 96365 or mefenamic acid, the peak amplitude was severely reduced and the decay phase of hyperpolarization to bradykinin was greatly accelerated, which was apparently similar to the response obtained in Ca2+-free medium.	Mefenamic Acid	37-51	kininogen 1	Homo sapiens	137-147
11444496-6	2001	In rings of coronary artery precontracted with U46619, bradykinin and cyclopiazonic acid produced endothelium-dependent relaxations even in the presence of N(G)-nitro-L-arginine and indomethacin.	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	47-53	kininogen 1	Homo sapiens	55-65
11444496-6	2001	In rings of coronary artery precontracted with U46619, bradykinin and cyclopiazonic acid produced endothelium-dependent relaxations even in the presence of N(G)-nitro-L-arginine and indomethacin.	Nitroarginine	156-177	kininogen 1	Homo sapiens	55-65
11444496-6	2001	In rings of coronary artery precontracted with U46619, bradykinin and cyclopiazonic acid produced endothelium-dependent relaxations even in the presence of N(G)-nitro-L-arginine and indomethacin.	Indomethacin	182-194	kininogen 1	Homo sapiens	55-65
11433227-10	2001	BK caused a transient increase in [Ca2(+)]i, which was significantly decreased by ANG II; concurrent addition of Losartan and PD 123319 prevented ANG II effect.	Losartan	113-121	kininogen 1	Homo sapiens	0-2
11433227-13	2001	In summary, ANG II increases extracellular/intracellular calcium dependent bidirectional Ca2(+) transport in GECs, inhibits BK induced release of Ca2(+) from IP(3) sensitive stores, and, in addition, reduces refilling of endoplasmic reticulum [Ca2(+)] depleted by repeated BK stimulation.	Inositol 1,4,5-Trisphosphate	158-163	kininogen 1	Homo sapiens	124-126
11418861-0	2001	Bradykinin and nerve growth factor release the capsaicin receptor from PtdIns(4,5)P2-mediated inhibition.	Phosphatidylinositol 4,5-Diphosphate	71-84	kininogen 1	Homo sapiens	0-10
11418861-5	2001	Diminution of plasma membrane phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) levels through antibody sequestration or PLC-mediated hydrolysis mimics the potentiating effects of bradykinin or NGF at the cellular level.	Phosphatidylinositol 4,5-Diphosphate	30-67	kininogen 1	Homo sapiens	184-194
11516436-4	2001	Intraplantar injection of interleukin-1beta into the hindpaw elicited mechanical hyperalgesia in the ipsilateral paw, as well as in the contralateral paw, following intraplantar injection of the bradykinin B(1) receptor agonist des-Arg(9)-bradykinin.	des-arg	228-235	kininogen 1	Homo sapiens	195-205
11516436-6	2001	In addition, following interleukin-1beta injection into the ipsilateral paw, co-administration of SB203580 with des-Arg(9)-bradykinin into the contralateral paw inhibited the bradykinin B(1) receptor-mediated hyperalgesia.	des-arg	112-119	kininogen 1	Homo sapiens	123-133
11275357-9	2001	Prostaglandins also facilitate membrane currents and release of substance P and CGRP induced by low pH, bradykinin and capsaicin.	Prostaglandins	0-14	kininogen 1	Homo sapiens	104-114
11380514-9	2001	The non-peptide bradykinin B2 receptor antagonist FR173657 selectively antagonized bradykinin-induced acidification responses in INT-407 cells in a competitive manner (pKB = 8.76+/-0.10; Hill slope = 0.92+/-0.05) at lower concentrations (1 and 3 nmol/L) but in an insurmountable manner at higher concentrations (10 nmol/L; Hill slope = 1.04+/-0.09).	FR 173657	50-58	kininogen 1	Homo sapiens	16-26
11380514-9	2001	The non-peptide bradykinin B2 receptor antagonist FR173657 selectively antagonized bradykinin-induced acidification responses in INT-407 cells in a competitive manner (pKB = 8.76+/-0.10; Hill slope = 0.92+/-0.05) at lower concentrations (1 and 3 nmol/L) but in an insurmountable manner at higher concentrations (10 nmol/L; Hill slope = 1.04+/-0.09).	FR 173657	50-58	kininogen 1	Homo sapiens	83-93
11305980-3	2001	Increased bradykinin levels, with the consequent enhanced synthesis of vasodilatory prostaglandins, appear to mediate a significant benefit of ACE inhibitor therapy in these patients.	Prostaglandins	84-98	kininogen 1	Homo sapiens	10-20
11312298-5	2001	In astrocytes, 4-AP treatment potentiated the sustained phase of the [Ca(2+)](i) elevation induced by ATP and bradykinin.	4-Aminopyridine	15-19	kininogen 1	Homo sapiens	110-120
11392569-0	2001	Exudation of plasma and production of thromboxane in human bronchi after local bradykinin challenge.	Thromboxanes	38-49	kininogen 1	Homo sapiens	79-89
11392569-13	2001	In study two, there was no numeric increase in plasma proteins after local bradykinin challenge, but the concentration of thromboxane was significantly increased in lavages from bradykinin-challenged bronchi.	Thromboxanes	122-133	kininogen 1	Homo sapiens	178-188
11392569-14	2001	Thus, local bronchial administration of bradykinin has the capacity to induce exudation of large plasma macromolecules into the bronchial lumen, as well as local thromboxane production.	Thromboxanes	162-173	kininogen 1	Homo sapiens	40-50
11247797-7	2001	Simultaneous with kallikrein formation, bradykinin (5.0 or 10.3 pmol/10(6) HUVEC in the absence or presence of lisinopril, respectively) is liberated from cell-bound HK.	Lisinopril	111-121	kininogen 1	Homo sapiens	40-50
11247797-8	2001	Liberated bradykinin stimulates the endothelial cell bradykinin B2 receptor to form nitric oxide.	Nitric Oxide	84-96	kininogen 1	Homo sapiens	10-20
11247797-8	2001	Liberated bradykinin stimulates the endothelial cell bradykinin B2 receptor to form nitric oxide.	Nitric Oxide	84-96	kininogen 1	Homo sapiens	53-63
11392476-5	2001	In addition, ACE inhibition of kininase inhibits the breakdown of bradykinin, a direct stimulant of nitric oxide release from the intact endothelial cell.	Nitric Oxide	100-112	kininogen 1	Homo sapiens	66-76
11397791-3	2001	eNOS Thr(495) was constitutively phosphorylated in porcine aortic endothelial cells and was rapidly dephosphorylated after bradykinin stimulation.	Threonine	5-8	kininogen 1	Homo sapiens	123-133
11397791-4	2001	In the same cells, bradykinin enhanced the phosphorylation of Ser(1177), which was maximal after 5 minutes, and abolished by the CaM-dependent kinase II (CaMKII) inhibitor KN-93.	Serine	62-65	kininogen 1	Homo sapiens	19-29
11397791-4	2001	In the same cells, bradykinin enhanced the phosphorylation of Ser(1177), which was maximal after 5 minutes, and abolished by the CaM-dependent kinase II (CaMKII) inhibitor KN-93.	KN 93	172-177	kininogen 1	Homo sapiens	19-29
11356600-4	2001	Infusion of KCl (0.33 mmol/min) into the brachial artery caused baseline vasodilation and inhibited the vasodilator response to bradykinin, but not to sodium nitroprusside.	Potassium Chloride	12-15	kininogen 1	Homo sapiens	128-138
11356600-5	2001	Thus the incremental vasodilation induced by bradykinin was reduced from 14.3 +/- 2 to 7.1 +/- 2 ml x min(-1) x 100 g(-1) (P &lt; 0.001) after KCl infusion.	Potassium Chloride	143-146	kininogen 1	Homo sapiens	45-55
11356600-6	2001	A similar inhibition of the bradykinin (P = 0.014), but not the sodium nitroprusside (not significant), response was observed with KCl after the study was repeated during preconstriction with phenylephrine to restore resting blood flow to basal values after KCl.	Potassium Chloride	131-134	kininogen 1	Homo sapiens	28-38
11356600-6	2001	A similar inhibition of the bradykinin (P = 0.014), but not the sodium nitroprusside (not significant), response was observed with KCl after the study was repeated during preconstriction with phenylephrine to restore resting blood flow to basal values after KCl.	Phenylephrine	192-205	kininogen 1	Homo sapiens	28-38
11356600-8	2001	However, after inhibition of cyclooxygenase and nitric oxide synthase with aspirin and NG-monomethyl-L-arginine, the forearm blood flow response to bradykinin (P = 0.003), but not to sodium nitroprusside (not significant), was significantly suppressed by miconazole.	Aspirin	75-82	kininogen 1	Homo sapiens	148-158
11356600-8	2001	However, after inhibition of cyclooxygenase and nitric oxide synthase with aspirin and NG-monomethyl-L-arginine, the forearm blood flow response to bradykinin (P = 0.003), but not to sodium nitroprusside (not significant), was significantly suppressed by miconazole.	omega-N-Methylarginine	87-111	kininogen 1	Homo sapiens	148-158
11356600-9	2001	Thus nitric oxide- and prostaglandin-independent, bradykinin-mediated forearm vasodilation is suppressed by high intravascular K+ concentrations, indicating a contribution of EDHF.	Nitric Oxide	5-17	kininogen 1	Homo sapiens	50-60
11356600-9	2001	Thus nitric oxide- and prostaglandin-independent, bradykinin-mediated forearm vasodilation is suppressed by high intravascular K+ concentrations, indicating a contribution of EDHF.	Prostaglandins	23-36	kininogen 1	Homo sapiens	50-60
11356600-9	2001	Thus nitric oxide- and prostaglandin-independent, bradykinin-mediated forearm vasodilation is suppressed by high intravascular K+ concentrations, indicating a contribution of EDHF.	edhf	175-179	kininogen 1	Homo sapiens	50-60
11356613-4	2001	Inhibiting nitric oxide synthase with 10(-5) M N(omega)-nitro-L-arginine methyl ester (L-NAME) blocked bradykinin-induced vasodilation but did not affect the flow-diameter relation or the maximum change in diameter from static conditions (67 +/- 10 microm in control vs. 71 +/- 8 microm after L-NAME, P = not significant).	Nitric Oxide	11-23	kininogen 1	Homo sapiens	103-113
11356613-4	2001	Inhibiting nitric oxide synthase with 10(-5) M N(omega)-nitro-L-arginine methyl ester (L-NAME) blocked bradykinin-induced vasodilation but did not affect the flow-diameter relation or the maximum change in diameter from static conditions (67 +/- 10 microm in control vs. 71 +/- 8 microm after L-NAME, P = not significant).	NG-Nitroarginine Methyl Ester	47-85	kininogen 1	Homo sapiens	103-113
11356613-4	2001	Inhibiting nitric oxide synthase with 10(-5) M N(omega)-nitro-L-arginine methyl ester (L-NAME) blocked bradykinin-induced vasodilation but did not affect the flow-diameter relation or the maximum change in diameter from static conditions (67 +/- 10 microm in control vs. 71 +/- 8 microm after L-NAME, P = not significant).	NG-Nitroarginine Methyl Ester	87-93	kininogen 1	Homo sapiens	103-113
11356613-6	2001	Depolarizing vascular smooth muscle with KCl (60 mM) or removing the endothelium blocked bradykinin vasodilation and completely abolished flow-mediated responses.	Potassium Chloride	41-44	kininogen 1	Homo sapiens	89-99
11458709-9	2001	Finally, regional changes in pH from lactic acid (but not hypercapnia), stimulate ventricular afferents and may activate kallikrein to increase bradykinin (BK), which, in turn, breaks down arachidonic acid to form prostaglandins.	Lactic Acid	37-48	kininogen 1	Homo sapiens	144-154
11458709-9	2001	Finally, regional changes in pH from lactic acid (but not hypercapnia), stimulate ventricular afferents and may activate kallikrein to increase bradykinin (BK), which, in turn, breaks down arachidonic acid to form prostaglandins.	Lactic Acid	37-48	kininogen 1	Homo sapiens	156-158
11458709-9	2001	Finally, regional changes in pH from lactic acid (but not hypercapnia), stimulate ventricular afferents and may activate kallikrein to increase bradykinin (BK), which, in turn, breaks down arachidonic acid to form prostaglandins.	Arachidonic Acid	189-205	kininogen 1	Homo sapiens	144-154
11458709-9	2001	Finally, regional changes in pH from lactic acid (but not hypercapnia), stimulate ventricular afferents and may activate kallikrein to increase bradykinin (BK), which, in turn, breaks down arachidonic acid to form prostaglandins.	Arachidonic Acid	189-205	kininogen 1	Homo sapiens	156-158
11458709-9	2001	Finally, regional changes in pH from lactic acid (but not hypercapnia), stimulate ventricular afferents and may activate kallikrein to increase bradykinin (BK), which, in turn, breaks down arachidonic acid to form prostaglandins.	Prostaglandins	214-228	kininogen 1	Homo sapiens	156-158
11458709-10	2001	Prostaglandins sensitize cardiac sympathetic afferents to BK.	Prostaglandins	0-14	kininogen 1	Homo sapiens	58-60
11352510-1	2001	We have previously demonstrated that bradykinin potentiates prostaglandin E(2)release in human gingival fibroblasts pretreated with interleukin-1 beta (priming).	Dinoprostone	60-78	kininogen 1	Homo sapiens	37-47
11352510-5	2001	In the primed fibroblasts, ionomycin and thapsigargin mimicked the potentiating effect of bradykinin on the cyclooxygenase-2 mRNA expression.	Ionomycin	27-36	kininogen 1	Homo sapiens	90-100
11352510-5	2001	In the primed fibroblasts, ionomycin and thapsigargin mimicked the potentiating effect of bradykinin on the cyclooxygenase-2 mRNA expression.	Thapsigargin	41-53	kininogen 1	Homo sapiens	90-100
11352510-6	2001	Dexamethasone and actinomycin D completely suppressed not only the interleukin-1 beta-induced cyclooxygenase-2 mRNA expression, but also the bradykinin-induced cyclooxygenase-2 mRNA expression in the interleukin-1 beta-primed fibroblasts, although cycloheximide did not inhibit the effects of interleukin-1 beta and bradykinin.	Dexamethasone	0-13	kininogen 1	Homo sapiens	141-151
11352510-6	2001	Dexamethasone and actinomycin D completely suppressed not only the interleukin-1 beta-induced cyclooxygenase-2 mRNA expression, but also the bradykinin-induced cyclooxygenase-2 mRNA expression in the interleukin-1 beta-primed fibroblasts, although cycloheximide did not inhibit the effects of interleukin-1 beta and bradykinin.	Dexamethasone	0-13	kininogen 1	Homo sapiens	316-326
11352510-6	2001	Dexamethasone and actinomycin D completely suppressed not only the interleukin-1 beta-induced cyclooxygenase-2 mRNA expression, but also the bradykinin-induced cyclooxygenase-2 mRNA expression in the interleukin-1 beta-primed fibroblasts, although cycloheximide did not inhibit the effects of interleukin-1 beta and bradykinin.	Dactinomycin	18-31	kininogen 1	Homo sapiens	141-151
11352510-6	2001	Dexamethasone and actinomycin D completely suppressed not only the interleukin-1 beta-induced cyclooxygenase-2 mRNA expression, but also the bradykinin-induced cyclooxygenase-2 mRNA expression in the interleukin-1 beta-primed fibroblasts, although cycloheximide did not inhibit the effects of interleukin-1 beta and bradykinin.	Dactinomycin	18-31	kininogen 1	Homo sapiens	316-326
11352510-6	2001	Dexamethasone and actinomycin D completely suppressed not only the interleukin-1 beta-induced cyclooxygenase-2 mRNA expression, but also the bradykinin-induced cyclooxygenase-2 mRNA expression in the interleukin-1 beta-primed fibroblasts, although cycloheximide did not inhibit the effects of interleukin-1 beta and bradykinin.	Cycloheximide	248-261	kininogen 1	Homo sapiens	141-151
11352510-7	2001	These results suggest that bradykinin-induced prostaglandin E2 synthesis is regulated at the level of the transcription of cyclooxygenase-2 mRNA via Ca2+ mobilization in the interleukin-1 beta-primed human gingival fibroblasts.	Dinoprostone	46-62	kininogen 1	Homo sapiens	27-37
11964841-2	2001	At physiological concentrations, vasodilator prostaglandins enhance the vascular permeability effects of histamine and bradykinin, and leukotrienes are important mediators of leukocyte accumulation during acute inflammation.	Prostaglandins	45-59	kininogen 1	Homo sapiens	119-129
11397846-5	2001	Vasodilator response to bradykinin, expressed as the within-subject mean difference in the area under the dose-response curve between phases, was significantly increased at midcycle compared with that in the early menstrual phase (486.5 +/- 165.0; P = 0.01), whereas there was no significant difference in response to glyceryl trinitrate (185.8 +/- 239.0; P = 0.45).	Nitroglycerin	318-337	kininogen 1	Homo sapiens	24-34
11342663-4	2001	The intracellular calcium increases in astrocytes, occurring spontaneously or as a result of mechanical or bradykinin stimulation, induced the release of ATP, which, in turn, was responsible for triggering a delayed calcium response in microglial cells.	Calcium	18-25	kininogen 1	Homo sapiens	107-117
11342663-4	2001	The intracellular calcium increases in astrocytes, occurring spontaneously or as a result of mechanical or bradykinin stimulation, induced the release of ATP, which, in turn, was responsible for triggering a delayed calcium response in microglial cells.	Adenosine Triphosphate	154-157	kininogen 1	Homo sapiens	107-117
11342663-4	2001	The intracellular calcium increases in astrocytes, occurring spontaneously or as a result of mechanical or bradykinin stimulation, induced the release of ATP, which, in turn, was responsible for triggering a delayed calcium response in microglial cells.	Calcium	216-223	kininogen 1	Homo sapiens	107-117
11393693-6	2001	The orthophosphoric acid initially added to the saliva allowed BK to be stabilized from enzymic degradation at 20 degrees C for 5 days and at 4 degrees C for 60 days.	phosphoric acid	4-24	kininogen 1	Homo sapiens	63-65
11392474-9	2001	Prevention of breakdown of bradykinin, substance P and neurotensin may result in direct vasodilation or release of nitrous oxide from the endothelium.	Nitrous Oxide	115-128	kininogen 1	Homo sapiens	27-37
11392475-13	2001	Furthermore, inhibition of ACE prolongs the half-life of bradykinin and stabilizes bradykinin receptors linked to the formation of nitric oxide and prostacyclin.	Nitric Oxide	131-143	kininogen 1	Homo sapiens	83-93
11392475-13	2001	Furthermore, inhibition of ACE prolongs the half-life of bradykinin and stabilizes bradykinin receptors linked to the formation of nitric oxide and prostacyclin.	Epoprostenol	148-160	kininogen 1	Homo sapiens	83-93
11292368-3	2001	In this study, we demonstrate that exogenous citrulline was as effective as exogenous arginine in stimulating nitric oxide production and that citrulline in the presence of excess intracellular and extracellular arginine further enhanced bradykinin stimulated endothelial nitric oxide production.	Citrulline	143-153	kininogen 1	Homo sapiens	238-248
11292368-3	2001	In this study, we demonstrate that exogenous citrulline was as effective as exogenous arginine in stimulating nitric oxide production and that citrulline in the presence of excess intracellular and extracellular arginine further enhanced bradykinin stimulated endothelial nitric oxide production.	Arginine	212-220	kininogen 1	Homo sapiens	238-248
11306421-8	2001	The soluble guanylyl cyclase inhibitor ODQ (10 micromol/L; n = 8) markedly reduced (P &lt;0.01) the relaxations induced by TSV, ACh, glyceryl trinitrate, and bradykinin.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	39-42	kininogen 1	Homo sapiens	158-168
11306421-9	2001	7-Nitroindazole (10 micromol/L; n = 8) inhibited the relaxations induced by TSV by 84% (P &lt;0.01) and also caused small, but significant, reductions in the ACh and bradykinin-induced HCC relaxations (P &lt;0.05).	7-nitroindazole	0-15	kininogen 1	Homo sapiens	166-176
11306421-9	2001	7-Nitroindazole (10 micromol/L; n = 8) inhibited the relaxations induced by TSV by 84% (P &lt;0.01) and also caused small, but significant, reductions in the ACh and bradykinin-induced HCC relaxations (P &lt;0.05).	(2r,6s,12z,13as,14ar,16as)-6-[(Tert-Butoxycarbonyl)amino]-14a-[(Cyclopropylsulfonyl)carbamoyl]-5,16-Dioxo-1,2,3,5,6,7,8,9,10,11,13a,14,14a,15,16,16a-Hexadecahydrocyclopropa[e]pyrrolo[1,2-A][1,4]diazacyclopentadecin-2-Yl 4-Fluoro-2h-Isoindole-2-Carboxylate	76-79	kininogen 1	Homo sapiens	166-176
11171630-8	2001	Indomethacin abolished gel thickening due to acid, bradykinin, and capsaicin.	Indomethacin	0-12	kininogen 1	Homo sapiens	51-61
11181410-3	2001	Here we demonstrate that acute exposure of human endothelial cells to glucose, at levels found in plasma of diabetic patients, results in a significant blunting of NO responses to the endothelial nitric oxide synthase (eNOS) agonists bradykinin and A-23187.	Glucose	70-77	kininogen 1	Homo sapiens	234-244
11181940-6	2001	administration of MEN 11270, Icatibant, or FR 173657 induced a dose-dependent (10-100 nmol/kg) inhibition of both hypotension and bronchoconstriction induced by bradykinin (10 nmol/kg i.v.).	FR 173657	43-52	kininogen 1	Homo sapiens	161-171
11411021-5	2001	RESULTS: Phorbol-12-myristate-13-acetate significantly upregulated the nephrin expression in A293 cells, while no change was found after treatment with additional stimulants for other main signalling pathways, e.g. okadaic acid, lysophosphatidic acid, bradykinin, angiotensin II (ANG II) and arginine vasopressin (AVP).	Tetradecanoylphorbol Acetate	9-40	kininogen 1	Homo sapiens	252-262
11287092-3	2001	The present study was designed to further characterize calcium signalling by NPY and bradykinin (BK) in LN319 cells.	Calcium	55-62	kininogen 1	Homo sapiens	85-95
11287092-3	2001	The present study was designed to further characterize calcium signalling by NPY and bradykinin (BK) in LN319 cells.	Calcium	55-62	kininogen 1	Homo sapiens	97-99
11287092-8	2001	The calcium release induced by BK on the other hand was largely PTX-insensitive, PLC-dependent, and from both thapsigargin- and ryanodine-sensitive stores.	Calcium	4-11	kininogen 1	Homo sapiens	31-33
11287092-8	2001	The calcium release induced by BK on the other hand was largely PTX-insensitive, PLC-dependent, and from both thapsigargin- and ryanodine-sensitive stores.	Thapsigargin	110-122	kininogen 1	Homo sapiens	31-33
11287092-8	2001	The calcium release induced by BK on the other hand was largely PTX-insensitive, PLC-dependent, and from both thapsigargin- and ryanodine-sensitive stores.	Ryanodine	128-137	kininogen 1	Homo sapiens	31-33
11330881-9	2001	A bradykinin B2 receptor antagonist abolished the suppressive effect of captopril on PAI-1 antigen.	Captopril	72-81	kininogen 1	Homo sapiens	2-12
11158972-3	2001	In porcine coronary artery precontracted with U-46619, bradykinin (BK) and cyclopiazonic acid (CPA) caused endothelium-dependent relaxations in the presence of N(G)-nitro-L-arginine (L-NNA).	Nitroarginine	160-181	kininogen 1	Homo sapiens	55-65
11158972-3	2001	In porcine coronary artery precontracted with U-46619, bradykinin (BK) and cyclopiazonic acid (CPA) caused endothelium-dependent relaxations in the presence of N(G)-nitro-L-arginine (L-NNA).	Nitroarginine	160-181	kininogen 1	Homo sapiens	67-69
11158972-3	2001	In porcine coronary artery precontracted with U-46619, bradykinin (BK) and cyclopiazonic acid (CPA) caused endothelium-dependent relaxations in the presence of N(G)-nitro-L-arginine (L-NNA).	Nitroarginine	183-188	kininogen 1	Homo sapiens	55-65
11158972-3	2001	In porcine coronary artery precontracted with U-46619, bradykinin (BK) and cyclopiazonic acid (CPA) caused endothelium-dependent relaxations in the presence of N(G)-nitro-L-arginine (L-NNA).	Nitroarginine	183-188	kininogen 1	Homo sapiens	67-69
11158972-5	2001	In the presence of Ni(2+), which inhibits Ca(2+) influx through nonselective cation channels, the BK-induced EDHF relaxant response was greatly diminished and the CPA-induced response was abolished.	Nickel(2+)	19-25	kininogen 1	Homo sapiens	98-100
11158972-5	2001	In the presence of Ni(2+), which inhibits Ca(2+) influx through nonselective cation channels, the BK-induced EDHF relaxant response was greatly diminished and the CPA-induced response was abolished.	edhf	109-113	kininogen 1	Homo sapiens	98-100
11158972-5	2001	In the presence of Ni(2+), which inhibits Ca(2+) influx through nonselective cation channels, the BK-induced EDHF relaxant response was greatly diminished and the CPA-induced response was abolished.	cyclopiazonic acid	163-166	kininogen 1	Homo sapiens	98-100
11158972-8	2001	EDHF-mediated relaxations and hyperpolarizations evoked by BK and CPA in porcine coronary artery showed a temporal correlation with the increases in [Ca(2+)](i) in porcine aortic endothelial cells.	edhf	0-4	kininogen 1	Homo sapiens	59-61
11235721-9	2001	Concentration-relaxation curves for bradykinin (n = 8 in each group) related to endothelium-derived hyperpolarizing factor (EDHF) were established in the rings precontracted with U46619 (30 microM) in the presence of Nomega-nitro-L-arginine (L-NNA, 300 microM) and indomethacin (7 microM).	edhf	124-128	kininogen 1	Homo sapiens	36-46
11245257-0	2001	NMR and simulated annealing investigations of bradykinin in presence of polyphenols.	Polyphenols	72-83	kininogen 1	Homo sapiens	46-56
11245257-8	2001	Thus, the biological activities of bradykinin in the presence of polyphenols could be affected.	Polyphenols	65-76	kininogen 1	Homo sapiens	35-45
11217909-11	2001	These findings provide further evidence of a link between ACEI-induced cough and I/D polymorphism of the ACE gene and suggest that ACEIs induce cough by modulating the tissue level of bradykinin.	acei	58-62	kininogen 1	Homo sapiens	184-194
11160513-12	2001	In amphotericin-perforated patches bradykinin (1 microM) activated TEA-sensitive currents that were abolished by preincubation with bis-(o-aminophenoxy)-N,N,N",N"-tetraacetic acid-AM (BAPTA-AM).	Amphotericin B	3-15	kininogen 1	Homo sapiens	35-45
11160513-12	2001	In amphotericin-perforated patches bradykinin (1 microM) activated TEA-sensitive currents that were abolished by preincubation with bis-(o-aminophenoxy)-N,N,N",N"-tetraacetic acid-AM (BAPTA-AM).	Tetraethylammonium	67-70	kininogen 1	Homo sapiens	35-45
11160513-12	2001	In amphotericin-perforated patches bradykinin (1 microM) activated TEA-sensitive currents that were abolished by preincubation with bis-(o-aminophenoxy)-N,N,N",N"-tetraacetic acid-AM (BAPTA-AM).	bis-(o-aminophenoxy)-n,n,n",n"-tetraacetic acid-am	132-182	kininogen 1	Homo sapiens	35-45
11160513-12	2001	In amphotericin-perforated patches bradykinin (1 microM) activated TEA-sensitive currents that were abolished by preincubation with bis-(o-aminophenoxy)-N,N,N",N"-tetraacetic acid-AM (BAPTA-AM).	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	184-192	kininogen 1	Homo sapiens	35-45
11217909-11	2001	These findings provide further evidence of a link between ACEI-induced cough and I/D polymorphism of the ACE gene and suggest that ACEIs induce cough by modulating the tissue level of bradykinin.	aceis	131-136	kininogen 1	Homo sapiens	184-194
11258664-2	2001	Here we show that the G protein-coupled bradykinin B2 receptor activates sphingosine kinase leading to a time- and dose-dependent elevation of cellular sphingosine 1-phosphate levels that was blocked by the sphingosine kinase inhibitor dihydrosphingosine.	sphingosine 1-phosphate	152-175	kininogen 1	Homo sapiens	40-50
11139472-3	2001	In bradykinin-stimulated coronary arteries, antisense oligonucleotides against CYP 2C almost abolished EDHF-mediated responses but potentiated nitric oxide (NO)-mediated relaxation.	Oligonucleotides	54-70	kininogen 1	Homo sapiens	3-13
11139472-4	2001	The selective CYP 2C9 inhibitor sulfaphenazole and the superoxide anion (O(2-)) scavengers Tiron and nordihydroguaretic acid also induced a leftward shift in the NO-mediated concentration-relaxation curve to bradykinin.	Sulfaphenazole	32-46	kininogen 1	Homo sapiens	208-218
11139472-4	2001	The selective CYP 2C9 inhibitor sulfaphenazole and the superoxide anion (O(2-)) scavengers Tiron and nordihydroguaretic acid also induced a leftward shift in the NO-mediated concentration-relaxation curve to bradykinin.	Superoxides	73-78	kininogen 1	Homo sapiens	208-218
11139472-4	2001	The selective CYP 2C9 inhibitor sulfaphenazole and the superoxide anion (O(2-)) scavengers Tiron and nordihydroguaretic acid also induced a leftward shift in the NO-mediated concentration-relaxation curve to bradykinin.	1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt	91-96	kininogen 1	Homo sapiens	208-218
11139472-4	2001	The selective CYP 2C9 inhibitor sulfaphenazole and the superoxide anion (O(2-)) scavengers Tiron and nordihydroguaretic acid also induced a leftward shift in the NO-mediated concentration-relaxation curve to bradykinin.	Masoprocol	101-124	kininogen 1	Homo sapiens	208-218
11139472-9	2001	In isolated coronary endothelial cells, bradykinin elicited a sulfaphenazole-sensitive increase in ROS production.	Sulfaphenazole	62-76	kininogen 1	Homo sapiens	40-50
11139472-9	2001	In isolated coronary endothelial cells, bradykinin elicited a sulfaphenazole-sensitive increase in ROS production.	Reactive Oxygen Species	99-102	kininogen 1	Homo sapiens	40-50
11137083-4	2001	The purpose of this investigation was to verify in vivo and in vitro vasoreactivity to bradykinin (BK) and serotonin (5-hydroxytryptamine; 5-HT) (endothelial dependent agonists) as well as to nitroglycerin (NTG) (exogenous nitric oxide donor) at different times after oversized balloon angioplasty intervention ranging from 1 h to 12 weeks, in normal porcine coronary arteries.	Nitroglycerin	192-205	kininogen 1	Homo sapiens	87-97
11137083-4	2001	The purpose of this investigation was to verify in vivo and in vitro vasoreactivity to bradykinin (BK) and serotonin (5-hydroxytryptamine; 5-HT) (endothelial dependent agonists) as well as to nitroglycerin (NTG) (exogenous nitric oxide donor) at different times after oversized balloon angioplasty intervention ranging from 1 h to 12 weeks, in normal porcine coronary arteries.	Nitroglycerin	207-210	kininogen 1	Homo sapiens	87-97
11137083-4	2001	The purpose of this investigation was to verify in vivo and in vitro vasoreactivity to bradykinin (BK) and serotonin (5-hydroxytryptamine; 5-HT) (endothelial dependent agonists) as well as to nitroglycerin (NTG) (exogenous nitric oxide donor) at different times after oversized balloon angioplasty intervention ranging from 1 h to 12 weeks, in normal porcine coronary arteries.	Nitric Oxide	223-235	kininogen 1	Homo sapiens	87-97
11258664-2	2001	Here we show that the G protein-coupled bradykinin B2 receptor activates sphingosine kinase leading to a time- and dose-dependent elevation of cellular sphingosine 1-phosphate levels that was blocked by the sphingosine kinase inhibitor dihydrosphingosine.	safingol	236-254	kininogen 1	Homo sapiens	40-50
11394922-9	2001	Bradykinin (10(-7)M) induced a significant PE, whereas serotonin was effective only at a concentration of 10(-3)M. While serotonin in lower concentrations induced moderate burning pain and an axon reflex flare but no PE, bradykinin provoked PE without pain or axon reflex flare at a concentration of 10(-7)M. Application of histamine similarly evoked PE at lower concentrations as compared to the induction of itch sensation and axon reflex flare.	Serotonin	121-130	kininogen 1	Homo sapiens	221-231
11347721-4	2001	Some of the beneficial effects of ACE inhibitors might be related to reduced degradation of bradykinin that enhances the synthesis of prostaglandins, while aspirin, through inhibiting the enzyme cyclo-oxygenase, inhibits the production of prostaglandins.	Prostaglandins	134-148	kininogen 1	Homo sapiens	92-102
11230284-9	2001	In addition, vasodilator response of balloon-injured coronary arteries to bradykinin was restored by perindopril treatment, whereas no vasodilator response was observed in balloon-injured vessels treated with vehicle.	Perindopril	101-112	kininogen 1	Homo sapiens	74-84
11805429-1	2001	BACKGROUND: The effect of bradykinin on intracellular free Ca(2+) levels ([Ca(2+)](i)) in MG63 human osteosarcoma cells was explored using fura-2 as a Ca(2+) dye.	Fura-2	139-145	kininogen 1	Homo sapiens	26-36
11805429-6	2001	Bradykinin (1 nM)-induced intracellular Ca(2+) release was nearly abolished by inhibiting phospholipase C with 2 microM 1-(6-((17 beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122).	1-(6-((17 beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1h-pyrrole-2,5-dione	120-205	kininogen 1	Homo sapiens	0-10
11805429-6	2001	Bradykinin (1 nM)-induced intracellular Ca(2+) release was nearly abolished by inhibiting phospholipase C with 2 microM 1-(6-((17 beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122).	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	207-213	kininogen 1	Homo sapiens	0-10
11805429-7	2001	The [Ca(2+)](i )increase induced by 1 nM bradykinin in Ca(2+)- free medium was abolished by 1 nM HOE 140 (a B2 bradykinin receptor antagonist) but was not altered by 100 nM Des-Arg-HOE 140 (a B1 bradykinin receptor antagonist).	4-hydroxy-2-octenal	97-100	kininogen 1	Homo sapiens	41-51
11805429-7	2001	The [Ca(2+)](i )increase induced by 1 nM bradykinin in Ca(2+)- free medium was abolished by 1 nM HOE 140 (a B2 bradykinin receptor antagonist) but was not altered by 100 nM Des-Arg-HOE 140 (a B1 bradykinin receptor antagonist).	des-arg	173-180	kininogen 1	Homo sapiens	41-51
11805429-7	2001	The [Ca(2+)](i )increase induced by 1 nM bradykinin in Ca(2+)- free medium was abolished by 1 nM HOE 140 (a B2 bradykinin receptor antagonist) but was not altered by 100 nM Des-Arg-HOE 140 (a B1 bradykinin receptor antagonist).	4-hydroxy-2-octenal	181-184	kininogen 1	Homo sapiens	41-51
11805429-8	2001	Pretreatment with 1 pM pertussis toxin for 5 h in Ca(2+) medium inhibited 30 +/- 3% of 1 nM bradykinin-induced peak [Ca(2+)](i) increase.	ca(2+) medium	50-63	kininogen 1	Homo sapiens	92-102
11805429-9	2001	CONCLUSIONS: Together, this study shows that bradykinin induced [Ca(2+)](i) increases in a concentration-dependent manner, by stimulating B2 bradykinin receptors leading to mobilization of Ca(2+) from the thapsigargin-sensitive stores in a manner dependent on inositol-1,4,5-trisphosphate, and also by inducing extracellular Ca(2+) influx.	Thapsigargin	205-217	kininogen 1	Homo sapiens	45-55
11805429-9	2001	CONCLUSIONS: Together, this study shows that bradykinin induced [Ca(2+)](i) increases in a concentration-dependent manner, by stimulating B2 bradykinin receptors leading to mobilization of Ca(2+) from the thapsigargin-sensitive stores in a manner dependent on inositol-1,4,5-trisphosphate, and also by inducing extracellular Ca(2+) influx.	Thapsigargin	205-217	kininogen 1	Homo sapiens	141-151
11805429-9	2001	CONCLUSIONS: Together, this study shows that bradykinin induced [Ca(2+)](i) increases in a concentration-dependent manner, by stimulating B2 bradykinin receptors leading to mobilization of Ca(2+) from the thapsigargin-sensitive stores in a manner dependent on inositol-1,4,5-trisphosphate, and also by inducing extracellular Ca(2+) influx.	Inositol 1,4,5-Trisphosphate	260-288	kininogen 1	Homo sapiens	45-55
11805429-9	2001	CONCLUSIONS: Together, this study shows that bradykinin induced [Ca(2+)](i) increases in a concentration-dependent manner, by stimulating B2 bradykinin receptors leading to mobilization of Ca(2+) from the thapsigargin-sensitive stores in a manner dependent on inositol-1,4,5-trisphosphate, and also by inducing extracellular Ca(2+) influx.	Inositol 1,4,5-Trisphosphate	260-288	kininogen 1	Homo sapiens	141-151
11715356-9	2001	In addition to their role in inhibiting the renin-angiotensin system, angiotensin-converting enzyme (ACE) inhibitors raise the activity of bradykinin, thereby leading to an increase in nitric oxide release.	Nitric Oxide	185-197	kininogen 1	Homo sapiens	139-149
11394922-9	2001	Bradykinin (10(-7)M) induced a significant PE, whereas serotonin was effective only at a concentration of 10(-3)M. While serotonin in lower concentrations induced moderate burning pain and an axon reflex flare but no PE, bradykinin provoked PE without pain or axon reflex flare at a concentration of 10(-7)M. Application of histamine similarly evoked PE at lower concentrations as compared to the induction of itch sensation and axon reflex flare.	Histamine	324-333	kininogen 1	Homo sapiens	0-10
11120633-6	2001	Increases in diaminofluorescein fluorescence were used to measure bradykinin activation of endothelial nitric oxide synthase (eNOS) with or without N-nitro-l-arginine (L-NNA).	diaminofluorescein	13-31	kininogen 1	Homo sapiens	66-76
11120633-10	2001	A two- to threefold increase in eNOS activity was observed upon activation by bradykinin which was completely inhibited in L-NNA-treated samples.	Nitroarginine	123-128	kininogen 1	Homo sapiens	78-88
11686395-9	2001	Acetylcholine and bradykinin induced a biphasic elevation of cytosolic calcium, which was antagonized by their receptor antagonists.	Calcium	71-78	kininogen 1	Homo sapiens	18-28
11208485-10	2001	RESULTS: In BAEC Bk via kinin B2 receptors raised in a concentration-dependent manner (1 pM-10 nM) free cytoplasmic calcium ions [Ca2+]i, that triggered the release of NO from BAEC.	Calcium	116-123	kininogen 1	Homo sapiens	17-19
11208485-12	2001	"Tissue type" ACE-Is, e.g. quinapril or perindopril acted through accumulation of endogenous Bk.	Quinapril	27-36	kininogen 1	Homo sapiens	93-95
11208485-12	2001	"Tissue type" ACE-Is, e.g. quinapril or perindopril acted through accumulation of endogenous Bk.	Perindopril	40-51	kininogen 1	Homo sapiens	93-95
11208485-17	2001	Bradykinin as a mediator of pleiotropic endothelial action of several cardiovascular drugs (e.g. ACE-I) may complete its mission not only through B2 receptor and [Ca2+]i--mediated release of PGI2 or NO.	Epoprostenol	191-195	kininogen 1	Homo sapiens	0-10
11208485-19	2001	Bk mediated induction of the [Ca2+]i-independent, so called "inducible", endothelial isoenzymes required for generation of CO, PGI2 and PGE2.	Carbon Monoxide	123-125	kininogen 1	Homo sapiens	0-2
11208485-19	2001	Bk mediated induction of the [Ca2+]i-independent, so called "inducible", endothelial isoenzymes required for generation of CO, PGI2 and PGE2.	Epoprostenol	127-131	kininogen 1	Homo sapiens	0-2
11208485-19	2001	Bk mediated induction of the [Ca2+]i-independent, so called "inducible", endothelial isoenzymes required for generation of CO, PGI2 and PGE2.	Dinoprostone	136-140	kininogen 1	Homo sapiens	0-2
11208485-26	2001	For instance, thrombolytic action of "tissue type" ACE-I depends on the Bk-released PGI2.	Epoprostenol	84-88	kininogen 1	Homo sapiens	72-74
11208485-29	2001	Moreover, acting as "microcytokine" Bk induces mRNAs for HO-1, COX-2 and PGE S, the isoenzymes responsible for a delayed endothelial biosynthesis of CO, PGI2 and PGE2.	Carbon Monoxide	63-65	kininogen 1	Homo sapiens	36-38
11208485-29	2001	Moreover, acting as "microcytokine" Bk induces mRNAs for HO-1, COX-2 and PGE S, the isoenzymes responsible for a delayed endothelial biosynthesis of CO, PGI2 and PGE2.	Epoprostenol	153-157	kininogen 1	Homo sapiens	36-38
11208485-29	2001	Moreover, acting as "microcytokine" Bk induces mRNAs for HO-1, COX-2 and PGE S, the isoenzymes responsible for a delayed endothelial biosynthesis of CO, PGI2 and PGE2.	Dinoprostone	162-166	kininogen 1	Homo sapiens	36-38
11507759-0	2001	Gas-phase conformers of the [M + 2H](2+) ion of bradykinin investigated by combining high-field asymmetric waveform ion mobility spectrometry, hydrogen/deuterium exchange, and energy-loss measurements.	Deuterium	33-35	kininogen 1	Homo sapiens	48-58
11507759-2	2001	Gas-phase conformers of the [M + 2H](2+) ion of bradykinin were examined using a combination of FAIMS, H/D exchange, and energy-loss measurements.	Deuterium	33-35	kininogen 1	Homo sapiens	48-58
11507759-3	2001	When FAIMS data and H/D exchange data were analyzed separately, the presence of only two conformers of the [M + 2H](2+) ion of bradykinin could be detected.	Deuterium	112-114	kininogen 1	Homo sapiens	127-137
11507759-4	2001	However, in an experiment in which FAIMS and H/D exchange were combined, at least four different conformers of the gas-phase [M + 2H](2+) ion of bradykinin were detected, including one of very low abundance.	Deuterium	130-132	kininogen 1	Homo sapiens	145-155
11675666-5	2001	Oligonucleotides (2- to 12-mer) and peptides (bradykinin, neurotensin) yield singly and doubly charged molecular ions with no detectable fragmentation.	Oligonucleotides	0-16	kininogen 1	Homo sapiens	46-56
11770034-12	2001	We conclude that removal of bradykinin and a decrease in the levels of NH3, potassium, and pH play a significant role in reducing water retention and postoperative lung injury.	Water	130-135	kininogen 1	Homo sapiens	28-38
11165666-2	2001	12-Lipoxygenase metabolites of arachidonic acid, produced by pain-inducing mediators such as bradykinin, might trigger vanilloid receptor activation by interacting with an intracellular site on the receptor.	Arachidonic Acid	31-47	kininogen 1	Homo sapiens	93-103
11164180-9	2001	RESULTS: In vitro, BK, forskolin, and sodium nitroprusside elicited dose-dependent relaxation of norepinephrine-induced tension of isolated HCC, and AN II evoked dose-dependent contraction of the HCC strips.	Norepinephrine	97-111	kininogen 1	Homo sapiens	19-21
11164180-10	2001	The relaxing potency of BK was paralleled by its ability to elevate the intracellular levels of cAMP and cGMP.	Cyclic AMP	96-100	kininogen 1	Homo sapiens	24-26
11164180-10	2001	The relaxing potency of BK was paralleled by its ability to elevate the intracellular levels of cAMP and cGMP.	Cyclic GMP	105-109	kininogen 1	Homo sapiens	24-26
11517684-0	2001	[Effects of anti-atherosclerotic low-sodium diet on dynamics of natural antibodies to angiotensin II, bradykinin and vasopressin in blood of patients with hypertension and obesity].	Sodium	37-43	kininogen 1	Homo sapiens	102-112
11106490-1	2000	The mammalian bradykinin-degrading enzyme aminopeptidase P (AP-P; E. C. 3.4.11.9) is a metal-dependent enzyme and is a member of the peptidase clan MG. AP-P exists as membrane-bound and cytosolic forms, which represent distinct gene products.	Metals	87-92	kininogen 1	Homo sapiens	14-24
11106490-6	2000	Hydrolysis of bradykinin was inhibited by 1,10-phenanthroline and by the specific inhibitor of the membrane-bound form of mammalian AP-P, apstatin.	1,10-phenanthroline	42-61	kininogen 1	Homo sapiens	14-24
11106490-6	2000	Hydrolysis of bradykinin was inhibited by 1,10-phenanthroline and by the specific inhibitor of the membrane-bound form of mammalian AP-P, apstatin.	apstatin	138-146	kininogen 1	Homo sapiens	14-24
11104833-2	2000	In organ bath experiments, Icatibant and FR173657 exerted a non-competitive antagonism (pKB 9.5 and 9.2, respectively) of the contractile response to bradykinin, whereas MEN 11270 showed competitive antagonism (pKB 8.3, slope -0.90).	FR 173657	41-49	kininogen 1	Homo sapiens	150-160
11104833-8	2000	In radioligand binding experiments, MEN 11270 and Icatibant displaced the [3H]bradykinin binding with pKi of 10.2 and 10.5 (Hill slope not different from unity), respectively.	Tritium	75-77	kininogen 1	Homo sapiens	78-88
11104833-9	2000	The non-peptide ligands displaced the [3H]bradykinin binding with similar affinity, their pKi being 8.7 and 8.6 for FR173657 and FR190997, respectively (both Hill slopes &lt;1).	Tritium	39-41	kininogen 1	Homo sapiens	42-52
11007574-11	2000	We conclude that, in sheep, PPE-induced bronchoconstriction is in part mediated by the generation of bradykinin.	ppe	28-31	kininogen 1	Homo sapiens	101-111
11419696-3	2001	The PLD activation induced by BK was blocked by pretreatment of A-431 cells with staurosporine, or by prolonged treatment with phorbol-12-myristate-13-acetate (PMA).	Staurosporine	81-94	kininogen 1	Homo sapiens	30-32
11419696-3	2001	The PLD activation induced by BK was blocked by pretreatment of A-431 cells with staurosporine, or by prolonged treatment with phorbol-12-myristate-13-acetate (PMA).	Tetradecanoylphorbol Acetate	127-158	kininogen 1	Homo sapiens	30-32
11419696-3	2001	The PLD activation induced by BK was blocked by pretreatment of A-431 cells with staurosporine, or by prolonged treatment with phorbol-12-myristate-13-acetate (PMA).	Tetradecanoylphorbol Acetate	160-163	kininogen 1	Homo sapiens	30-32
11419696-4	2001	PKC inhibitors Ro-31-8220 and bisindolylmaleimide I, showed the same inhibitory effects on the BK-stimulated increase of PLD activity, indicating a role of PKC in this activation process.	Ro 31-8220	15-25	kininogen 1	Homo sapiens	95-97
11419696-4	2001	PKC inhibitors Ro-31-8220 and bisindolylmaleimide I, showed the same inhibitory effects on the BK-stimulated increase of PLD activity, indicating a role of PKC in this activation process.	bisindolylmaleimide I	30-51	kininogen 1	Homo sapiens	95-97
11419696-7	2001	Furthermore, rottlerin and Go 6976, the PKC inhibitors specific for PKC-delta, -alpha and -betaI, respectively, markedly inhibited the PLD activity stimulated by BK.	rottlerin	13-22	kininogen 1	Homo sapiens	162-164
11419696-7	2001	Furthermore, rottlerin and Go 6976, the PKC inhibitors specific for PKC-delta, -alpha and -betaI, respectively, markedly inhibited the PLD activity stimulated by BK.	Go 6976	27-34	kininogen 1	Homo sapiens	162-164
11087238-4	2000	VSMC treated with BK (10(-8) M) for 24 h significantly increased alpha(2)(I) collagen mRNA levels.	vsmc	0-4	kininogen 1	Homo sapiens	18-20
11139431-3	2000	In these cells BK as well as Hoe 140 increased the rate of DNA synthesis measured with the [(3)H]-thymidine uptake assay.	Thymidine	98-107	kininogen 1	Homo sapiens	15-17
11139431-10	2000	In the cell lines SW-480 and H-69 both BK and Hoe 140 but not FR 173657 stimulated phosphatidylinositol hydrolysis.	Phosphatidylinositols	83-103	kininogen 1	Homo sapiens	39-41
11344778-3	2000	On the other hand, ACE inhibitors can increase bradykinin, and thus, nitric oxide, which may cause potent cardioprotection, inhibition of smooth muscle proliferation and attenuation of inflammation mechanisms.	Nitric Oxide	69-81	kininogen 1	Homo sapiens	47-57
11062335-4	2000	In the innervated skin histamine evoked a significant, dose-dependent plasma extravasation which was markedly augmented by the coadministration of a specific galanin receptor antagonist, galanin-1-16-bradykinin-2-9-amide (M35).	Histamine	23-32	kininogen 1	Homo sapiens	200-210
11092662-7	2000	Decrease in MVO2 was greater in LVAD hearts (n = 8) compared with heart failure controls (n = 18) in response to the following drugs: bradykinin (-34+/-3% vs. -24+/-5%), enalaprilat (-37+/-5% vs. -23+/-5%) and amlodipine (-43+/-13% vs. -16+/-5%; p&lt;0.05 from controls).	mvo2	12-16	kininogen 1	Homo sapiens	134-144
11092662-7	2000	Decrease in MVO2 was greater in LVAD hearts (n = 8) compared with heart failure controls (n = 18) in response to the following drugs: bradykinin (-34+/-3% vs. -24+/-5%), enalaprilat (-37+/-5% vs. -23+/-5%) and amlodipine (-43+/-13% vs. -16+/-5%; p&lt;0.05 from controls).	lvad	32-36	kininogen 1	Homo sapiens	134-144
11092662-9	2000	N(w)-nitro-L-arginine methyl ester, inhibitor of NO synthase, attenuated the response to bradykinin, enalaprilat and amlodipine.	n(w)-nitro-l-arginine methyl ester	0-34	kininogen 1	Homo sapiens	89-99
11068028-5	2000	Both retinoids produced a concentration-dependent rightward shift of the concentration-response curves for the bradykinin B1 receptor agonist, des-Arg(9)-bradykinin.	Retinoids	5-14	kininogen 1	Homo sapiens	111-121
11068028-5	2000	Both retinoids produced a concentration-dependent rightward shift of the concentration-response curves for the bradykinin B1 receptor agonist, des-Arg(9)-bradykinin.	des-arg	143-150	kininogen 1	Homo sapiens	111-121
11054467-4	2000	The B(1) receptor is activated by the des-Arg(9)kinin metabolites namely des-Arg(9)BK and Lys-des-Arg(9)BK, the synthesis of which are increased during inflammation.	des-arg	38-45	kininogen 1	Homo sapiens	83-85
11054467-4	2000	The B(1) receptor is activated by the des-Arg(9)kinin metabolites namely des-Arg(9)BK and Lys-des-Arg(9)BK, the synthesis of which are increased during inflammation.	des-arg	38-45	kininogen 1	Homo sapiens	104-106
11054467-4	2000	The B(1) receptor is activated by the des-Arg(9)kinin metabolites namely des-Arg(9)BK and Lys-des-Arg(9)BK, the synthesis of which are increased during inflammation.	des-arg	73-80	kininogen 1	Homo sapiens	83-85
11054467-4	2000	The B(1) receptor is activated by the des-Arg(9)kinin metabolites namely des-Arg(9)BK and Lys-des-Arg(9)BK, the synthesis of which are increased during inflammation.	lys-des-arg	90-101	kininogen 1	Homo sapiens	104-106
11046097-4	2000	Ramiprilat significantly increased the half-life of BK (P &lt;.01), but the effect was similar for the three kinds of tissues (297 +/- 104, 267 +/- 157, and 407 +/- 146 s, respectively; P = NS).	ramiprilat	0-10	kininogen 1	Homo sapiens	52-54
11046097-8	2000	Omapatrilat, a VPI, has a greater protective effect on BK metabolism than that of a pure ACE inhibitor.	omapatrilat	0-11	kininogen 1	Homo sapiens	55-57
11056091-2	2000	Although bradykinin is known to cause vasodilation through B(2) receptor-dependent effects on NO, prostacyclin, and endothelium-derived hyperpolarizing factor production, the mechanism(s) underlying tPA release is unknown.	Epoprostenol	98-110	kininogen 1	Homo sapiens	9-19
11056091-2	2000	Although bradykinin is known to cause vasodilation through B(2) receptor-dependent effects on NO, prostacyclin, and endothelium-derived hyperpolarizing factor production, the mechanism(s) underlying tPA release is unknown.	derived hyperpolarizing factor	128-158	kininogen 1	Homo sapiens	9-19
11056091-10	2000	The vasodilator response to endothelium-dependent (P:=0.019 for bradykinin) and endothelium-independent (P:=0.019) vasodilators was enhanced during indomethacin administration.	Indomethacin	148-160	kininogen 1	Homo sapiens	64-74
10997917-4	2000	We addressed this problem by using amperometric electrochemical NO detection with a porphyrinic microelectrode to study responses of endothelial cells incubated with homocysteine (Hcy) to the stimulation with bradykinin, calcium ionophore, or L-arginine.	Homocysteine	166-178	kininogen 1	Homo sapiens	209-219
10997917-4	2000	We addressed this problem by using amperometric electrochemical NO detection with a porphyrinic microelectrode to study responses of endothelial cells incubated with homocysteine (Hcy) to the stimulation with bradykinin, calcium ionophore, or L-arginine.	Homocysteine	180-183	kininogen 1	Homo sapiens	209-219
11027555-2	2000	Bradykinin (10 nM) and thapsigargin (1 microM) provoked large Ca(2+) influxes under fura-2/AM fluoroscopy.	Fura-2	84-90	kininogen 1	Homo sapiens	0-10
11003455-11	2000	In atopic subjects, cetirizine induced a significant reduction of flare reactions after the BK test (80% for IDT, and 94% for PT [P&lt;0.01]).	Cetirizine	20-30	kininogen 1	Homo sapiens	92-94
19667535-4	2000	Oxidized lipoproteins inhibit the release of the vasodilative substance nitric oxide, and angiotensin II degrades bradykinin, a potent stimulator of nitric oxide production in endothelial cells that is known to protect against atherosclerosis.	Nitric Oxide	149-161	kininogen 1	Homo sapiens	114-124
10852903-5	2000	After ATP or bradykinin stimulation, IICR-inhibited ECs showed a marked reduction of basal Ca(2+)(i), which was abolished by N(G)-monomethyl-l-arginine monoacetate pretreatment.	iicr	37-41	kininogen 1	Homo sapiens	13-23
10852903-5	2000	After ATP or bradykinin stimulation, IICR-inhibited ECs showed a marked reduction of basal Ca(2+)(i), which was abolished by N(G)-monomethyl-l-arginine monoacetate pretreatment.	n(g)-monomethyl-l-arginine monoacetate	125-163	kininogen 1	Homo sapiens	13-23
11003455-0	2000	Cetirizine inhibits bradykinin-induced cutaneous wheal and flare in atopic and healthy subjects.	Cetirizine	0-10	kininogen 1	Homo sapiens	20-30
11003455-3	2000	The aim of this study was to compare the possible effect of cetirizine (an H1-antagonist) on wheal and flare responses to BK, histamine, and compound 48/80 in atopic and healthy subjects.	Cetirizine	60-70	kininogen 1	Homo sapiens	122-124
10978247-1	2000	Nitric oxide (NO) production by endothelial cells in response to bradykinin (Bk) treatment was markedly and synergistically enhanced by cotreatment with sodium orthovanadate (vanadate), a phosphotyrosine phosphatase inhibitor.	Nitric Oxide	0-12	kininogen 1	Homo sapiens	65-75
10978247-1	2000	Nitric oxide (NO) production by endothelial cells in response to bradykinin (Bk) treatment was markedly and synergistically enhanced by cotreatment with sodium orthovanadate (vanadate), a phosphotyrosine phosphatase inhibitor.	Nitric Oxide	0-12	kininogen 1	Homo sapiens	77-79
10978247-1	2000	Nitric oxide (NO) production by endothelial cells in response to bradykinin (Bk) treatment was markedly and synergistically enhanced by cotreatment with sodium orthovanadate (vanadate), a phosphotyrosine phosphatase inhibitor.	Sodium orthovanadate	153-173	kininogen 1	Homo sapiens	65-75
10978247-1	2000	Nitric oxide (NO) production by endothelial cells in response to bradykinin (Bk) treatment was markedly and synergistically enhanced by cotreatment with sodium orthovanadate (vanadate), a phosphotyrosine phosphatase inhibitor.	Sodium orthovanadate	153-173	kininogen 1	Homo sapiens	77-79
10978247-1	2000	Nitric oxide (NO) production by endothelial cells in response to bradykinin (Bk) treatment was markedly and synergistically enhanced by cotreatment with sodium orthovanadate (vanadate), a phosphotyrosine phosphatase inhibitor.	Vanadates	165-173	kininogen 1	Homo sapiens	65-75
10978247-1	2000	Nitric oxide (NO) production by endothelial cells in response to bradykinin (Bk) treatment was markedly and synergistically enhanced by cotreatment with sodium orthovanadate (vanadate), a phosphotyrosine phosphatase inhibitor.	Vanadates	165-173	kininogen 1	Homo sapiens	77-79
10978247-6	2000	Western blots of immunoprecipitated eNOS showed the presence of a major tyrosine-phosphorylated protein band at a mass corresponding to approximately 125 kDa and 2 minor bands corresponding to approximately 105 and 75 kDa after treatment with vanadate/Bk.	Tyrosine	72-80	kininogen 1	Homo sapiens	252-254
10978247-6	2000	Western blots of immunoprecipitated eNOS showed the presence of a major tyrosine-phosphorylated protein band at a mass corresponding to approximately 125 kDa and 2 minor bands corresponding to approximately 105 and 75 kDa after treatment with vanadate/Bk.	Vanadates	243-251	kininogen 1	Homo sapiens	252-254
10978247-8	2000	Geldanamycin, an inhibitor of heat shock protein 90, also inhibited the enhancement of NO production by vanadate/Bk or vanadate/A23187, and there was an increase in the amount of heat shock protein 90 that coimmunoprecipitated with eNOS after treatment with vanadate/Bk.	geldanamycin	0-12	kininogen 1	Homo sapiens	113-115
10978247-8	2000	Geldanamycin, an inhibitor of heat shock protein 90, also inhibited the enhancement of NO production by vanadate/Bk or vanadate/A23187, and there was an increase in the amount of heat shock protein 90 that coimmunoprecipitated with eNOS after treatment with vanadate/Bk.	geldanamycin	0-12	kininogen 1	Homo sapiens	267-269
10978247-8	2000	Geldanamycin, an inhibitor of heat shock protein 90, also inhibited the enhancement of NO production by vanadate/Bk or vanadate/A23187, and there was an increase in the amount of heat shock protein 90 that coimmunoprecipitated with eNOS after treatment with vanadate/Bk.	Vanadates	104-112	kininogen 1	Homo sapiens	113-115
10861382-6	2000	That effect could not be assigned to the BK higher concentration at the membrane surface, due to its higher net charge (2(+)) compared to the fragments (1(+)), because ten times more des-Arg(9)-BK (100 mol %) yielded opposite result.	des-arg	183-190	kininogen 1	Homo sapiens	194-196
10973143-0	2000	Bradykinin enhances membrane electrical activity of pancreatic beta cells in the presence of low glucose concentrations.	Glucose	97-104	kininogen 1	Homo sapiens	0-10
10973143-1	2000	In most of cells bradykinin (BK) induces intracellular calcium mobilization.	Calcium	55-62	kininogen 1	Homo sapiens	17-27
10973143-1	2000	In most of cells bradykinin (BK) induces intracellular calcium mobilization.	Calcium	55-62	kininogen 1	Homo sapiens	29-31
10973143-9	2000	Thus, the stimulatory process obtained in the presence of BK and of a non-stimulatory concentration of glucose in the present study suggests that BK may facilitate the action of glucose on beta cell secretion.	Glucose	103-110	kininogen 1	Homo sapiens	146-148
10973143-9	2000	Thus, the stimulatory process obtained in the presence of BK and of a non-stimulatory concentration of glucose in the present study suggests that BK may facilitate the action of glucose on beta cell secretion.	Glucose	178-185	kininogen 1	Homo sapiens	58-60
10973143-9	2000	Thus, the stimulatory process obtained in the presence of BK and of a non-stimulatory concentration of glucose in the present study suggests that BK may facilitate the action of glucose on beta cell secretion.	Glucose	178-185	kininogen 1	Homo sapiens	146-148
10991911-0	2000	L-NAME-resistant bradykinin-induced relaxation in porcine coronary arteries is NO-dependent: effect of ACE inhibition.	NG-Nitroarginine Methyl Ester	0-6	kininogen 1	Homo sapiens	17-27
10991911-16	2000	Adding quinaprilat to the bath following repeated exposure (with or without L-NAME), at the time BK and HT-BK no longer induced relaxation, fully restored vasorelaxation, while quinaprilat alone had no effect.	quinaprilat	7-18	kininogen 1	Homo sapiens	97-99
10991911-19	2000	In conclusion, L-NAME-resistant BK-induced relaxation in PCAs depends on NO from storage sites, and is mediated via stimulation of guanylyl cyclase and/or Ca(2+)-dependent K(+)-channels.	NG-Nitroarginine Methyl Ester	15-21	kininogen 1	Homo sapiens	32-34
10969039-11	2000	Basal NO-dependent and bradykinin-stimulated levels of cGMP were higher (P:&lt;0.05) in P than in NP arteries.	Cyclic GMP	55-59	kininogen 1	Homo sapiens	23-33
10969042-8	2000	ACE2 can also cleave des-Arg bradykinin and neurotensin but not bradykinin or 15 other vasoactive and hormonal peptides tested.	des-arg	21-28	kininogen 1	Homo sapiens	29-39
10973545-11	2000	The bradykinin level in the hypothermic group was significantly higher just after cardiopulmonary bypass than that in the tepid group (2.40+/-0.32 vs. 1.85+/-0.21 log(10) (pg/ml), P=0.005).	tepid	122-127	kininogen 1	Homo sapiens	4-14
11003455-12	2000	Moreover, cetirizine reduced significantly BK-induced wheals by 70% for IDT (P&lt;0.01) and 65% for PT (P&lt;0.01).	Cetirizine	10-20	kininogen 1	Homo sapiens	43-45
11003455-12	2000	Moreover, cetirizine reduced significantly BK-induced wheals by 70% for IDT (P&lt;0.01) and 65% for PT (P&lt;0.01).	Platinum	100-102	kininogen 1	Homo sapiens	43-45
11003455-14	2000	CONCLUSIONS: These findings showed that the wheal and flare reactions induced by BK challenge were markedly inhibited by previous intake of cetirizine.	Cetirizine	140-150	kininogen 1	Homo sapiens	81-83
11028659-8	2000	Furthermore, PD98059 or SB203580 significantly suppressed BK-induced IL-6 and IL-8 production and their gene expression.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	13-20	kininogen 1	Homo sapiens	58-60
11028659-8	2000	Furthermore, PD98059 or SB203580 significantly suppressed BK-induced IL-6 and IL-8 production and their gene expression.	SB 203580	24-32	kininogen 1	Homo sapiens	58-60
11129088-4	2000	The effect of various concentrations of CLT (2-15 microM) on BK-induced proliferation of HSMC was quantitated by spectrometry following [3H]-thymidine incorporation, and intracellular calcium [Ca+]i was determined by spectrofluorimetry using Fura 2-AM assay.	Clotrimazole	40-43	kininogen 1	Homo sapiens	61-63
11129088-4	2000	The effect of various concentrations of CLT (2-15 microM) on BK-induced proliferation of HSMC was quantitated by spectrometry following [3H]-thymidine incorporation, and intracellular calcium [Ca+]i was determined by spectrofluorimetry using Fura 2-AM assay.	hsmc	89-93	kininogen 1	Homo sapiens	61-63
11129088-7	2000	The results showed that 10 microM CLT: (i) inhibits the BK-induced proliferation of HSMC by 45-50%: (ii) prevents the rise of [Ca2+]i induced by BK (120.8 +/- 12.4 nM vs. 235.8 +/- 34.1 nM), an cffect similar to that of "classic" L-type calcium channels blockers: (iii) reduces the release of Ca2+ entry induced by thapsigargin suggesting a possible inhibition of the capacitative Ca2+ entry.	hsmc	84-88	kininogen 1	Homo sapiens	56-58
11129088-7	2000	The results showed that 10 microM CLT: (i) inhibits the BK-induced proliferation of HSMC by 45-50%: (ii) prevents the rise of [Ca2+]i induced by BK (120.8 +/- 12.4 nM vs. 235.8 +/- 34.1 nM), an cffect similar to that of "classic" L-type calcium channels blockers: (iii) reduces the release of Ca2+ entry induced by thapsigargin suggesting a possible inhibition of the capacitative Ca2+ entry.	Thapsigargin	315-327	kininogen 1	Homo sapiens	145-147
11129088-8	2000	Organ bath assays showed that CLT enhanced the BK-induced relaxation of the resistance arteries by an endothelium NO-independent pathway.	Clotrimazole	30-33	kininogen 1	Homo sapiens	47-49
10994858-8	2000	The NOS inhibitor L-nitroarginine methylester (L-NAME) caused significantly greater contraction in AdCMVeNOS-transduced rings (P &lt; 0.001; n = 4) and inhibited bradykinin-induced relaxations in control and transduced rings (P &lt; 0.001; n = 6).	H-Arg(NO2)-OH	18-33	kininogen 1	Homo sapiens	162-172
10994858-8	2000	The NOS inhibitor L-nitroarginine methylester (L-NAME) caused significantly greater contraction in AdCMVeNOS-transduced rings (P &lt; 0.001; n = 4) and inhibited bradykinin-induced relaxations in control and transduced rings (P &lt; 0.001; n = 6).	NG-Nitroarginine Methyl Ester	47-53	kininogen 1	Homo sapiens	162-172
11016880-0	2000	Bradykinin analogues with beta-amino acid substitutions reveal subtle differences in substrate specificity between the endopeptidases EC 3.4.24.15 and EC 3.4.24.16.	beta-amino acid	26-41	kininogen 1	Homo sapiens	0-10
11016880-0	2000	Bradykinin analogues with beta-amino acid substitutions reveal subtle differences in substrate specificity between the endopeptidases EC 3.4.24.15 and EC 3.4.24.16.	ec	134-136	kininogen 1	Homo sapiens	0-10
11016880-5	2000	Alanine-substituted analogues were generally better substrates than BK itself, although differences between the peptidases were observed.	Alanine	0-7	kininogen 1	Homo sapiens	68-70
10801799-0	2000	Activation of NF-kappa B by bradykinin through a Galpha(q)- and Gbeta gamma-dependent pathway that involves phosphoinositide 3-kinase and Akt.	galpha(q)	49-58	kininogen 1	Homo sapiens	28-38
10940387-3	2000	Here we show that the depletion of cellular Ca2+ stores by thapsigargin or bradykinin is functionally linked to a phosphoinositide-specific phospholipase D (PLD) activity in cultured vascular smooth muscle cells (VSMC), and that phosphatidic acid formed via PLD enhances sustained calcium entry in this cell type.	Phosphatidic Acids	229-246	kininogen 1	Homo sapiens	75-85
10940387-3	2000	Here we show that the depletion of cellular Ca2+ stores by thapsigargin or bradykinin is functionally linked to a phosphoinositide-specific phospholipase D (PLD) activity in cultured vascular smooth muscle cells (VSMC), and that phosphatidic acid formed via PLD enhances sustained calcium entry in this cell type.	Calcium	281-288	kininogen 1	Homo sapiens	75-85
10924042-3	2000	Bradykinin (BK)-induced dilation was mediated by EDHF, when NO and prostaglandin syntheses were inhibited, or by NO when EDHF and prostaglandin syntheses were blocked.	edhf	49-53	kininogen 1	Homo sapiens	0-10
10924042-3	2000	Bradykinin (BK)-induced dilation was mediated by EDHF, when NO and prostaglandin syntheses were inhibited, or by NO when EDHF and prostaglandin syntheses were blocked.	edhf	49-53	kininogen 1	Homo sapiens	12-14
10924042-3	2000	Bradykinin (BK)-induced dilation was mediated by EDHF, when NO and prostaglandin syntheses were inhibited, or by NO when EDHF and prostaglandin syntheses were blocked.	Prostaglandins	67-80	kininogen 1	Homo sapiens	0-10
10924042-3	2000	Bradykinin (BK)-induced dilation was mediated by EDHF, when NO and prostaglandin syntheses were inhibited, or by NO when EDHF and prostaglandin syntheses were blocked.	Prostaglandins	67-80	kininogen 1	Homo sapiens	12-14
10924042-3	2000	Bradykinin (BK)-induced dilation was mediated by EDHF, when NO and prostaglandin syntheses were inhibited, or by NO when EDHF and prostaglandin syntheses were blocked.	edhf	121-125	kininogen 1	Homo sapiens	0-10
10924042-3	2000	Bradykinin (BK)-induced dilation was mediated by EDHF, when NO and prostaglandin syntheses were inhibited, or by NO when EDHF and prostaglandin syntheses were blocked.	edhf	121-125	kininogen 1	Homo sapiens	12-14
10924042-3	2000	Bradykinin (BK)-induced dilation was mediated by EDHF, when NO and prostaglandin syntheses were inhibited, or by NO when EDHF and prostaglandin syntheses were blocked.	Prostaglandins	130-143	kininogen 1	Homo sapiens	0-10
10924042-3	2000	Bradykinin (BK)-induced dilation was mediated by EDHF, when NO and prostaglandin syntheses were inhibited, or by NO when EDHF and prostaglandin syntheses were blocked.	Prostaglandins	130-143	kininogen 1	Homo sapiens	12-14
10924042-7	2000	The residual dilation to BK with L-NMMA and Indo was completely abolished by suffusion of miconazole or an isosmotic buffer containing high KCl (60 mM), suggesting that this arteriolar vasodilation is mediated by the cytochrome P-450 derivative EDHF.	omega-N-Methylarginine	33-39	kininogen 1	Homo sapiens	25-27
10924042-7	2000	The residual dilation to BK with L-NMMA and Indo was completely abolished by suffusion of miconazole or an isosmotic buffer containing high KCl (60 mM), suggesting that this arteriolar vasodilation is mediated by the cytochrome P-450 derivative EDHF.	Indomethacin	44-48	kininogen 1	Homo sapiens	25-27
10924042-7	2000	The residual dilation to BK with L-NMMA and Indo was completely abolished by suffusion of miconazole or an isosmotic buffer containing high KCl (60 mM), suggesting that this arteriolar vasodilation is mediated by the cytochrome P-450 derivative EDHF.	Miconazole	90-100	kininogen 1	Homo sapiens	25-27
10924042-7	2000	The residual dilation to BK with L-NMMA and Indo was completely abolished by suffusion of miconazole or an isosmotic buffer containing high KCl (60 mM), suggesting that this arteriolar vasodilation is mediated by the cytochrome P-450 derivative EDHF.	Potassium Chloride	140-143	kininogen 1	Homo sapiens	25-27
10924042-7	2000	The residual dilation to BK with L-NMMA and Indo was completely abolished by suffusion of miconazole or an isosmotic buffer containing high KCl (60 mM), suggesting that this arteriolar vasodilation is mediated by the cytochrome P-450 derivative EDHF.	edhf	245-249	kininogen 1	Homo sapiens	25-27
10924042-8	2000	BK-induced dilation was reduced by 39% after inhibition of EDHF and prostaglandin synthesis, and dilation was further inhibited by combined blockade with L-NMMA to a 74% reduction in the response.	edhf	59-63	kininogen 1	Homo sapiens	0-2
10924042-8	2000	BK-induced dilation was reduced by 39% after inhibition of EDHF and prostaglandin synthesis, and dilation was further inhibited by combined blockade with L-NMMA to a 74% reduction in the response.	Prostaglandins	68-81	kininogen 1	Homo sapiens	0-2
10924042-8	2000	BK-induced dilation was reduced by 39% after inhibition of EDHF and prostaglandin synthesis, and dilation was further inhibited by combined blockade with L-NMMA to a 74% reduction in the response.	omega-N-Methylarginine	154-160	kininogen 1	Homo sapiens	0-2
10924042-13	2000	Dilation to BK was virtually abolished when administered concomitantly with SNP during L-NMMA and Indo (P &lt; 0.01 vs. before SNP), suggesting that NO inhibits EDHF-induced dilation.	omega-N-Methylarginine	87-93	kininogen 1	Homo sapiens	12-14
10924042-13	2000	Dilation to BK was virtually abolished when administered concomitantly with SNP during L-NMMA and Indo (P &lt; 0.01 vs. before SNP), suggesting that NO inhibits EDHF-induced dilation.	Indomethacin	98-102	kininogen 1	Homo sapiens	12-14
10924042-13	2000	Dilation to BK was virtually abolished when administered concomitantly with SNP during L-NMMA and Indo (P &lt; 0.01 vs. before SNP), suggesting that NO inhibits EDHF-induced dilation.	edhf	161-165	kininogen 1	Homo sapiens	12-14
10943881-10	2000	Indeed, in arterioles constricted with phenylephrine, the endothelial stimuli acetylcholine or bradykinin evoked endothelium-dependent relaxation that was similar in control and SSc arterioles.	Phenylephrine	39-52	kininogen 1	Homo sapiens	95-105
10976548-6	2000	RESULTS: Transdermal nicotine reduced the venous responsiveness to bradykinin in nonsmokers (Emax = 88.0% +/- 17.9% and 54.3% +/- 14.9%, respectively, before and after the nicotine patch; P &lt; .05); the latter response was similar to that in smokers (Emax = 56.3% +/- 16.6%).	Nicotine	21-29	kininogen 1	Homo sapiens	67-77
10976548-6	2000	RESULTS: Transdermal nicotine reduced the venous responsiveness to bradykinin in nonsmokers (Emax = 88.0% +/- 17.9% and 54.3% +/- 14.9%, respectively, before and after the nicotine patch; P &lt; .05); the latter response was similar to that in smokers (Emax = 56.3% +/- 16.6%).	Nicotine	172-180	kininogen 1	Homo sapiens	67-77
10948078-0	2000	Effects of bradykinin on prostaglandin I(2) synthesis in human vascular endothelial cells.	Epoprostenol	25-43	kininogen 1	Homo sapiens	11-21
10948078-1	2000	The effects of bradykinin on the regulatory mechanisms of prostacyclin synthesis in endothelial cells were investigated in association with intracellular Ca(2+) kinetics, cytosolic phospholipase A(2) (cPLA(2)) activity, and mRNA expression of cPLA(2) and prostaglandin H synthase (PGHS) isoforms.	Epoprostenol	58-70	kininogen 1	Homo sapiens	15-25
10948078-2	2000	Bradykinin enhanced prostacyclin release from endothelial cells time-dependently, but pretreatment with EGTA H-7 or HOE 140 inhibited bradykinin-induced prostacyclin release.	Epoprostenol	20-32	kininogen 1	Homo sapiens	0-10
10948078-2	2000	Bradykinin enhanced prostacyclin release from endothelial cells time-dependently, but pretreatment with EGTA H-7 or HOE 140 inhibited bradykinin-induced prostacyclin release.	Egtazic Acid	104-108	kininogen 1	Homo sapiens	134-144
10948078-2	2000	Bradykinin enhanced prostacyclin release from endothelial cells time-dependently, but pretreatment with EGTA H-7 or HOE 140 inhibited bradykinin-induced prostacyclin release.	Epoprostenol	153-165	kininogen 1	Homo sapiens	134-144
10948078-10	2000	These findings suggest that the elevation of cPLA(2) activity caused by the increase of intracellular Ca(2+) concentration is important in the early phase of bradykinin-induced prostacyclin synthesis and that the mechanisms regulating cPLA(2) are different from those regulating PGHS isoforms in endothelial cells.	Epoprostenol	177-189	kininogen 1	Homo sapiens	158-168
10948084-1	2000	We investigated the effect of angiotensin-converting enzyme inhibitors on glucose uptake regulation as well as the effect of bradykinin (BK) on glucose uptake and its regulation by using inhibitors of phospholipase C, BK B2 receptor, protein kinase C, phosphatidylinositol 3-kinase, tyrosine kinase, and intracellular Ca(2+).	Glucose	144-151	kininogen 1	Homo sapiens	125-135
10948084-1	2000	We investigated the effect of angiotensin-converting enzyme inhibitors on glucose uptake regulation as well as the effect of bradykinin (BK) on glucose uptake and its regulation by using inhibitors of phospholipase C, BK B2 receptor, protein kinase C, phosphatidylinositol 3-kinase, tyrosine kinase, and intracellular Ca(2+).	Glucose	144-151	kininogen 1	Homo sapiens	137-139
10948084-6	2000	In the presence of 1 nmol/L of insulin, exposure to 10 micromol/L BK stimulated glucose uptake from 89.2+/-8.1 to 171.6+/-10.1 pmol/h per mg protein.	Glucose	80-87	kininogen 1	Homo sapiens	66-68
10948084-8	2000	One hundred nanomoles per liter of tyrphostin A-23 and genistein, which are tyrosine kinase inhibitors, significantly decreased the BK-induced glucose uptake from 142.0+/-8.4 to 87.6+/-6.	tyrphostin A23	35-50	kininogen 1	Homo sapiens	132-134
10948084-8	2000	One hundred nanomoles per liter of tyrphostin A-23 and genistein, which are tyrosine kinase inhibitors, significantly decreased the BK-induced glucose uptake from 142.0+/-8.4 to 87.6+/-6.	Genistein	55-64	kininogen 1	Homo sapiens	132-134
10948084-8	2000	One hundred nanomoles per liter of tyrphostin A-23 and genistein, which are tyrosine kinase inhibitors, significantly decreased the BK-induced glucose uptake from 142.0+/-8.4 to 87.6+/-6.	Glucose	143-150	kininogen 1	Homo sapiens	132-134
10948084-10	2000	BK-induced glucose uptake was inhibited significantly by 10 micromol/L U73122 (a phospholipase C antagonist) from 142.0+/-8.4 to 95.7+/-9.5 pmol/h per mg protein.	Glucose	11-18	kininogen 1	Homo sapiens	0-2
10948084-10	2000	BK-induced glucose uptake was inhibited significantly by 10 micromol/L U73122 (a phospholipase C antagonist) from 142.0+/-8.4 to 95.7+/-9.5 pmol/h per mg protein.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	71-77	kininogen 1	Homo sapiens	0-2
10948084-11	2000	One and 20 micromol/L of TMB-8 (an intracellular calcium antagonist) significantly decreased BK-induced glucose uptake from 142.0+/-8.4 to 108.0+/-9.6 and 100.8+/-11.4 pmol/h per mg protein.	8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate	25-30	kininogen 1	Homo sapiens	93-95
10948084-11	2000	One and 20 micromol/L of TMB-8 (an intracellular calcium antagonist) significantly decreased BK-induced glucose uptake from 142.0+/-8.4 to 108.0+/-9.6 and 100.8+/-11.4 pmol/h per mg protein.	Calcium	49-56	kininogen 1	Homo sapiens	93-95
10948084-11	2000	One and 20 micromol/L of TMB-8 (an intracellular calcium antagonist) significantly decreased BK-induced glucose uptake from 142.0+/-8.4 to 108.0+/-9.6 and 100.8+/-11.4 pmol/h per mg protein.	Glucose	104-111	kininogen 1	Homo sapiens	93-95
10948084-13	2000	BK-stimulated glucose uptake is related to phospholipase C, tyrosine kinase, and an increase in intracellular calcium.	Glucose	14-21	kininogen 1	Homo sapiens	0-2
10948084-13	2000	BK-stimulated glucose uptake is related to phospholipase C, tyrosine kinase, and an increase in intracellular calcium.	Calcium	110-117	kininogen 1	Homo sapiens	0-2
10948089-7	2000	In organ bath experiments, pretreatment with nifedipine enhanced bradykinin-induced, EDHF-mediated relaxations as well as the concomitant hyperpolarization of smooth muscle cells.	Nifedipine	45-55	kininogen 1	Homo sapiens	65-75
10948089-7	2000	In organ bath experiments, pretreatment with nifedipine enhanced bradykinin-induced, EDHF-mediated relaxations as well as the concomitant hyperpolarization of smooth muscle cells.	edhf	85-89	kininogen 1	Homo sapiens	65-75
10948089-9	2000	These results demonstrate that in porcine coronary arteries, the elevated expression of a CYP epoxygenase, homologous to CYP2C8/9, is associated with enhanced EDHF-mediated hyperpolarization in response to bradykinin.	edhf	159-163	kininogen 1	Homo sapiens	206-216
10900238-3	2000	BK and its ACE-resistant peptide analog activated the B(2) receptor to release arachidonic acid and elevate [Ca(2+)](i) and subsequently desensitized it.	Arachidonic Acid	79-95	kininogen 1	Homo sapiens	0-2
11016327-1	2000	BACKGROUND: The bradykinin (BK)-induced endothelium-dependent relaxation is impaired in the presence of elevated potassium concentration enhancing the vasospastic tendency of large coronary arteries.	Potassium	113-122	kininogen 1	Homo sapiens	16-26
11016327-1	2000	BACKGROUND: The bradykinin (BK)-induced endothelium-dependent relaxation is impaired in the presence of elevated potassium concentration enhancing the vasospastic tendency of large coronary arteries.	Potassium	113-122	kininogen 1	Homo sapiens	28-30
11016327-5	2000	The rings were isometrically contracted with potassium chloride (30 mmol/L) and the response to BK (1 to 1,000 nmol/L)-induced relaxation was investigated in the presence of nitric oxide synthase inhibitor Nomega-nitro-L-arginine (300 micromol/L) alone and in combination with the cyclooxygenase inhibitor indomethacin (10 micromol/L), and that of the inhibitor of calcium-dependent potassium channels tetraethylammonium (7 mmol/L).	Nitroarginine	206-229	kininogen 1	Homo sapiens	96-98
11016327-5	2000	The rings were isometrically contracted with potassium chloride (30 mmol/L) and the response to BK (1 to 1,000 nmol/L)-induced relaxation was investigated in the presence of nitric oxide synthase inhibitor Nomega-nitro-L-arginine (300 micromol/L) alone and in combination with the cyclooxygenase inhibitor indomethacin (10 micromol/L), and that of the inhibitor of calcium-dependent potassium channels tetraethylammonium (7 mmol/L).	Indomethacin	306-318	kininogen 1	Homo sapiens	96-98
11016327-5	2000	The rings were isometrically contracted with potassium chloride (30 mmol/L) and the response to BK (1 to 1,000 nmol/L)-induced relaxation was investigated in the presence of nitric oxide synthase inhibitor Nomega-nitro-L-arginine (300 micromol/L) alone and in combination with the cyclooxygenase inhibitor indomethacin (10 micromol/L), and that of the inhibitor of calcium-dependent potassium channels tetraethylammonium (7 mmol/L).	Tetraethylammonium	402-420	kininogen 1	Homo sapiens	96-98
11016327-9	2000	CONCLUSIONS: In the present study phosphoramidon potentiated the effect of BK in the absence of nitric oxide and prostaglandins in porcine-isolated coronary artery.	phosphoramidon	34-48	kininogen 1	Homo sapiens	75-77
10900238-9	2000	Protein kinase C or phosphatase inhibitors, however, blocked the effects of BK on the receptor resensitized by enalaprilat or ramiprilat.	Enalaprilat	111-122	kininogen 1	Homo sapiens	76-78
10900238-9	2000	Protein kinase C or phosphatase inhibitors, however, blocked the effects of BK on the receptor resensitized by enalaprilat or ramiprilat.	ramiprilat	126-136	kininogen 1	Homo sapiens	76-78
11035208-4	2000	On the other hand, morphine-induced blockade of bradykinin (BK, a B(2)-receptor agonist)-responses was attenuated by pertussis toxin (PTX) treatment, whereas that of spinorphin was not.	Morphine	19-27	kininogen 1	Homo sapiens	48-58
10916114-2	2000	Some of the effects of BK are mediated by nitric oxide (NO).	Nitric Oxide	42-54	kininogen 1	Homo sapiens	23-25
11035208-4	2000	On the other hand, morphine-induced blockade of bradykinin (BK, a B(2)-receptor agonist)-responses was attenuated by pertussis toxin (PTX) treatment, whereas that of spinorphin was not.	Morphine	19-27	kininogen 1	Homo sapiens	60-62
10913258-2	2000	We assayed two series of bradykinin-related peptides flanked by o-aminobenzoic acid (Abz) and N-(2,4-dinitrophenyl)ethylenediamine (EDDnp), namely, Abz-GFSPFXQ-EDDnp and Abz-GFSPFRX-EDDnp (X = natural amino acids), in which the fluorescence appeared when Abz/EDDnp are separated by substrate hydrolysis.	ortho-Aminobenzoates	64-83	kininogen 1	Homo sapiens	25-35
10913258-2	2000	We assayed two series of bradykinin-related peptides flanked by o-aminobenzoic acid (Abz) and N-(2,4-dinitrophenyl)ethylenediamine (EDDnp), namely, Abz-GFSPFXQ-EDDnp and Abz-GFSPFRX-EDDnp (X = natural amino acids), in which the fluorescence appeared when Abz/EDDnp are separated by substrate hydrolysis.	ortho-Aminobenzoates	85-88	kininogen 1	Homo sapiens	25-35
10913258-2	2000	We assayed two series of bradykinin-related peptides flanked by o-aminobenzoic acid (Abz) and N-(2,4-dinitrophenyl)ethylenediamine (EDDnp), namely, Abz-GFSPFXQ-EDDnp and Abz-GFSPFRX-EDDnp (X = natural amino acids), in which the fluorescence appeared when Abz/EDDnp are separated by substrate hydrolysis.	N-(2,4-dinitrophenyl)ethylenediamine	94-130	kininogen 1	Homo sapiens	25-35
10913258-2	2000	We assayed two series of bradykinin-related peptides flanked by o-aminobenzoic acid (Abz) and N-(2,4-dinitrophenyl)ethylenediamine (EDDnp), namely, Abz-GFSPFXQ-EDDnp and Abz-GFSPFRX-EDDnp (X = natural amino acids), in which the fluorescence appeared when Abz/EDDnp are separated by substrate hydrolysis.	n1-(2,4-dinitrophenyl)ethane-1,2-diamine	132-137	kininogen 1	Homo sapiens	25-35
10913258-2	2000	We assayed two series of bradykinin-related peptides flanked by o-aminobenzoic acid (Abz) and N-(2,4-dinitrophenyl)ethylenediamine (EDDnp), namely, Abz-GFSPFXQ-EDDnp and Abz-GFSPFRX-EDDnp (X = natural amino acids), in which the fluorescence appeared when Abz/EDDnp are separated by substrate hydrolysis.	abz-gfspfxq-eddnp	148-165	kininogen 1	Homo sapiens	25-35
10913258-2	2000	We assayed two series of bradykinin-related peptides flanked by o-aminobenzoic acid (Abz) and N-(2,4-dinitrophenyl)ethylenediamine (EDDnp), namely, Abz-GFSPFXQ-EDDnp and Abz-GFSPFRX-EDDnp (X = natural amino acids), in which the fluorescence appeared when Abz/EDDnp are separated by substrate hydrolysis.	abz-gfspfrx-eddnp	170-187	kininogen 1	Homo sapiens	25-35
10913258-2	2000	We assayed two series of bradykinin-related peptides flanked by o-aminobenzoic acid (Abz) and N-(2,4-dinitrophenyl)ethylenediamine (EDDnp), namely, Abz-GFSPFXQ-EDDnp and Abz-GFSPFRX-EDDnp (X = natural amino acids), in which the fluorescence appeared when Abz/EDDnp are separated by substrate hydrolysis.	ortho-Aminobenzoates	148-151	kininogen 1	Homo sapiens	25-35
10913258-2	2000	We assayed two series of bradykinin-related peptides flanked by o-aminobenzoic acid (Abz) and N-(2,4-dinitrophenyl)ethylenediamine (EDDnp), namely, Abz-GFSPFXQ-EDDnp and Abz-GFSPFRX-EDDnp (X = natural amino acids), in which the fluorescence appeared when Abz/EDDnp are separated by substrate hydrolysis.	n1-(2,4-dinitrophenyl)ethane-1,2-diamine	160-165	kininogen 1	Homo sapiens	25-35
10919570-4	2000	RESULTS: In the rings (normalized diameter: 200-500 microM) precontracted by U46619, EDHF-mediated relaxation and hyperpolarization were initiated by bradykinin (BK) or A23187 in the presence of indomethacin and NG-nitro-L-arginine.	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	77-83	kininogen 1	Homo sapiens	150-160
10919570-4	2000	RESULTS: In the rings (normalized diameter: 200-500 microM) precontracted by U46619, EDHF-mediated relaxation and hyperpolarization were initiated by bradykinin (BK) or A23187 in the presence of indomethacin and NG-nitro-L-arginine.	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	77-83	kininogen 1	Homo sapiens	162-164
10919570-4	2000	RESULTS: In the rings (normalized diameter: 200-500 microM) precontracted by U46619, EDHF-mediated relaxation and hyperpolarization were initiated by bradykinin (BK) or A23187 in the presence of indomethacin and NG-nitro-L-arginine.	edhf	85-89	kininogen 1	Homo sapiens	150-160
10919570-4	2000	RESULTS: In the rings (normalized diameter: 200-500 microM) precontracted by U46619, EDHF-mediated relaxation and hyperpolarization were initiated by bradykinin (BK) or A23187 in the presence of indomethacin and NG-nitro-L-arginine.	edhf	85-89	kininogen 1	Homo sapiens	162-164
10919570-4	2000	RESULTS: In the rings (normalized diameter: 200-500 microM) precontracted by U46619, EDHF-mediated relaxation and hyperpolarization were initiated by bradykinin (BK) or A23187 in the presence of indomethacin and NG-nitro-L-arginine.	Indomethacin	195-207	kininogen 1	Homo sapiens	150-160
10919570-4	2000	RESULTS: In the rings (normalized diameter: 200-500 microM) precontracted by U46619, EDHF-mediated relaxation and hyperpolarization were initiated by bradykinin (BK) or A23187 in the presence of indomethacin and NG-nitro-L-arginine.	Indomethacin	195-207	kininogen 1	Homo sapiens	162-164
10919570-4	2000	RESULTS: In the rings (normalized diameter: 200-500 microM) precontracted by U46619, EDHF-mediated relaxation and hyperpolarization were initiated by bradykinin (BK) or A23187 in the presence of indomethacin and NG-nitro-L-arginine.	Nitroarginine	212-231	kininogen 1	Homo sapiens	150-160
10919570-4	2000	RESULTS: In the rings (normalized diameter: 200-500 microM) precontracted by U46619, EDHF-mediated relaxation and hyperpolarization were initiated by bradykinin (BK) or A23187 in the presence of indomethacin and NG-nitro-L-arginine.	Nitroarginine	212-231	kininogen 1	Homo sapiens	162-164
10919570-5	2000	In the human coronary arteries, the EDHF-mediated relaxation to BK was reduced by UW solution from 53.2+/-5.6% to 24.0+/-2.7% (P=0.006).	edhf	36-40	kininogen 1	Homo sapiens	64-66
10919570-6	2000	The reduced EDHF-mediated relaxation occurred concurrently with the decreased hyperpolarization to BK (17.0+/-1.5 vs. 10.5+/-1.1 mV, n=10, P=0.004) or A23187 in porcine coronary arteries.	edhf	12-16	kininogen 1	Homo sapiens	99-101
10871321-7	2000	BK1-5 (Arg-Pro-Pro-Gly-Phe), the 1-to-5 amino acid fragment of bradykinin, was identified as a major stable plasma metabolite of bradykinin.	Arginine	7-10	kininogen 1	Homo sapiens	63-73
10893317-6	2000	Incubation with a high-glucose concentration for 7 days significantly downregulated, whereas insulin significantly upregulated, basal and bradykinin-stimulated NO production and eNOS expression in cultured endothelial cells.	Glucose	23-30	kininogen 1	Homo sapiens	138-148
10874500-8	2000	In cultured RMIC, AngII, ET, BK, ANP and AVP act on their respective receptors to induce various cellular responses, including contraction, prostaglandin synthesis, cell proliferation and/or extracellular matrix synthesis.	Prostaglandins	140-153	kininogen 1	Homo sapiens	29-31
10904025-8	2000	Our study indicates that the bradykinin B(2) receptor antagonist icatibant attenuates the short-term blood pressure-lowering effect of acute ACE inhibition in normal men on a normal sodium diet.	Sodium	182-188	kininogen 1	Homo sapiens	29-39
10871321-7	2000	BK1-5 (Arg-Pro-Pro-Gly-Phe), the 1-to-5 amino acid fragment of bradykinin, was identified as a major stable plasma metabolite of bradykinin.	Arginine	7-10	kininogen 1	Homo sapiens	129-139
10871321-7	2000	BK1-5 (Arg-Pro-Pro-Gly-Phe), the 1-to-5 amino acid fragment of bradykinin, was identified as a major stable plasma metabolite of bradykinin.	Proline	11-14	kininogen 1	Homo sapiens	63-73
10871321-7	2000	BK1-5 (Arg-Pro-Pro-Gly-Phe), the 1-to-5 amino acid fragment of bradykinin, was identified as a major stable plasma metabolite of bradykinin.	Proline	11-14	kininogen 1	Homo sapiens	129-139
10871321-7	2000	BK1-5 (Arg-Pro-Pro-Gly-Phe), the 1-to-5 amino acid fragment of bradykinin, was identified as a major stable plasma metabolite of bradykinin.	Proline	15-18	kininogen 1	Homo sapiens	63-73
10871321-7	2000	BK1-5 (Arg-Pro-Pro-Gly-Phe), the 1-to-5 amino acid fragment of bradykinin, was identified as a major stable plasma metabolite of bradykinin.	Proline	15-18	kininogen 1	Homo sapiens	129-139
10871321-7	2000	BK1-5 (Arg-Pro-Pro-Gly-Phe), the 1-to-5 amino acid fragment of bradykinin, was identified as a major stable plasma metabolite of bradykinin.	Glycine	19-22	kininogen 1	Homo sapiens	63-73
10871321-7	2000	BK1-5 (Arg-Pro-Pro-Gly-Phe), the 1-to-5 amino acid fragment of bradykinin, was identified as a major stable plasma metabolite of bradykinin.	Glycine	19-22	kininogen 1	Homo sapiens	129-139
10871321-7	2000	BK1-5 (Arg-Pro-Pro-Gly-Phe), the 1-to-5 amino acid fragment of bradykinin, was identified as a major stable plasma metabolite of bradykinin.	Phenylalanine	23-26	kininogen 1	Homo sapiens	63-73
10871321-7	2000	BK1-5 (Arg-Pro-Pro-Gly-Phe), the 1-to-5 amino acid fragment of bradykinin, was identified as a major stable plasma metabolite of bradykinin.	Phenylalanine	23-26	kininogen 1	Homo sapiens	129-139
10910005-4	2000	In rat studies, plasma bradykinin concentrations also significantly increased after 1 hour of swimming in nondiabetic and mildly diabetic (streptozotocin [STZ] 45 mg/kg intravenously [IV]) rats, but not in rats with severe diabetes (STZ 65 mg/kg IV).	Streptozocin	139-153	kininogen 1	Homo sapiens	23-33
10910005-2	2000	In this study, we evaluated the involvement of bradykinin in exercise-induced glucose uptake in humans and rats.	Glucose	78-85	kininogen 1	Homo sapiens	47-57
16604161-6	2000	The lowest energy structure of the salt-bridge form of bradykinin is 10.6 kcal/mol lower in energy (EDF1) than the lowest energy simple protonated form at the 6-311G* level.	Salts	35-39	kininogen 1	Homo sapiens	55-65
10871044-5	2000	How hsAmP relates to hmAmP has clinical significance in that both can inactivate bradykinin, and AmP deficiency states have been described.	hsamp	4-9	kininogen 1	Homo sapiens	81-91
10871044-5	2000	How hsAmP relates to hmAmP has clinical significance in that both can inactivate bradykinin, and AmP deficiency states have been described.	hmamp	21-26	kininogen 1	Homo sapiens	81-91
10912465-4	2000	RESULTS: In large arteries pretreated with indomethacin, bradykinin (BK) evoked a rise in [NO] from 5.5+/-2.4 nM to 105.0+/-19.6 nM and hyperpolarization.	Indomethacin	43-55	kininogen 1	Homo sapiens	57-67
10912465-4	2000	RESULTS: In large arteries pretreated with indomethacin, bradykinin (BK) evoked a rise in [NO] from 5.5+/-2.4 nM to 105.0+/-19.6 nM and hyperpolarization.	Indomethacin	43-55	kininogen 1	Homo sapiens	69-71
10912465-5	2000	L-NNA treatment significantly reduced the BK-stimulated rise in [NO] to 32.1+/-11.3 nM but did not affect the hyperpolarization.	Nitroarginine	0-5	kininogen 1	Homo sapiens	42-44
10912465-9	2000	Tetraethylammonium, charybdotoxin, and iberiotoxin partially decreased the BK-induced responses.	Tetraethylammonium	0-18	kininogen 1	Homo sapiens	75-77
10912465-9	2000	Tetraethylammonium, charybdotoxin, and iberiotoxin partially decreased the BK-induced responses.	Charybdotoxin	20-33	kininogen 1	Homo sapiens	75-77
10912465-9	2000	Tetraethylammonium, charybdotoxin, and iberiotoxin partially decreased the BK-induced responses.	iberiotoxin	39-50	kininogen 1	Homo sapiens	75-77
10912465-10	2000	Apamin alone did not affect the relaxation by BK; however, in combination with charybdotoxin it almost completely abolished the BK-induced relaxation and hyperpolarization.	Charybdotoxin	79-92	kininogen 1	Homo sapiens	128-130
10912465-11	2000	CONCLUSIONS: In porcine coronary arteries, both EDHF and NO contribute to BK-induced relaxation resistance to indomethacin and L-NNA.	edhf	48-52	kininogen 1	Homo sapiens	74-76
10912465-11	2000	CONCLUSIONS: In porcine coronary arteries, both EDHF and NO contribute to BK-induced relaxation resistance to indomethacin and L-NNA.	Indomethacin	110-122	kininogen 1	Homo sapiens	74-76
10912465-11	2000	CONCLUSIONS: In porcine coronary arteries, both EDHF and NO contribute to BK-induced relaxation resistance to indomethacin and L-NNA.	Nitroarginine	127-132	kininogen 1	Homo sapiens	74-76
10949162-2	2000	A detailed NMR study is carried out in acetonitrile/water solutions on three novel cyclic bradykinin antagonist analogues, BKM-824, BKM-870, and BKM-872, to examine their solution structures, and to correlate the structures with bradykinin antagonist and anti-cancer activities.	bkm-824	123-130	kininogen 1	Homo sapiens	90-100
10949162-2	2000	A detailed NMR study is carried out in acetonitrile/water solutions on three novel cyclic bradykinin antagonist analogues, BKM-824, BKM-870, and BKM-872, to examine their solution structures, and to correlate the structures with bradykinin antagonist and anti-cancer activities.	BKM 870	132-139	kininogen 1	Homo sapiens	90-100
10949162-2	2000	A detailed NMR study is carried out in acetonitrile/water solutions on three novel cyclic bradykinin antagonist analogues, BKM-824, BKM-870, and BKM-872, to examine their solution structures, and to correlate the structures with bradykinin antagonist and anti-cancer activities.	BKM 872	145-152	kininogen 1	Homo sapiens	90-100
10826452-3	2000	Currently, it is perceived that a significant part of the beneficial effect of ACE inhibitors is related to augmentation of bradykinin levels, which among other effects stimulate the release of prostacyclin.	Epoprostenol	194-206	kininogen 1	Homo sapiens	124-134
10882364-1	2000	We recently described a potent bradykinin B(2) receptor agonist (JMV1116) obtained by replacing the D-Tic-Oic dipeptide moiety of HOE140 by a (3S)-amino-5-(carbonylmethyl)-2,3-dihydro-1, 5-benzothiazepin-4(5H)-one (D-BT) moiety.	Dipeptides	110-119	kininogen 1	Homo sapiens	31-41
10882364-1	2000	We recently described a potent bradykinin B(2) receptor agonist (JMV1116) obtained by replacing the D-Tic-Oic dipeptide moiety of HOE140 by a (3S)-amino-5-(carbonylmethyl)-2,3-dihydro-1, 5-benzothiazepin-4(5H)-one (D-BT) moiety.	(3s)-amino-5-(carbonylmethyl)-2,3-dihydro-1, 5-benzothiazepin-4(5h)-one	142-213	kininogen 1	Homo sapiens	31-41
10882364-1	2000	We recently described a potent bradykinin B(2) receptor agonist (JMV1116) obtained by replacing the D-Tic-Oic dipeptide moiety of HOE140 by a (3S)-amino-5-(carbonylmethyl)-2,3-dihydro-1, 5-benzothiazepin-4(5H)-one (D-BT) moiety.	d-bt	215-219	kininogen 1	Homo sapiens	31-41
10856283-1	2000	Bradykinin (BK) stimulates endothelial cells to release a number of relaxing factors, such as NO, prostanoids (PGs), and an endothelium-derived hyperpolarizing factor (EDHF).	Prostaglandins	98-109	kininogen 1	Homo sapiens	0-10
10856283-1	2000	Bradykinin (BK) stimulates endothelial cells to release a number of relaxing factors, such as NO, prostanoids (PGs), and an endothelium-derived hyperpolarizing factor (EDHF).	Prostaglandins	98-109	kininogen 1	Homo sapiens	12-14
10856283-1	2000	Bradykinin (BK) stimulates endothelial cells to release a number of relaxing factors, such as NO, prostanoids (PGs), and an endothelium-derived hyperpolarizing factor (EDHF).	Phosphatidylglycerols	111-114	kininogen 1	Homo sapiens	0-10
10856283-1	2000	Bradykinin (BK) stimulates endothelial cells to release a number of relaxing factors, such as NO, prostanoids (PGs), and an endothelium-derived hyperpolarizing factor (EDHF).	Phosphatidylglycerols	111-114	kininogen 1	Homo sapiens	12-14
10856283-1	2000	Bradykinin (BK) stimulates endothelial cells to release a number of relaxing factors, such as NO, prostanoids (PGs), and an endothelium-derived hyperpolarizing factor (EDHF).	endothelium-derived hyperpolarizing factor	124-166	kininogen 1	Homo sapiens	0-10
10856283-1	2000	Bradykinin (BK) stimulates endothelial cells to release a number of relaxing factors, such as NO, prostanoids (PGs), and an endothelium-derived hyperpolarizing factor (EDHF).	endothelium-derived hyperpolarizing factor	124-166	kininogen 1	Homo sapiens	12-14
10856283-1	2000	Bradykinin (BK) stimulates endothelial cells to release a number of relaxing factors, such as NO, prostanoids (PGs), and an endothelium-derived hyperpolarizing factor (EDHF).	edhf	168-172	kininogen 1	Homo sapiens	0-10
10856283-1	2000	Bradykinin (BK) stimulates endothelial cells to release a number of relaxing factors, such as NO, prostanoids (PGs), and an endothelium-derived hyperpolarizing factor (EDHF).	edhf	168-172	kininogen 1	Homo sapiens	12-14
10856283-2	2000	However, the contributions of NO, PG, and EDHF in the vascular relaxation to BK vary with species and anatomic origin of blood vessels used.	edhf	42-46	kininogen 1	Homo sapiens	77-79
10856283-3	2000	Therefore, the present study was designed to investigate the contributions of NO, PG, and EDHF in vasodilation caused by BK in human forearm resistance vessels.	edhf	90-94	kininogen 1	Homo sapiens	121-123
10856283-23	2000	However, vasodilation caused by the 2 lower doses of BK were significantly attenuated after K(Ca) channel activity was blocked with tetraethylammonium chloride (0.1 mg. 100 mL FAV(-1).	Tetraethylammonium	132-159	kininogen 1	Homo sapiens	53-55
10856283-25	2000	In conclusion, BK is a potent vasodilator peptide in human forearm resistance vessels, causing vasodilation through hyperpolarization of the vascular wall independent of NO and PG production.	Prostaglandins	177-179	kininogen 1	Homo sapiens	15-17
10888199-1	2000	Different types of dipeptide building units containing N- or C-terminal arginine were prepared for synthesis of the backbone cyclic analogues of the peptide hormone bradykinin (BK: Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg).	Dipeptides	19-28	kininogen 1	Homo sapiens	165-175
10888199-1	2000	Different types of dipeptide building units containing N- or C-terminal arginine were prepared for synthesis of the backbone cyclic analogues of the peptide hormone bradykinin (BK: Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg).	Arginine	72-80	kininogen 1	Homo sapiens	165-175
10812056-0	2000	Bradykinin potentiates prostaglandin E(2) release in the human gingival fibroblasts pretreated with interleukin-1beta via Ca(2+) mobilization.	Dinoprostone	23-41	kininogen 1	Homo sapiens	0-10
10812056-2	2000	On the other hand, bradykinin, a chemical mediator for inflammation, induces a rapid prostaglandin E(2) release.	prostaglandin e(2) release	85-111	kininogen 1	Homo sapiens	19-29
10812056-3	2000	Simultaneous stimulation with interleukin-1beta (200 pg/ml) and bradykinin (1 microM) evoked a moderately synergistic increase in prostaglandin E(2) release in human gingival fibroblasts.	Dinoprostone	130-148	kininogen 1	Homo sapiens	64-74
10812056-4	2000	However, in the human gingival fibroblasts pretreated with interleukin-1beta, bradykinin drastically enhanced prostaglandin E(2) release.	Dinoprostone	110-128	kininogen 1	Homo sapiens	78-88
10812056-5	2000	NS-398, a specific inhibitor of cyclooxygenase-2, inhibited not only interleukin-1beta-induced prostaglandin E(2) release but also bradykinin-induced prostaglandin E(2) release in the human gingival fibroblasts pretreated with interleukin-1beta.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	0-6	kininogen 1	Homo sapiens	131-141
10812056-5	2000	NS-398, a specific inhibitor of cyclooxygenase-2, inhibited not only interleukin-1beta-induced prostaglandin E(2) release but also bradykinin-induced prostaglandin E(2) release in the human gingival fibroblasts pretreated with interleukin-1beta.	Prostaglandins E	150-165	kininogen 1	Homo sapiens	131-141
10812056-6	2000	Transcriptional and translational inhibitors such as actinomycin D, cycloheximide, and dexamethasone also suppressed the interleukin-1beta-induced prostaglandin E(2) release and the bradykinin-induced prostaglandin E(2) release in interleukin-1beta-pretreated human gingival fibroblasts.	Dactinomycin	53-66	kininogen 1	Homo sapiens	182-192
10812056-6	2000	Transcriptional and translational inhibitors such as actinomycin D, cycloheximide, and dexamethasone also suppressed the interleukin-1beta-induced prostaglandin E(2) release and the bradykinin-induced prostaglandin E(2) release in interleukin-1beta-pretreated human gingival fibroblasts.	Cycloheximide	68-81	kininogen 1	Homo sapiens	182-192
10812056-6	2000	Transcriptional and translational inhibitors such as actinomycin D, cycloheximide, and dexamethasone also suppressed the interleukin-1beta-induced prostaglandin E(2) release and the bradykinin-induced prostaglandin E(2) release in interleukin-1beta-pretreated human gingival fibroblasts.	Dexamethasone	87-100	kininogen 1	Homo sapiens	182-192
10812056-6	2000	Transcriptional and translational inhibitors such as actinomycin D, cycloheximide, and dexamethasone also suppressed the interleukin-1beta-induced prostaglandin E(2) release and the bradykinin-induced prostaglandin E(2) release in interleukin-1beta-pretreated human gingival fibroblasts.	Prostaglandins E	201-216	kininogen 1	Homo sapiens	182-192
10773231-4	2000	The arterial changes are chronically modulated by hormonal counterregulatory mechanisms since, when sodium intake is high, bradykinin blockade produces more carotid hypertrophy, and when sodium intake is normal, less aortic collagen accumulates because of AT(1)-receptor blockade.	Sodium	100-106	kininogen 1	Homo sapiens	123-133
10825662-6	2000	The enzyme hydrolyzed angiotensin I to angiotensin II and sequentially released Phe-Arg and Ser-Pro from the C-terminus bradykinin, but does not cleave imido-bonds.	phenylalanylarginine	80-87	kininogen 1	Homo sapiens	120-130
10825662-6	2000	The enzyme hydrolyzed angiotensin I to angiotensin II and sequentially released Phe-Arg and Ser-Pro from the C-terminus bradykinin, but does not cleave imido-bonds.	seryl-proline	92-99	kininogen 1	Homo sapiens	120-130
10910005-4	2000	In rat studies, plasma bradykinin concentrations also significantly increased after 1 hour of swimming in nondiabetic and mildly diabetic (streptozotocin [STZ] 45 mg/kg intravenously [IV]) rats, but not in rats with severe diabetes (STZ 65 mg/kg IV).	Streptozocin	155-158	kininogen 1	Homo sapiens	23-33
10910005-4	2000	In rat studies, plasma bradykinin concentrations also significantly increased after 1 hour of swimming in nondiabetic and mildly diabetic (streptozotocin [STZ] 45 mg/kg intravenously [IV]) rats, but not in rats with severe diabetes (STZ 65 mg/kg IV).	Streptozocin	233-236	kininogen 1	Homo sapiens	23-33
10910005-8	2000	Moreover, the exercise-induced increase in bradykinin may be involved in modulating exercise-induced glucose transport through an increase of GLUT-4 translocation, as well as enhancement of the insulin signal pathway, during the postexercise period in skeletal muscle, resulting in a decrease of blood glucose.	Glucose	101-108	kininogen 1	Homo sapiens	43-53
10769288-5	2000	The specific agonists for endothelial release of NO, bradykinin (10 nmol/L), and substance P (100 nmol/L) both induced earlier onset of LV relaxation in shams (time to LV dP/dt(min) [tdP/dt(min)], -13.4+/-3.0 and -10.4+/-2.5 ms, respectively) without altering peak LV pressure or LV dP/dt(max).	dp	171-173	kininogen 1	Homo sapiens	53-63
10769288-5	2000	The specific agonists for endothelial release of NO, bradykinin (10 nmol/L), and substance P (100 nmol/L) both induced earlier onset of LV relaxation in shams (time to LV dP/dt(min) [tdP/dt(min)], -13.4+/-3.0 and -10.4+/-2.5 ms, respectively) without altering peak LV pressure or LV dP/dt(max).	Thymidine	174-176	kininogen 1	Homo sapiens	53-63
10769288-7	2000	The ACE inhibitor captopril (1 micromol/L) also selectively reduced tdP/dt(min) in shams via a bradykinin/NO-dependent mechanism but had no effect in banded animals.	Captopril	18-27	kininogen 1	Homo sapiens	95-105
10749673-4	2000	Three lines of evidence suggest the activation of a protein tyrosine phosphatase (PTP) by bradykinin: (i) treatment of A431 cells with bradykinin decreases both basal and EGF-induced EGFR tyrosine phosphorylation, (ii) this effect of bradykinin can be blocked by two different PTP inhibitors, and (iii) bradykinin significantly increased the PTP activity in total A431 cell lysates when measured in vitro.	Tyrosine	60-68	kininogen 1	Homo sapiens	90-100
10749673-4	2000	Three lines of evidence suggest the activation of a protein tyrosine phosphatase (PTP) by bradykinin: (i) treatment of A431 cells with bradykinin decreases both basal and EGF-induced EGFR tyrosine phosphorylation, (ii) this effect of bradykinin can be blocked by two different PTP inhibitors, and (iii) bradykinin significantly increased the PTP activity in total A431 cell lysates when measured in vitro.	Tyrosine	60-68	kininogen 1	Homo sapiens	135-145
10749673-4	2000	Three lines of evidence suggest the activation of a protein tyrosine phosphatase (PTP) by bradykinin: (i) treatment of A431 cells with bradykinin decreases both basal and EGF-induced EGFR tyrosine phosphorylation, (ii) this effect of bradykinin can be blocked by two different PTP inhibitors, and (iii) bradykinin significantly increased the PTP activity in total A431 cell lysates when measured in vitro.	Tyrosine	60-68	kininogen 1	Homo sapiens	135-145
10749673-4	2000	Three lines of evidence suggest the activation of a protein tyrosine phosphatase (PTP) by bradykinin: (i) treatment of A431 cells with bradykinin decreases both basal and EGF-induced EGFR tyrosine phosphorylation, (ii) this effect of bradykinin can be blocked by two different PTP inhibitors, and (iii) bradykinin significantly increased the PTP activity in total A431 cell lysates when measured in vitro.	Tyrosine	60-68	kininogen 1	Homo sapiens	135-145
10749673-6	2000	Activation of MAPK in response to bradykinin was insensitive towards AG 1478, a specific inhibitor of EGFR tyrosine kinase, but was blocked by wortmannin or bisindolylmaleimide, inhibitors of phosphatidylinositol 3-kinase (PI3-K) and protein kinase C (PKC) respectively.	Wortmannin	143-153	kininogen 1	Homo sapiens	34-44
10749673-6	2000	Activation of MAPK in response to bradykinin was insensitive towards AG 1478, a specific inhibitor of EGFR tyrosine kinase, but was blocked by wortmannin or bisindolylmaleimide, inhibitors of phosphatidylinositol 3-kinase (PI3-K) and protein kinase C (PKC) respectively.	bisindolylmaleimide	157-176	kininogen 1	Homo sapiens	34-44
10749673-9	2000	Although Src does not participate in bradykinin-induced stimulation of PTP activity, inhibition of Src by 4-amino-5-(4-methylphenyl)-7-(t-butyl)pyrazolo(3,4-d)pyrimidine leads to an increase in MAPK activation by bradykinin.	4-amino-5-(4-methylphenyl)-7-(t-butyl)pyrazolo(3,4-d)pyrimidine	106-169	kininogen 1	Homo sapiens	213-223
10742606-2	2000	The fluorescent probe aminobenzoic acid (Abz) bound to the amino terminal of bradykinin maintained its fluorescence characteristics, like high quantum yield and excited state decay dominated by a lifetime of 8.3 ns.	Aminobenzoates	22-39	kininogen 1	Homo sapiens	77-87
10742606-2	2000	The fluorescent probe aminobenzoic acid (Abz) bound to the amino terminal of bradykinin maintained its fluorescence characteristics, like high quantum yield and excited state decay dominated by a lifetime of 8.3 ns.	Aminobenzoates	41-44	kininogen 1	Homo sapiens	77-87
10742606-3	2000	The binding of the acceptor group N-[2, 4-dinitrophenyl]-ethylenediamine (EDDnp) to the carboxy terminal of Abz labeled bradykinin resulted in a drastic decrease of the fluorescence intensity and in a fastening of the excited state decay.	N-(2,4-dinitrophenyl)ethylenediamine	34-72	kininogen 1	Homo sapiens	120-130
10742606-3	2000	The binding of the acceptor group N-[2, 4-dinitrophenyl]-ethylenediamine (EDDnp) to the carboxy terminal of Abz labeled bradykinin resulted in a drastic decrease of the fluorescence intensity and in a fastening of the excited state decay.	n1-(2,4-dinitrophenyl)ethane-1,2-diamine	74-79	kininogen 1	Homo sapiens	120-130
10742606-3	2000	The binding of the acceptor group N-[2, 4-dinitrophenyl]-ethylenediamine (EDDnp) to the carboxy terminal of Abz labeled bradykinin resulted in a drastic decrease of the fluorescence intensity and in a fastening of the excited state decay.	Aminobenzoates	108-111	kininogen 1	Homo sapiens	120-130
10742606-7	2000	We observed three distance populations for bradykinin in water, that merged to two populations when the solvent was trifluoroethanol (TFE).	Water	57-62	kininogen 1	Homo sapiens	43-53
10742606-7	2000	We observed three distance populations for bradykinin in water, that merged to two populations when the solvent was trifluoroethanol (TFE).	Trifluoroethanol	116-132	kininogen 1	Homo sapiens	43-53
10742606-7	2000	We observed three distance populations for bradykinin in water, that merged to two populations when the solvent was trifluoroethanol (TFE).	Trifluoroethanol	134-137	kininogen 1	Homo sapiens	43-53
10742606-9	2000	We also studied several peptides related to bradykinin, and the results emphasized the formation of turns involving the proline residues and the decrease of conformational flexibility induced by using TFE as the solvent.	Proline	120-127	kininogen 1	Homo sapiens	44-54
10742606-9	2000	We also studied several peptides related to bradykinin, and the results emphasized the formation of turns involving the proline residues and the decrease of conformational flexibility induced by using TFE as the solvent.	Trifluoroethanol	201-204	kininogen 1	Homo sapiens	44-54
10782524-0	2000	Cetirizine inhibits bradykinin-induced cutaneous wheal and flare in atopic and healthy subjects.	Cetirizine	0-10	kininogen 1	Homo sapiens	20-30
10782524-3	2000	The aim of this study was to compare the possible effect of cetirizine (an H1-antagonist) on wheal and flare responses to BK, histamine, and compound 48/80 in atopic and healthy subjects.	Cetirizine	60-70	kininogen 1	Homo sapiens	122-124
10782524-11	2000	In atopic subjects, cetirizine induced a significant reduction of flare reactions after the BK test (80% for IDT, and 94% for PT [P &lt; 0.01]).	Cetirizine	20-30	kininogen 1	Homo sapiens	92-94
10782524-12	2000	Moreover, cetirizine reduced significantly BK-induced wheals by 70% for IDT (P &lt; 0.01) and 65% for PT (P &lt; 0.01).	Cetirizine	10-20	kininogen 1	Homo sapiens	43-45
10782524-12	2000	Moreover, cetirizine reduced significantly BK-induced wheals by 70% for IDT (P &lt; 0.01) and 65% for PT (P &lt; 0.01).	Platinum	102-104	kininogen 1	Homo sapiens	43-45
10782524-14	2000	CONCLUSIONS: These findings showed that the wheal and flare reactions induced by BK challenge were markedly inhibited by previous intake of cetirizine.	Cetirizine	140-150	kininogen 1	Homo sapiens	81-83
10749777-3	2000	Moreover, a proportion of kinin peptides is hydroxylated on proline(3) of the bradykinin sequence.	Proline	60-67	kininogen 1	Homo sapiens	78-88
10751218-3	2000	We found that the cytosolic Ca(2+) release triggered by either ionomycin or by several IP(3)-generating mitogens, namely bradykinin, thrombin, platelet-derived growth factor (PDGF), and epidermal growth factor (EGF), was attenuated markedly in senescent HDFs.	Inositol 1,4,5-Trisphosphate	87-92	kininogen 1	Homo sapiens	121-131
10751218-7	2000	In parallel, IP(3) formation in response to bradykinin or EGF was also attenuated in senescent HDFs.	Inositol 1,4,5-Trisphosphate	13-18	kininogen 1	Homo sapiens	44-54
10801248-8	2000	RESULTS: After a 10-minute preinfusion, nicotine administration was associated with a loss in sensitivity to bradykinin (P &lt; .001).	Nicotine	40-48	kininogen 1	Homo sapiens	109-119
10812056-7	2000	In the fibroblasts pretreated with interleukin-1beta, Ca(2+)-mobilizing reagents such as ionomycin and thapsigargin mimicked the potentiating effect of bradykinin on prostaglandin E(2) release.	Ionomycin	89-98	kininogen 1	Homo sapiens	152-162
10812056-7	2000	In the fibroblasts pretreated with interleukin-1beta, Ca(2+)-mobilizing reagents such as ionomycin and thapsigargin mimicked the potentiating effect of bradykinin on prostaglandin E(2) release.	Thapsigargin	103-115	kininogen 1	Homo sapiens	152-162
10812056-7	2000	In the fibroblasts pretreated with interleukin-1beta, Ca(2+)-mobilizing reagents such as ionomycin and thapsigargin mimicked the potentiating effect of bradykinin on prostaglandin E(2) release.	prostaglandin e(2) release	166-192	kininogen 1	Homo sapiens	152-162
10812056-8	2000	These results suggest that interleukin-1beta- and bradykinin-induced prostaglandin E(2) release is dependent on cyclooxygenase-2 and the potentiated effect of bradykinin in the human gingival fibroblasts primed with interleukin-1beta is caused by Ca(2+) mobilization.	Dinoprostone	69-87	kininogen 1	Homo sapiens	50-60
10812056-8	2000	These results suggest that interleukin-1beta- and bradykinin-induced prostaglandin E(2) release is dependent on cyclooxygenase-2 and the potentiated effect of bradykinin in the human gingival fibroblasts primed with interleukin-1beta is caused by Ca(2+) mobilization.	Dinoprostone	69-87	kininogen 1	Homo sapiens	159-169
10696506-19	2000	The downstream events reported include elevation of [Ca2+]i, activation of phospholipase A2, release of arachidonic acid, and production of free radicals, with evidence that IL-1 beta potentiates the actions of Bk in ischemia.	Arachidonic Acid	104-120	kininogen 1	Homo sapiens	211-213
10801248-9	2000	After 30 and 60 minutes of preinfusion with nicotine, the venorelaxant effect of bradykinin was further reduced (P &lt; .001).	Nicotine	44-52	kininogen 1	Homo sapiens	81-91
10801248-10	2000	A similar inhibition of the response to bradykinin by nicotine persisted in the presence of indomethacin (INN, indomethacin).	Nicotine	54-62	kininogen 1	Homo sapiens	40-50
10801248-10	2000	A similar inhibition of the response to bradykinin by nicotine persisted in the presence of indomethacin (INN, indomethacin).	Indomethacin	92-104	kininogen 1	Homo sapiens	40-50
10801248-10	2000	A similar inhibition of the response to bradykinin by nicotine persisted in the presence of indomethacin (INN, indomethacin).	Indomethacin	111-123	kininogen 1	Homo sapiens	40-50
10775566-2	2000	We investigated the action of bradykinin on the phosphorylation state of the mitogen-activated protein kinases p42(mapk) and p44(mapk) in VSMCs and tested the hypothesis that reactive oxygen species (ROS) might be involved in the signal transduction pathway linking bradykinin activation of nuclear transcription factors to the phosphorylation of p42(mapk) and p44(mapk).	Reactive Oxygen Species	175-198	kininogen 1	Homo sapiens	266-276
10775566-0	2000	Role of reactive oxygen species in bradykinin-induced mitogen-activated protein kinase and c-fos induction in vascular cells.	Reactive Oxygen Species	8-31	kininogen 1	Homo sapiens	35-45
10775566-8	2000	These findings demonstrate that the phosphorylation of cytosolic and nuclear p42(mapk) and p44(mapk) and the expression of c-fos mRNA in VSMCs in response to bradykinin are mediated via the generation of ROS and implicate ROS as important mediators in the signal transduction pathway through which bradykinin promotes VSMC proliferation in states of vascular injury.	Reactive Oxygen Species	204-207	kininogen 1	Homo sapiens	158-168
10775566-8	2000	These findings demonstrate that the phosphorylation of cytosolic and nuclear p42(mapk) and p44(mapk) and the expression of c-fos mRNA in VSMCs in response to bradykinin are mediated via the generation of ROS and implicate ROS as important mediators in the signal transduction pathway through which bradykinin promotes VSMC proliferation in states of vascular injury.	Reactive Oxygen Species	204-207	kininogen 1	Homo sapiens	298-308
10775566-8	2000	These findings demonstrate that the phosphorylation of cytosolic and nuclear p42(mapk) and p44(mapk) and the expression of c-fos mRNA in VSMCs in response to bradykinin are mediated via the generation of ROS and implicate ROS as important mediators in the signal transduction pathway through which bradykinin promotes VSMC proliferation in states of vascular injury.	Reactive Oxygen Species	222-225	kininogen 1	Homo sapiens	158-168
10757171-3	2000	Based on PSD analyses of serine- or threonine-containing bradykinin and its analogs, which have been ethyl-esterified or 18O labeled at their C termini, the [b(k) + H2O] (where k denotes the position adjacent to the left of the Ser/Thr residue) ion is generally thought to be formed by the transfer of the hydroxyl moiety of a serine or threonine residue to the carbonyl group of the residue to its left accompanied by the loss of the remaining C-terminal portion of the peptide.	Serine	25-31	kininogen 1	Homo sapiens	57-67
10785507-6	2000	In cultures from regenerated endothelium, cGMP production was decreased under basal conditions and during stimulation with serotonin, bradykinin, and A23187.	Cyclic GMP	42-46	kininogen 1	Homo sapiens	134-144
10775566-4	2000	Preincubation of VSMCs with either N-acetyl-L-cysteine and/or alpha-lipoic acid significantly decreased bradykinin-induced cytosolic and nuclear phosphorylation of p42(mapk) and p44(mapk).	vsmcs	17-22	kininogen 1	Homo sapiens	104-114
10775566-4	2000	Preincubation of VSMCs with either N-acetyl-L-cysteine and/or alpha-lipoic acid significantly decreased bradykinin-induced cytosolic and nuclear phosphorylation of p42(mapk) and p44(mapk).	Acetylcysteine	35-54	kininogen 1	Homo sapiens	104-114
10775566-4	2000	Preincubation of VSMCs with either N-acetyl-L-cysteine and/or alpha-lipoic acid significantly decreased bradykinin-induced cytosolic and nuclear phosphorylation of p42(mapk) and p44(mapk).	Thioctic Acid	62-79	kininogen 1	Homo sapiens	104-114
10775566-5	2000	In addition, the induction c-fos mRNA levels by bradykinin was completely abolished by N-acetyl-L-cysteine and alpha-lipoic acid.	Acetylcysteine	87-106	kininogen 1	Homo sapiens	48-58
10775566-5	2000	In addition, the induction c-fos mRNA levels by bradykinin was completely abolished by N-acetyl-L-cysteine and alpha-lipoic acid.	Thioctic Acid	111-128	kininogen 1	Homo sapiens	48-58
10775566-6	2000	Using the cell-permeable fluorescent dye dichlorofluorescein diacetate, we determined that bradykinin (10(-8) mol/L) rapidly increased the generation of ROS in VSMCs.	dichlorofluorescein diacetate	41-70	kininogen 1	Homo sapiens	91-101
10775566-6	2000	Using the cell-permeable fluorescent dye dichlorofluorescein diacetate, we determined that bradykinin (10(-8) mol/L) rapidly increased the generation of ROS in VSMCs.	Reactive Oxygen Species	153-156	kininogen 1	Homo sapiens	91-101
10775566-7	2000	The NADPH oxidase inhibitor diphenylene iodonium (DPI) blocked bradykinin-induced c-fos mRNA expression and p42(mapk) and p44(mapk) activation, implicating NADPH oxidase as the source for the generation of ROS.	diphenyleneiodonium	28-48	kininogen 1	Homo sapiens	63-73
10775566-7	2000	The NADPH oxidase inhibitor diphenylene iodonium (DPI) blocked bradykinin-induced c-fos mRNA expression and p42(mapk) and p44(mapk) activation, implicating NADPH oxidase as the source for the generation of ROS.	diphenyleneiodonium	50-53	kininogen 1	Homo sapiens	63-73
10775566-7	2000	The NADPH oxidase inhibitor diphenylene iodonium (DPI) blocked bradykinin-induced c-fos mRNA expression and p42(mapk) and p44(mapk) activation, implicating NADPH oxidase as the source for the generation of ROS.	Reactive Oxygen Species	206-209	kininogen 1	Homo sapiens	63-73
10696094-1	2000	The mechanism of endothelium-dependent regulation of vascular tone of bradykinin was investigated by simultaneously monitoring the changes in the cytosolic Ca(2+) concentration and the force of smooth muscle in fura-2-loaded strips of the porcine renal artery with endothelium.	Fura-2	211-217	kininogen 1	Homo sapiens	70-80
10863961-5	2000	In contrast, 45Ca release induced by IL-1 alpha, IL-1 beta, thrombin and bradykinin was significantly reduced by indomethacin, whereas the effects of PTH and PTHrP were unaffected by indomethacin.	Indomethacin	113-125	kininogen 1	Homo sapiens	73-83
10748265-2	2000	The most potent agonist for Chinese hamster ovary (CHO) cells stably expressing recombinant human bradykinin B(1) receptors were Des-Arg(9)-bradykinin (EC(50)=7.9 nM) and Des-Arg(10)-kallidin (EC(50)=8.6 nM), while the most potent agonist for CHO cells expressing human bradykinin B(2) receptors was bradykinin (EC(50)=2.0 nM).	des-arg	129-136	kininogen 1	Homo sapiens	98-108
10748265-2	2000	The most potent agonist for Chinese hamster ovary (CHO) cells stably expressing recombinant human bradykinin B(1) receptors were Des-Arg(9)-bradykinin (EC(50)=7.9 nM) and Des-Arg(10)-kallidin (EC(50)=8.6 nM), while the most potent agonist for CHO cells expressing human bradykinin B(2) receptors was bradykinin (EC(50)=2.0 nM).	des-arg	129-136	kininogen 1	Homo sapiens	140-150
10748265-2	2000	The most potent agonist for Chinese hamster ovary (CHO) cells stably expressing recombinant human bradykinin B(1) receptors were Des-Arg(9)-bradykinin (EC(50)=7.9 nM) and Des-Arg(10)-kallidin (EC(50)=8.6 nM), while the most potent agonist for CHO cells expressing human bradykinin B(2) receptors was bradykinin (EC(50)=2.0 nM).	des-arg	129-136	kininogen 1	Homo sapiens	140-150
10748265-2	2000	The most potent agonist for Chinese hamster ovary (CHO) cells stably expressing recombinant human bradykinin B(1) receptors were Des-Arg(9)-bradykinin (EC(50)=7.9 nM) and Des-Arg(10)-kallidin (EC(50)=8.6 nM), while the most potent agonist for CHO cells expressing human bradykinin B(2) receptors was bradykinin (EC(50)=2.0 nM).	des-arg	129-136	kininogen 1	Homo sapiens	140-150
10748265-2	2000	The most potent agonist for Chinese hamster ovary (CHO) cells stably expressing recombinant human bradykinin B(1) receptors were Des-Arg(9)-bradykinin (EC(50)=7.9 nM) and Des-Arg(10)-kallidin (EC(50)=8.6 nM), while the most potent agonist for CHO cells expressing human bradykinin B(2) receptors was bradykinin (EC(50)=2.0 nM).	des-arg	171-178	kininogen 1	Homo sapiens	98-108
10748265-2	2000	The most potent agonist for Chinese hamster ovary (CHO) cells stably expressing recombinant human bradykinin B(1) receptors were Des-Arg(9)-bradykinin (EC(50)=7.9 nM) and Des-Arg(10)-kallidin (EC(50)=8.6 nM), while the most potent agonist for CHO cells expressing human bradykinin B(2) receptors was bradykinin (EC(50)=2.0 nM).	cho	51-54	kininogen 1	Homo sapiens	98-108
10748265-2	2000	The most potent agonist for Chinese hamster ovary (CHO) cells stably expressing recombinant human bradykinin B(1) receptors were Des-Arg(9)-bradykinin (EC(50)=7.9 nM) and Des-Arg(10)-kallidin (EC(50)=8.6 nM), while the most potent agonist for CHO cells expressing human bradykinin B(2) receptors was bradykinin (EC(50)=2.0 nM).	cho	51-54	kininogen 1	Homo sapiens	140-150
10748265-2	2000	The most potent agonist for Chinese hamster ovary (CHO) cells stably expressing recombinant human bradykinin B(1) receptors were Des-Arg(9)-bradykinin (EC(50)=7.9 nM) and Des-Arg(10)-kallidin (EC(50)=8.6 nM), while the most potent agonist for CHO cells expressing human bradykinin B(2) receptors was bradykinin (EC(50)=2.0 nM).	cho	51-54	kininogen 1	Homo sapiens	140-150
10748265-2	2000	The most potent agonist for Chinese hamster ovary (CHO) cells stably expressing recombinant human bradykinin B(1) receptors were Des-Arg(9)-bradykinin (EC(50)=7.9 nM) and Des-Arg(10)-kallidin (EC(50)=8.6 nM), while the most potent agonist for CHO cells expressing human bradykinin B(2) receptors was bradykinin (EC(50)=2.0 nM).	cho	51-54	kininogen 1	Homo sapiens	140-150
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	[d-arg	110-116	kininogen 1	Homo sapiens	44-54
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	[d-arg	110-116	kininogen 1	Homo sapiens	58-68
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	[d-arg	110-116	kininogen 1	Homo sapiens	58-68
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	Hydroxyproline	120-123	kininogen 1	Homo sapiens	44-54
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	Hydroxyproline	120-123	kininogen 1	Homo sapiens	58-68
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	Hydroxyproline	120-123	kininogen 1	Homo sapiens	58-68
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	beta-(2-thienyl)-ala	128-148	kininogen 1	Homo sapiens	44-54
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	beta-(2-thienyl)-ala	128-148	kininogen 1	Homo sapiens	58-68
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	beta-(2-thienyl)-ala	128-148	kininogen 1	Homo sapiens	58-68
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	Dacarbazine	152-157	kininogen 1	Homo sapiens	44-54
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	Dacarbazine	152-157	kininogen 1	Homo sapiens	58-68
10748265-4	2000	The concentration-response relationship for bradykinin at bradykinin B(2) receptors was potently inhibited by [D-Arg(0),Hyp(3), beta-(2-thienyl)-Ala(5),D-Tic(7),Oic(8)]-bradykinin (Hoe140) (IC(50)=71 nM), which was 500-fold more potent against the B(2)-expressing cells than the B(1) cells.	Dacarbazine	152-157	kininogen 1	Homo sapiens	58-68
10730637-3	2000	METHODS: Forty-six patients were enrolled in a Phase II study of intra-arterial chemotherapy with carboplatin and Cereport (Alkermes Inc.; Cambridge, MA), a bradykinin analog that selectively increases permeability of the blood-tumor barrier.	Carboplatin	98-109	kininogen 1	Homo sapiens	157-167
10728427-6	2000	Short-term exposure (20 min) to low levels of testosterone (1-100 nM), which were ineffective on their own on vascular function, significantly diminished relaxation to bradykinin and calcium ionophore A23187 but not those produced by levcromakalim and sodium nitroprusside.	Testosterone	46-58	kininogen 1	Homo sapiens	168-178
10696094-2	2000	During phenylephrine-induced sustained contraction, bradykinin (&gt;3x10(-9) M) caused endothelium-dependent triphasic changes in the force of the strips, composed of an initial relaxation, a subsequent transient contraction and a late sustained relaxation.	Phenylephrine	7-20	kininogen 1	Homo sapiens	52-62
10696094-4	2000	A thromboxane A(2) (TXA(2))/prostaglandin H(2) (PGH(2)) receptor antagonist (10(-5) M ONO-3708) completely inhibited, while a TXA(2) synthase inhibitor (10(-5) M OKY-046) only partially inhibited, the transient contraction induced by bradykinin.	thromboxane a	2-15	kininogen 1	Homo sapiens	234-244
10696094-5	2000	Under conditions where the bradykinin-induced contraction was inhibited by ONO-3708 during the phenylephrine-induced contraction, bradykinin induced only a transient relaxation in the presence of N(Omega)-nitro-L-arginine methyl ester (L-NAME).	ONO 3708	75-83	kininogen 1	Homo sapiens	27-37
10696094-5	2000	Under conditions where the bradykinin-induced contraction was inhibited by ONO-3708 during the phenylephrine-induced contraction, bradykinin induced only a transient relaxation in the presence of N(Omega)-nitro-L-arginine methyl ester (L-NAME).	ONO 3708	75-83	kininogen 1	Homo sapiens	130-140
10696094-5	2000	Under conditions where the bradykinin-induced contraction was inhibited by ONO-3708 during the phenylephrine-induced contraction, bradykinin induced only a transient relaxation in the presence of N(Omega)-nitro-L-arginine methyl ester (L-NAME).	Phenylephrine	95-108	kininogen 1	Homo sapiens	27-37
10696094-5	2000	Under conditions where the bradykinin-induced contraction was inhibited by ONO-3708 during the phenylephrine-induced contraction, bradykinin induced only a transient relaxation in the presence of N(Omega)-nitro-L-arginine methyl ester (L-NAME).	Phenylephrine	95-108	kininogen 1	Homo sapiens	130-140
10696094-5	2000	Under conditions where the bradykinin-induced contraction was inhibited by ONO-3708 during the phenylephrine-induced contraction, bradykinin induced only a transient relaxation in the presence of N(Omega)-nitro-L-arginine methyl ester (L-NAME).	NG-Nitroarginine Methyl Ester	196-234	kininogen 1	Homo sapiens	130-140
10696094-5	2000	Under conditions where the bradykinin-induced contraction was inhibited by ONO-3708 during the phenylephrine-induced contraction, bradykinin induced only a transient relaxation in the presence of N(Omega)-nitro-L-arginine methyl ester (L-NAME).	NG-Nitroarginine Methyl Ester	236-242	kininogen 1	Homo sapiens	27-37
10696094-5	2000	Under conditions where the bradykinin-induced contraction was inhibited by ONO-3708 during the phenylephrine-induced contraction, bradykinin induced only a transient relaxation in the presence of N(Omega)-nitro-L-arginine methyl ester (L-NAME).	NG-Nitroarginine Methyl Ester	236-242	kininogen 1	Homo sapiens	130-140
10696094-10	2000	Both TXA(2) and PGH(2) were involved in the bradykinin-induced contraction.	Thromboxane A2	5-11	kininogen 1	Homo sapiens	44-54
10696094-10	2000	Both TXA(2) and PGH(2) were involved in the bradykinin-induced contraction.	Prostaglandin H2	16-22	kininogen 1	Homo sapiens	44-54
10703672-7	2000	In the third series, lisinopril reduced BP from 121 +/- 5 to 68 +/- 2 mmHg and proteinuria from 355 +/- 90 to 101 +/- 10 mg/24 h. Subsequent intraperitoneal infusion of bradykinin antagonist (HOE 140; 1 mg/kg per 24 h) for 2 wk did not affect BP (72 +/- 2 mmHg) or proteinuria (92 +/- 15 mg/24 h).	Lisinopril	21-31	kininogen 1	Homo sapiens	169-179
10726715-5	2000	In cultured porcine aortic endothelial cells, the bradykinin-induced increase of intracellular calcium was also investigated before and after insulin administration.	Calcium	95-102	kininogen 1	Homo sapiens	50-60
10741903-8	2000	The enzymes were able to hydrolyze angiotensin I (AI) (P0 and P0N about 25%, P1 and P1N about 70%, P2 100% and P2N 66%) and bradykinin (BK) (P0N 22%, P1N 81%, P2N 62%, P0 and P1 50% and P2 35%), and their activities were inhibited by captopril.	Captopril	234-243	kininogen 1	Homo sapiens	124-134
10741903-8	2000	The enzymes were able to hydrolyze angiotensin I (AI) (P0 and P0N about 25%, P1 and P1N about 70%, P2 100% and P2N 66%) and bradykinin (BK) (P0N 22%, P1N 81%, P2N 62%, P0 and P1 50% and P2 35%), and their activities were inhibited by captopril.	Captopril	234-243	kininogen 1	Homo sapiens	136-138
10726715-6	2000	RESULTS: Insulin significantly attenuated bradykinin-induced increase in intracellular calcium and venodilation in cultured endothelial cells and human dorsal hand veins, respectively.	Calcium	87-94	kininogen 1	Homo sapiens	42-52
10726715-7	2000	CONCLUSIONS: These findings suggest that insulin attenuates the bradykinin-induced calcium elevation in endothelial cells and may decrease the production of vasodilative substances from endothelial cells, resulting in the reduction of vasodilation.	Calcium	83-90	kininogen 1	Homo sapiens	64-74
10731036-2	2000	We reported previously that IL-1beta induced a prostanoid-dependent increase in the density of bradykinin B2 receptors in cultured human bronchial smooth muscle cells.	Prostaglandins	47-57	kininogen 1	Homo sapiens	95-105
10731036-7	2000	These data demonstrate that the activation of p38 MAP kinase elicited by IL-1beta leads to the phosphorylation of cPLA2 and Cox-2 overexpression, allowing rapid synthesis of PGE2 as a prerequisite for bradykinin B2 gene expression in human bronchial smooth muscle cells which could explain the hyperresponsiveness of asthmatic patients to bradykinin.	Dinoprostone	174-178	kininogen 1	Homo sapiens	201-211
10731036-7	2000	These data demonstrate that the activation of p38 MAP kinase elicited by IL-1beta leads to the phosphorylation of cPLA2 and Cox-2 overexpression, allowing rapid synthesis of PGE2 as a prerequisite for bradykinin B2 gene expression in human bronchial smooth muscle cells which could explain the hyperresponsiveness of asthmatic patients to bradykinin.	Dinoprostone	174-178	kininogen 1	Homo sapiens	339-349
10666071-8	2000	However, in endothelium-denuded arteries transduced with recombinant eNOS, bradykinin and substance P caused relaxations that were abolished in the presence of the NOS inhibitor N(G)-nitro-L-arginine methyl ester.	NG-Nitroarginine Methyl Ester	178-212	kininogen 1	Homo sapiens	75-85
10681501-12	2000	This interaction of nNOS with the B2R may recruit the enzyme to allow for the effective coupling of bradykinin signaling to the nitric oxide pathway.	Nitric Oxide	128-140	kininogen 1	Homo sapiens	100-110
10711351-5	2000	This effect was abolished by pretreatment with the bradykinin B2 receptor antagonists icatibant and [1-adamantaneacetyl-D-Arg0,Hyp3,beta-(2-thienyl)-Al a5,8,D-Phe7]-bradykinin ([Ad]-BK), both at 200 micrograms, every 2 h following PAF administration.	[1-adamantaneacetyl-d-arg0	100-126	kininogen 1	Homo sapiens	51-61
10711351-5	2000	This effect was abolished by pretreatment with the bradykinin B2 receptor antagonists icatibant and [1-adamantaneacetyl-D-Arg0,Hyp3,beta-(2-thienyl)-Al a5,8,D-Phe7]-bradykinin ([Ad]-BK), both at 200 micrograms, every 2 h following PAF administration.	[1-adamantaneacetyl-d-arg0	100-126	kininogen 1	Homo sapiens	165-175
10711351-5	2000	This effect was abolished by pretreatment with the bradykinin B2 receptor antagonists icatibant and [1-adamantaneacetyl-D-Arg0,Hyp3,beta-(2-thienyl)-Al a5,8,D-Phe7]-bradykinin ([Ad]-BK), both at 200 micrograms, every 2 h following PAF administration.	Berkelium	180-184	kininogen 1	Homo sapiens	51-61
10757171-3	2000	Based on PSD analyses of serine- or threonine-containing bradykinin and its analogs, which have been ethyl-esterified or 18O labeled at their C termini, the [b(k) + H2O] (where k denotes the position adjacent to the left of the Ser/Thr residue) ion is generally thought to be formed by the transfer of the hydroxyl moiety of a serine or threonine residue to the carbonyl group of the residue to its left accompanied by the loss of the remaining C-terminal portion of the peptide.	Threonine	36-45	kininogen 1	Homo sapiens	57-67
10757171-3	2000	Based on PSD analyses of serine- or threonine-containing bradykinin and its analogs, which have been ethyl-esterified or 18O labeled at their C termini, the [b(k) + H2O] (where k denotes the position adjacent to the left of the Ser/Thr residue) ion is generally thought to be formed by the transfer of the hydroxyl moiety of a serine or threonine residue to the carbonyl group of the residue to its left accompanied by the loss of the remaining C-terminal portion of the peptide.	Water	165-168	kininogen 1	Homo sapiens	57-67
10706487-7	2000	Steroid inhalation therapy was associated with a reduction in eosinophil and bradykinin concentration in sputum and NO levels in exhaled air and an improvement in FEV1 and AHR.	Steroids	0-7	kininogen 1	Homo sapiens	77-87
10640624-14	2000	In addition, PPTs were significantly decreased (P&lt;0.05) after 5-HT+BKN at 5 cm (5 and 20 min) and 10 cm (5 min).	Pyridinium p-toluenesulfonate	13-17	kininogen 1	Homo sapiens	70-73
10640624-15	2000	Serotonin may enhance the effect of bradykinin in producing experimental muscle pain and muscle hyperalgesia to mechanical stimuli.	Serotonin	0-9	kininogen 1	Homo sapiens	36-46
10694205-6	2000	Bradyzide inhibits bradykinin-induced [(3)H]-inositol trisphosphate (IP(3)) formation with IC(50) values of 11.6+/-1.4 nM (n=3) at the rat and 2.4+/-0.3 microM (n=3) at the human receptor.	ip	69-71	kininogen 1	Homo sapiens	19-29
10666510-2	2000	Bradykinin evoked a concentration-dependent contraction of human (pD(2)=7.2) and rat (pD(2)=7.7) detrusor muscle strips.	pd(2)	66-71	kininogen 1	Homo sapiens	0-10
10666510-2	2000	Bradykinin evoked a concentration-dependent contraction of human (pD(2)=7.2) and rat (pD(2)=7.7) detrusor muscle strips.	pd(2)	86-91	kininogen 1	Homo sapiens	0-10
11270506-8	2000	Quinaprilat could ameliorate both apoptosis and necrosis through the upregulation of constitutive endothelial nitric oxide synthase via an increase of bradykinin, with the resulting increase of nitric oxide.	quinaprilat	0-11	kininogen 1	Homo sapiens	151-161
11270506-8	2000	Quinaprilat could ameliorate both apoptosis and necrosis through the upregulation of constitutive endothelial nitric oxide synthase via an increase of bradykinin, with the resulting increase of nitric oxide.	Nitric Oxide	110-122	kininogen 1	Homo sapiens	151-161
10694205-1	2000	Bradyzide is from a novel class of rodent-selective non-peptide B(2) bradykinin antagonists (1-(2-Nitrophenyl)thiosemicarbazides).	bradyzide	0-9	kininogen 1	Homo sapiens	69-79
10694205-1	2000	Bradyzide is from a novel class of rodent-selective non-peptide B(2) bradykinin antagonists (1-(2-Nitrophenyl)thiosemicarbazides).	1-(2-nitrophenyl)thiosemicarbazides	93-128	kininogen 1	Homo sapiens	69-79
10694205-2	2000	Bradyzide has high affinity for the rodent B(2) receptor, displacing [(3)H]-bradykinin binding in NG108-15 cells and in Cos-7 cells expressing the rat receptor with K(I) values of 0.51+/-0.18 nM (n=3) and 0.89+/-0.27 nM (n=3), respectively.	bradyzide	0-9	kininogen 1	Homo sapiens	76-86
10694205-4	2000	In the rat spinal cord and tail preparation, bradyzide inhibits bradykinin-induced ventral root depolarizations (IC(50) value; 1.6+/-0.05 nM (n=3)).	bradyzide	45-54	kininogen 1	Homo sapiens	64-74
10694205-5	2000	Bradyzide is much less potent at the human than at the rodent B(2) receptor, displacing [(3)H]-bradykinin binding in human fibroblasts and in Cos-7 cells expressing the human B(2) receptor with K(I) values of 393+/-90 nM (n=3) and 772+/-144 nM (n=3), respectively.	bradyzide	0-9	kininogen 1	Homo sapiens	95-105
10694205-6	2000	Bradyzide inhibits bradykinin-induced [(3)H]-inositol trisphosphate (IP(3)) formation with IC(50) values of 11.6+/-1.4 nM (n=3) at the rat and 2.4+/-0.3 microM (n=3) at the human receptor.	bradyzide	0-9	kininogen 1	Homo sapiens	19-29
10694205-6	2000	Bradyzide inhibits bradykinin-induced [(3)H]-inositol trisphosphate (IP(3)) formation with IC(50) values of 11.6+/-1.4 nM (n=3) at the rat and 2.4+/-0.3 microM (n=3) at the human receptor.	[(3)h]-inositol trisphosphate	38-67	kininogen 1	Homo sapiens	19-29
10653985-5	2000	The effects of bradykinin were dose dependent (with an EC(50) of 50 nmol/L for calcium mobilization) and were inhibited by N-alpha-adamantaneacetyl-D-Arg-[Hyp(3),Thi(5,8),D-phe(7)]-Bk, a specific B2 receptor antagonist.	n-alpha-adamantaneacetyl-d-arg	123-153	kininogen 1	Homo sapiens	15-25
10653985-5	2000	The effects of bradykinin were dose dependent (with an EC(50) of 50 nmol/L for calcium mobilization) and were inhibited by N-alpha-adamantaneacetyl-D-Arg-[Hyp(3),Thi(5,8),D-phe(7)]-Bk, a specific B2 receptor antagonist.	2-acetyl-4(5)-tetrahydroxybutylimidazole	162-165	kininogen 1	Homo sapiens	15-25
10653985-5	2000	The effects of bradykinin were dose dependent (with an EC(50) of 50 nmol/L for calcium mobilization) and were inhibited by N-alpha-adamantaneacetyl-D-Arg-[Hyp(3),Thi(5,8),D-phe(7)]-Bk, a specific B2 receptor antagonist.	D-phenylalanine	171-176	kininogen 1	Homo sapiens	15-25
10653985-5	2000	The effects of bradykinin were dose dependent (with an EC(50) of 50 nmol/L for calcium mobilization) and were inhibited by N-alpha-adamantaneacetyl-D-Arg-[Hyp(3),Thi(5,8),D-phe(7)]-Bk, a specific B2 receptor antagonist.	Berkelium	179-183	kininogen 1	Homo sapiens	15-25
10653985-9	2000	Bradykinin-induced [Ca(2+)](i) mobilization was increased by genistein and tyrphostin A51.	Genistein	61-70	kininogen 1	Homo sapiens	0-10
10653985-9	2000	Bradykinin-induced [Ca(2+)](i) mobilization was increased by genistein and tyrphostin A51.	tyrphostin A51	75-89	kininogen 1	Homo sapiens	0-10
10653985-11	2000	Homologous desensitization of the B2 receptor was observed after repeated applications of bradykinin, which resulted in attenuated changes in intracellular calcium.	Calcium	156-163	kininogen 1	Homo sapiens	90-100
10653985-12	2000	In addition, genistein promoted an increased response to a third exposure to the agonist when applied after washing the cells that had been previously challenged with two increasing doses of bradykinin.	Genistein	13-22	kininogen 1	Homo sapiens	191-201
10653985-16	2000	Phosphoaminoacid analysis revealed the presence of phosphoserine and traces of phosphothreonine, but not phosphotyrosine, suggesting that the putative tyrosine kinase(s), activated by bradykinin, could act in a step previous to receptor phosphorylation.	Phosphoamino Acids	0-16	kininogen 1	Homo sapiens	184-194
10653985-16	2000	Phosphoaminoacid analysis revealed the presence of phosphoserine and traces of phosphothreonine, but not phosphotyrosine, suggesting that the putative tyrosine kinase(s), activated by bradykinin, could act in a step previous to receptor phosphorylation.	Phosphoserine	51-64	kininogen 1	Homo sapiens	184-194
10653985-16	2000	Phosphoaminoacid analysis revealed the presence of phosphoserine and traces of phosphothreonine, but not phosphotyrosine, suggesting that the putative tyrosine kinase(s), activated by bradykinin, could act in a step previous to receptor phosphorylation.	Phosphothreonine	79-95	kininogen 1	Homo sapiens	184-194
10653985-17	2000	Interestingly, genistein prevented agonist-induced G protein uncoupling from B2 receptors, determined by in vitro bradykinin-stimulated [(35)S]-GTP(gamma)S binding, in membranes from bradykinin pretreated cells.	Genistein	15-24	kininogen 1	Homo sapiens	114-124
10653985-17	2000	Interestingly, genistein prevented agonist-induced G protein uncoupling from B2 receptors, determined by in vitro bradykinin-stimulated [(35)S]-GTP(gamma)S binding, in membranes from bradykinin pretreated cells.	Genistein	15-24	kininogen 1	Homo sapiens	183-193
10653985-17	2000	Interestingly, genistein prevented agonist-induced G protein uncoupling from B2 receptors, determined by in vitro bradykinin-stimulated [(35)S]-GTP(gamma)S binding, in membranes from bradykinin pretreated cells.	Guanosine Triphosphate	144-147	kininogen 1	Homo sapiens	114-124
10689670-1	2000	The gas phase H/D exchange reactions of bradykinin (M + 3H)3+ ions with D2O and DI were monitored in a quadrupole ion trap mass spectrometer.	Tritium	56-58	kininogen 1	Homo sapiens	40-50
10689670-1	2000	The gas phase H/D exchange reactions of bradykinin (M + 3H)3+ ions with D2O and DI were monitored in a quadrupole ion trap mass spectrometer.	Deuterium Oxide	72-75	kininogen 1	Homo sapiens	40-50
10689670-2	2000	The H/D exchange kinetics of both chemical probes (D2O and DI) indicate the presence of two noninterconverting reactive gas phase ion populations of bradykinin (M + 3H)3+ at room temperature.	Deuterium Oxide	51-54	kininogen 1	Homo sapiens	149-159
10689670-2	2000	The H/D exchange kinetics of both chemical probes (D2O and DI) indicate the presence of two noninterconverting reactive gas phase ion populations of bradykinin (M + 3H)3+ at room temperature.	Tritium	165-167	kininogen 1	Homo sapiens	149-159
10691781-4	2000	In the kidney, ANG II at the AT2 receptor stimulates a vasodilator cascade of bradykinin (BK), NO and cyclic GMP which is tonically activated only during conditions of increased ANG II, such as sodium depletion.	Sodium	194-200	kininogen 1	Homo sapiens	78-88
10691781-4	2000	In the kidney, ANG II at the AT2 receptor stimulates a vasodilator cascade of bradykinin (BK), NO and cyclic GMP which is tonically activated only during conditions of increased ANG II, such as sodium depletion.	Sodium	194-200	kininogen 1	Homo sapiens	90-92
10635057-5	2000	Conversely, ACE catalyzes the breakdown of bradykinin, a potent stimulus to t-PA secretion.	t-pa	76-80	kininogen 1	Homo sapiens	43-53
10644597-8	2000	Endothelium-dependent dilations to the cyclooxygenase activator arachidonic acid and to the cytochrome P-450 monooxygenase activator bradykinin and endothelium-independent vasodilation to sodium nitroprusside were also not altered by oxLDL.	Nitroprusside	188-208	kininogen 1	Homo sapiens	133-143
11012086-5	2000	G-protein-coupled activation of phospholipase was intact in both lines, as evidenced by the generation of similar amounts of IP3 in response to addition of bradykinin or guanosine 5"-[gamma-thio]-triphosphate.	Inositol 1,4,5-Trisphosphate	125-128	kininogen 1	Homo sapiens	156-166
10663220-4	2000	RESULTS: Cumulative vasodilatory responses to bradykinin (10 nmol/l to 3 mumol/l) were induced in vessels precontracted with 35-50 mmol/l potassium chloride.	Potassium Chloride	138-156	kininogen 1	Homo sapiens	46-56
10663220-5	2000	Addition of 100 mumol/l NG-nitro-L-arginine methyl ester reduced the relaxation evoked by bradykinin, but preincubation with both NG-nitro-L-arginine methyl ester and 10 mumol/l indomethacin was needed to abolish it.	NG-Nitroarginine Methyl Ester	24-56	kininogen 1	Homo sapiens	90-100
10663220-5	2000	Addition of 100 mumol/l NG-nitro-L-arginine methyl ester reduced the relaxation evoked by bradykinin, but preincubation with both NG-nitro-L-arginine methyl ester and 10 mumol/l indomethacin was needed to abolish it.	Indomethacin	178-190	kininogen 1	Homo sapiens	90-100
10653985-4	2000	In these cells, bradykinin induced a transient increase of intracellular calcium ([Ca(2+)](i)) in fura 2-AM loaded sf21 cells, and promoted [(35)S]-GTP(gamma)S binding to membranes.	Calcium	73-80	kininogen 1	Homo sapiens	16-26
10653985-4	2000	In these cells, bradykinin induced a transient increase of intracellular calcium ([Ca(2+)](i)) in fura 2-AM loaded sf21 cells, and promoted [(35)S]-GTP(gamma)S binding to membranes.	fura-2-am	98-107	kininogen 1	Homo sapiens	16-26
10653985-4	2000	In these cells, bradykinin induced a transient increase of intracellular calcium ([Ca(2+)](i)) in fura 2-AM loaded sf21 cells, and promoted [(35)S]-GTP(gamma)S binding to membranes.	Guanosine Triphosphate	148-151	kininogen 1	Homo sapiens	16-26
10653985-5	2000	The effects of bradykinin were dose dependent (with an EC(50) of 50 nmol/L for calcium mobilization) and were inhibited by N-alpha-adamantaneacetyl-D-Arg-[Hyp(3),Thi(5,8),D-phe(7)]-Bk, a specific B2 receptor antagonist.	Calcium	79-86	kininogen 1	Homo sapiens	15-25
10604961-8	2000	Pretreatment with 10 mg of quinapril significantly shifted the dose-response curve for bradykinin to the left (effect of quinapril; F = 77.96, P &lt;.001) and there was significant interaction between quinapril and bradykinin (F = 7.82, P =.041).	Quinapril	27-36	kininogen 1	Homo sapiens	87-97
10604961-8	2000	Pretreatment with 10 mg of quinapril significantly shifted the dose-response curve for bradykinin to the left (effect of quinapril; F = 77.96, P &lt;.001) and there was significant interaction between quinapril and bradykinin (F = 7.82, P =.041).	Quinapril	27-36	kininogen 1	Homo sapiens	215-225
10604961-8	2000	Pretreatment with 10 mg of quinapril significantly shifted the dose-response curve for bradykinin to the left (effect of quinapril; F = 77.96, P &lt;.001) and there was significant interaction between quinapril and bradykinin (F = 7.82, P =.041).	Quinapril	121-130	kininogen 1	Homo sapiens	87-97
10604961-8	2000	Pretreatment with 10 mg of quinapril significantly shifted the dose-response curve for bradykinin to the left (effect of quinapril; F = 77.96, P &lt;.001) and there was significant interaction between quinapril and bradykinin (F = 7.82, P =.041).	Quinapril	121-130	kininogen 1	Homo sapiens	87-97
10604961-9	2000	The effect of quinapril was significantly potentiated by coinjection of 10 microg of apstatin (effect of apstatin; F = 21.60, P =.006), such that there was significant interactive effect of quinapril and apstatin (F = 20.83, P =.006) on the wheal response to bradykinin.	Quinapril	14-23	kininogen 1	Homo sapiens	259-269
10604961-9	2000	The effect of quinapril was significantly potentiated by coinjection of 10 microg of apstatin (effect of apstatin; F = 21.60, P =.006), such that there was significant interactive effect of quinapril and apstatin (F = 20.83, P =.006) on the wheal response to bradykinin.	apstatin	85-93	kininogen 1	Homo sapiens	259-269
10604961-9	2000	The effect of quinapril was significantly potentiated by coinjection of 10 microg of apstatin (effect of apstatin; F = 21.60, P =.006), such that there was significant interactive effect of quinapril and apstatin (F = 20.83, P =.006) on the wheal response to bradykinin.	apstatin	105-113	kininogen 1	Homo sapiens	259-269
10604961-9	2000	The effect of quinapril was significantly potentiated by coinjection of 10 microg of apstatin (effect of apstatin; F = 21.60, P =.006), such that there was significant interactive effect of quinapril and apstatin (F = 20.83, P =.006) on the wheal response to bradykinin.	apstatin	105-113	kininogen 1	Homo sapiens	259-269
10694205-7	2000	Bradyzide does not interact with a range of other receptors, including human and rat B(1) bradykinin receptors.	bradyzide	0-9	kininogen 1	Homo sapiens	90-100
10694205-8	2000	Bradyzide is orally available and blocks bradykinin-induced hypotension and plasma extravasation.	bradyzide	0-9	kininogen 1	Homo sapiens	41-51
10690296-6	1999	Bradykinin and thapsigargin provoked large increases in [Ca2+]i, which were significantly diminished by removal of Cl-o and by pretreatment with the Cl(-)-channel inhibitor N-phenylanthranilic acid.	fenamic acid	173-197	kininogen 1	Homo sapiens	0-10
10714896-5	2000	During reverse microdialysis with bradykinin and enalaprilate a significant decrease in arterial-interstitial-gradient for glucose (AIG(glu)) was observed (from 1.49 +/- 0.08 mM to 0.12 +/- 0.63 mM (p = 0.018) for bradykinin and from 1.5 +/- 0.07 mM to 0.24 +/- 0.67 mM (p = 0.043) for enalaprilate).	Glucose	123-130	kininogen 1	Homo sapiens	34-44
10714896-5	2000	During reverse microdialysis with bradykinin and enalaprilate a significant decrease in arterial-interstitial-gradient for glucose (AIG(glu)) was observed (from 1.49 +/- 0.08 mM to 0.12 +/- 0.63 mM (p = 0.018) for bradykinin and from 1.5 +/- 0.07 mM to 0.24 +/- 0.67 mM (p = 0.043) for enalaprilate).	Glutamic Acid	123-126	kininogen 1	Homo sapiens	34-44
10714896-5	2000	During reverse microdialysis with bradykinin and enalaprilate a significant decrease in arterial-interstitial-gradient for glucose (AIG(glu)) was observed (from 1.49 +/- 0.08 mM to 0.12 +/- 0.63 mM (p = 0.018) for bradykinin and from 1.5 +/- 0.07 mM to 0.24 +/- 0.67 mM (p = 0.043) for enalaprilate).	Enalaprilat	49-61	kininogen 1	Homo sapiens	214-224
10714896-7	2000	The changes in transcapillary glucose transport during bradykinin and enalaprilate administration were accompanied by significant increases in interstitial lactate levels which was most pronounced for bradykinin (from 0.14 +/- 0.01 mM to 0.40 +/- 0.07 mM, p = 0.018).	Glucose	30-37	kininogen 1	Homo sapiens	55-65
10714896-7	2000	The changes in transcapillary glucose transport during bradykinin and enalaprilate administration were accompanied by significant increases in interstitial lactate levels which was most pronounced for bradykinin (from 0.14 +/- 0.01 mM to 0.40 +/- 0.07 mM, p = 0.018).	Glucose	30-37	kininogen 1	Homo sapiens	201-211
10714896-7	2000	The changes in transcapillary glucose transport during bradykinin and enalaprilate administration were accompanied by significant increases in interstitial lactate levels which was most pronounced for bradykinin (from 0.14 +/- 0.01 mM to 0.40 +/- 0.07 mM, p = 0.018).	Enalaprilat	70-82	kininogen 1	Homo sapiens	201-211
10714896-7	2000	The changes in transcapillary glucose transport during bradykinin and enalaprilate administration were accompanied by significant increases in interstitial lactate levels which was most pronounced for bradykinin (from 0.14 +/- 0.01 mM to 0.40 +/- 0.07 mM, p = 0.018).	Lactic Acid	156-163	kininogen 1	Homo sapiens	55-65
10714896-7	2000	The changes in transcapillary glucose transport during bradykinin and enalaprilate administration were accompanied by significant increases in interstitial lactate levels which was most pronounced for bradykinin (from 0.14 +/- 0.01 mM to 0.40 +/- 0.07 mM, p = 0.018).	Lactic Acid	156-163	kininogen 1	Homo sapiens	201-211
10961146-1	2000	The synthetic gene of bradykinin was built into the retrovirus vector pPS-3-neo under the guidance of LTR promotor, followed by pPS-3-neo (brd) vector transfection of strain 293 cells.	pps-3-neo	70-79	kininogen 1	Homo sapiens	22-32
10961146-1	2000	The synthetic gene of bradykinin was built into the retrovirus vector pPS-3-neo under the guidance of LTR promotor, followed by pPS-3-neo (brd) vector transfection of strain 293 cells.	Pentosan Sulfuric Polyester	70-73	kininogen 1	Homo sapiens	22-32
10961146-1	2000	The synthetic gene of bradykinin was built into the retrovirus vector pPS-3-neo under the guidance of LTR promotor, followed by pPS-3-neo (brd) vector transfection of strain 293 cells.	3-neo	74-79	kininogen 1	Homo sapiens	22-32
10690296-3	1999	RESULTS: Bradykinin and thapsigargin significantly decreased the MQAE fluorescence intensity, which indicates increased [Cl-]i; these changes were reversed by removal of extracellular chloride (Cl-o) and were significantly inhibited by Cl(-)-channel inhibitor N-phenylanthranilic acid but not by Na(+)-K(+)-Cl- cotransport inhibitor furosemide.	Chlorides	184-192	kininogen 1	Homo sapiens	9-19
10690296-3	1999	RESULTS: Bradykinin and thapsigargin significantly decreased the MQAE fluorescence intensity, which indicates increased [Cl-]i; these changes were reversed by removal of extracellular chloride (Cl-o) and were significantly inhibited by Cl(-)-channel inhibitor N-phenylanthranilic acid but not by Na(+)-K(+)-Cl- cotransport inhibitor furosemide.	Chlorides	194-198	kininogen 1	Homo sapiens	9-19
10690296-3	1999	RESULTS: Bradykinin and thapsigargin significantly decreased the MQAE fluorescence intensity, which indicates increased [Cl-]i; these changes were reversed by removal of extracellular chloride (Cl-o) and were significantly inhibited by Cl(-)-channel inhibitor N-phenylanthranilic acid but not by Na(+)-K(+)-Cl- cotransport inhibitor furosemide.	fenamic acid	260-284	kininogen 1	Homo sapiens	9-19
10690296-3	1999	RESULTS: Bradykinin and thapsigargin significantly decreased the MQAE fluorescence intensity, which indicates increased [Cl-]i; these changes were reversed by removal of extracellular chloride (Cl-o) and were significantly inhibited by Cl(-)-channel inhibitor N-phenylanthranilic acid but not by Na(+)-K(+)-Cl- cotransport inhibitor furosemide.	Furosemide	333-343	kininogen 1	Homo sapiens	9-19
10690296-6	1999	Bradykinin and thapsigargin provoked large increases in [Ca2+]i, which were significantly diminished by removal of Cl-o and by pretreatment with the Cl(-)-channel inhibitor N-phenylanthranilic acid.	Chlorides	115-119	kininogen 1	Homo sapiens	0-10
10585891-3	1999	In human subcutaneous arteries from uraemic subjects, noradrenaline- and KCl-induced vasoconstrictions were enhanced when nitric oxide (NO) production was blocked with N(G)-nitro-L-arginine methyl ester (L-NAME), but were unaffected by EPO, while acetylcholine- and bradykinin-induced concentration-dependent relaxations were markedly attenuated by L-NAME, but not by EPO.	Norepinephrine	54-67	kininogen 1	Homo sapiens	266-276
10614983-1	1999	Here we propose a molecular model for bradykinin receptor-operated and second messenger (inositol-1,3,4,5-tetrakisphosphate)-evoked Ca2+ influx and its potentiation by oncogenic Ras, which is not store-depletion-induced, so-called capacitative, Ca2+ influx.	inositol-1,3,4,5-tetrakisphosphate	89-123	kininogen 1	Homo sapiens	38-48
10614983-2	1999	The principal idea for this hypothesis stems from observation that two bradykinin B2 receptor-activated signal pathways, protein tyrosine phosphorylation and formation of inositol tetrakisphosphate, merge during the Ca2+ influx process and that GTPase activating-protein 1 (GAP 1) is inositol tetrakisphosphate binding protein.	Tyrosine	129-137	kininogen 1	Homo sapiens	71-81
10614983-2	1999	The principal idea for this hypothesis stems from observation that two bradykinin B2 receptor-activated signal pathways, protein tyrosine phosphorylation and formation of inositol tetrakisphosphate, merge during the Ca2+ influx process and that GTPase activating-protein 1 (GAP 1) is inositol tetrakisphosphate binding protein.	inositol tetrakisphosphate	171-197	kininogen 1	Homo sapiens	71-81
10614983-2	1999	The principal idea for this hypothesis stems from observation that two bradykinin B2 receptor-activated signal pathways, protein tyrosine phosphorylation and formation of inositol tetrakisphosphate, merge during the Ca2+ influx process and that GTPase activating-protein 1 (GAP 1) is inositol tetrakisphosphate binding protein.	inositol tetrakisphosphate	284-310	kininogen 1	Homo sapiens	71-81
10615015-5	1999	The enzyme hydrolyzed bradykinin (BK = RPPGFSPFR) at the F-S peptide bond, differing from the cleavage site F-R, in the fluorogenic substrates Abz-BKQ-EDDnp and Abz-FRQ-EDDnp.	abz-bkq-eddnp	143-156	kininogen 1	Homo sapiens	22-32
10615015-5	1999	The enzyme hydrolyzed bradykinin (BK = RPPGFSPFR) at the F-S peptide bond, differing from the cleavage site F-R, in the fluorogenic substrates Abz-BKQ-EDDnp and Abz-FRQ-EDDnp.	abz-frq-eddnp	161-174	kininogen 1	Homo sapiens	22-32
10594341-1	1999	The influence of the angiotensin-converting enzyme inhibitor captopril on bradykinin-and angiotensin I-induced responses with special regard to nitric oxide (NO) was studied.	Captopril	61-70	kininogen 1	Homo sapiens	74-84
10594341-3	1999	Captopril potentiated bradykinin-induced contraction of preparations with intact endothelium; this potentiation was not seen with the kininase I inhibitor mergepta or a bradykinin B(1)-receptor antagonist.	Captopril	0-9	kininogen 1	Homo sapiens	22-32
10594341-5	1999	The captopril-mediated increase of bradykinin-induced contraction was only seen in preparations with intact endothelium, while captopril did not affect arterial strips treated with Nomega-nitro-L-arginine.	Captopril	4-13	kininogen 1	Homo sapiens	35-45
10594341-9	1999	In conclusion, captopril increased bradykinin-induced contraction in a NO-dependent manner.	Captopril	15-24	kininogen 1	Homo sapiens	35-45
10658194-6	2000	Treatment of F-11 cells with bradykinin (BK) stimulated the hydrolysis of a different polyphosphoinositide, PtdIns(4,5)P2, and enhanced both wortmannin-induced caspase-3 (CPP32) activation and subsequent apoptosis.	Phosphatidylinositol Phosphates	86-106	kininogen 1	Homo sapiens	29-39
10658194-6	2000	Treatment of F-11 cells with bradykinin (BK) stimulated the hydrolysis of a different polyphosphoinositide, PtdIns(4,5)P2, and enhanced both wortmannin-induced caspase-3 (CPP32) activation and subsequent apoptosis.	Phosphatidylinositol Phosphates	86-106	kininogen 1	Homo sapiens	41-43
10658194-6	2000	Treatment of F-11 cells with bradykinin (BK) stimulated the hydrolysis of a different polyphosphoinositide, PtdIns(4,5)P2, and enhanced both wortmannin-induced caspase-3 (CPP32) activation and subsequent apoptosis.	Phosphatidylinositol 4,5-Diphosphate	108-121	kininogen 1	Homo sapiens	29-39
10658194-6	2000	Treatment of F-11 cells with bradykinin (BK) stimulated the hydrolysis of a different polyphosphoinositide, PtdIns(4,5)P2, and enhanced both wortmannin-induced caspase-3 (CPP32) activation and subsequent apoptosis.	Phosphatidylinositol 4,5-Diphosphate	108-121	kininogen 1	Homo sapiens	41-43
10658194-6	2000	Treatment of F-11 cells with bradykinin (BK) stimulated the hydrolysis of a different polyphosphoinositide, PtdIns(4,5)P2, and enhanced both wortmannin-induced caspase-3 (CPP32) activation and subsequent apoptosis.	Wortmannin	141-151	kininogen 1	Homo sapiens	29-39
10658194-6	2000	Treatment of F-11 cells with bradykinin (BK) stimulated the hydrolysis of a different polyphosphoinositide, PtdIns(4,5)P2, and enhanced both wortmannin-induced caspase-3 (CPP32) activation and subsequent apoptosis.	Wortmannin	141-151	kininogen 1	Homo sapiens	41-43
10585891-3	1999	In human subcutaneous arteries from uraemic subjects, noradrenaline- and KCl-induced vasoconstrictions were enhanced when nitric oxide (NO) production was blocked with N(G)-nitro-L-arginine methyl ester (L-NAME), but were unaffected by EPO, while acetylcholine- and bradykinin-induced concentration-dependent relaxations were markedly attenuated by L-NAME, but not by EPO.	Potassium Chloride	73-76	kininogen 1	Homo sapiens	266-276
10585891-3	1999	In human subcutaneous arteries from uraemic subjects, noradrenaline- and KCl-induced vasoconstrictions were enhanced when nitric oxide (NO) production was blocked with N(G)-nitro-L-arginine methyl ester (L-NAME), but were unaffected by EPO, while acetylcholine- and bradykinin-induced concentration-dependent relaxations were markedly attenuated by L-NAME, but not by EPO.	Nitric Oxide	122-134	kininogen 1	Homo sapiens	266-276
10666793-4	1999	The basal endothelial formation of NO can be increased by receptor-dependent agonists (i.e., bradykinin) in a calcium-calmodulin-dependent manner, and also by physical forces (i.e., shear stress), predominantly without changes in the intracellular concentration of free calcium.	Calcium	110-117	kininogen 1	Homo sapiens	93-103
10579714-4	1999	Here, we explore the spatial and temporal characteristics of [InsP(3)](cyt) during a bradykinin-induced calcium wave in a neuroblastoma cell.	Calcium	104-111	kininogen 1	Homo sapiens	85-95
10564232-1	1999	Bradykinin (BK)-induced changes in intracellular calcium level ([Ca(2+)](i)) were studied on fura 2-loaded afferent (AA) and efferent glomerular arterioles (EA) microdissected from juxtamedullary renal cortex.	Calcium	49-56	kininogen 1	Homo sapiens	0-10
10564232-1	1999	Bradykinin (BK)-induced changes in intracellular calcium level ([Ca(2+)](i)) were studied on fura 2-loaded afferent (AA) and efferent glomerular arterioles (EA) microdissected from juxtamedullary renal cortex.	Calcium	49-56	kininogen 1	Homo sapiens	12-14
10564232-1	1999	Bradykinin (BK)-induced changes in intracellular calcium level ([Ca(2+)](i)) were studied on fura 2-loaded afferent (AA) and efferent glomerular arterioles (EA) microdissected from juxtamedullary renal cortex.	Fura-2	93-99	kininogen 1	Homo sapiens	0-10
10564232-1	1999	Bradykinin (BK)-induced changes in intracellular calcium level ([Ca(2+)](i)) were studied on fura 2-loaded afferent (AA) and efferent glomerular arterioles (EA) microdissected from juxtamedullary renal cortex.	Fura-2	93-99	kininogen 1	Homo sapiens	12-14
10582733-9	1999	These techniques were also used to show that low concentrations of intradermal bradykinin release negligible quantities of histamine.	Histamine	123-132	kininogen 1	Homo sapiens	79-89
10535458-9	1999	After bradykinin stimulation either in the absence or in the presence of BHT, both cytoplasmic Ca2+ levels and NO production were increased in control HUVECs and in HUVECs incubated with control LDL, while a reduced response was observed in HUVECs incubated with type 1 LDL.	Butylated Hydroxytoluene	73-76	kininogen 1	Homo sapiens	6-16
10596684-0	1999	Prostaglandins mediate bradykinin-induced reduction of exhaled nitric oxide in asthma.	Prostaglandins	0-14	kininogen 1	Homo sapiens	23-33
10596684-0	1999	Prostaglandins mediate bradykinin-induced reduction of exhaled nitric oxide in asthma.	Nitric Oxide	63-75	kininogen 1	Homo sapiens	23-33
10596684-2	1999	Endogenous release of nitric oxide may inhibit BK-induced bronchoconstriction.	Nitric Oxide	22-34	kininogen 1	Homo sapiens	47-49
10596684-7	1999	In asthmatic subjects, pretreatment with inhaled L-ASA (90 x mg x mL(-1), 4 mL) did not alter exhaled NO levels, but prevented a BK-induced fall in exhaled NO concentration, as indicated by a significant increase in exhaled NO levels at the provocative concentration of BK causing a 20% fall in FEV1, (5.7 +/- 0.94 ppb after placebo and 12.0 +/- 1.8 ppb after L-ASA; p&lt;0.05).	l-asa	49-54	kininogen 1	Homo sapiens	129-131
10596684-7	1999	In asthmatic subjects, pretreatment with inhaled L-ASA (90 x mg x mL(-1), 4 mL) did not alter exhaled NO levels, but prevented a BK-induced fall in exhaled NO concentration, as indicated by a significant increase in exhaled NO levels at the provocative concentration of BK causing a 20% fall in FEV1, (5.7 +/- 0.94 ppb after placebo and 12.0 +/- 1.8 ppb after L-ASA; p&lt;0.05).	l-asa	49-54	kininogen 1	Homo sapiens	270-272
10596684-7	1999	In asthmatic subjects, pretreatment with inhaled L-ASA (90 x mg x mL(-1), 4 mL) did not alter exhaled NO levels, but prevented a BK-induced fall in exhaled NO concentration, as indicated by a significant increase in exhaled NO levels at the provocative concentration of BK causing a 20% fall in FEV1, (5.7 +/- 0.94 ppb after placebo and 12.0 +/- 1.8 ppb after L-ASA; p&lt;0.05).	l-asa	360-365	kininogen 1	Homo sapiens	129-131
10596684-8	1999	L-ASA significantly reduced bronchial responsiveness to BK 3.9-fold (p&lt;0.01).	l-asa	0-5	kininogen 1	Homo sapiens	56-58
10596684-9	1999	Inhaled bradykinin induced bronchoconstriction and a reduction in exhaled nitric oxide levels in asthmatic subjects, an effect that is partly mediated by cyclo-oxygenase products.	Nitric Oxide	74-86	kininogen 1	Homo sapiens	8-18
10548377-10	1999	Bradykinin (10(-6) M) significantly increased permeability to albumin, ioversol, and sinerem.	ioversol	71-79	kininogen 1	Homo sapiens	0-10
10548377-10	1999	Bradykinin (10(-6) M) significantly increased permeability to albumin, ioversol, and sinerem.	ferumoxtran-10	85-92	kininogen 1	Homo sapiens	0-10
10608722-1	1999	The negative charges of dextran sulfate cellulose (DSC) used for low-density lipoprotein (LDL) apheresis activate the intrinsic coagulation pathway, accompanied by bradykinin production.	dextran sulfate cellulose	24-49	kininogen 1	Homo sapiens	164-174
10564166-8	1999	In porcine coronary arteries, 4-PCO augmented 14,15-EET-induced potentiation of endothelium-dependent relaxation to bradykinin.	4-phenylchalcone oxide	30-35	kininogen 1	Homo sapiens	116-126
10564166-8	1999	In porcine coronary arteries, 4-PCO augmented 14,15-EET-induced potentiation of endothelium-dependent relaxation to bradykinin.	14,15-epoxy-5,8,11-eicosatrienoic acid	46-55	kininogen 1	Homo sapiens	116-126
10608722-1	1999	The negative charges of dextran sulfate cellulose (DSC) used for low-density lipoprotein (LDL) apheresis activate the intrinsic coagulation pathway, accompanied by bradykinin production.	N,N'-Disuccinimidyl carbonate	51-54	kininogen 1	Homo sapiens	164-174
10608722-6	1999	Bradykinin levels during LDL apheresis tended to be higher with losartan than without losartan (without versus with, 529 +/- 121 [n = 4, mean +/- SE] pg/ml vs. 1,058 +/- 49 at the 2,000 ml stage, p &lt; 0.01).	Losartan	64-72	kininogen 1	Homo sapiens	0-10
10608722-6	1999	Bradykinin levels during LDL apheresis tended to be higher with losartan than without losartan (without versus with, 529 +/- 121 [n = 4, mean +/- SE] pg/ml vs. 1,058 +/- 49 at the 2,000 ml stage, p &lt; 0.01).	Losartan	86-94	kininogen 1	Homo sapiens	0-10
10510297-4	1999	Furthermore, the B2 receptor is transiently phosphorylated on tyrosine residues in cultured endothelial cells in response to BK stimulation.	Tyrosine	62-70	kininogen 1	Homo sapiens	125-127
10604529-1	1999	Bradykinin (BK) increased carotid blood flow (CBF) and jugular nitric oxide (NO) levels when administered into the common carotid artery of rabbits, and potentiated selectively, when infused together with histamine (HIST) or serotonin (5-HT), their effects on both CBF and jugular NO levels (but not vice versa).	Nitric Oxide	63-75	kininogen 1	Homo sapiens	0-10
10604529-1	1999	Bradykinin (BK) increased carotid blood flow (CBF) and jugular nitric oxide (NO) levels when administered into the common carotid artery of rabbits, and potentiated selectively, when infused together with histamine (HIST) or serotonin (5-HT), their effects on both CBF and jugular NO levels (but not vice versa).	Histamine	205-214	kininogen 1	Homo sapiens	0-10
10604529-1	1999	Bradykinin (BK) increased carotid blood flow (CBF) and jugular nitric oxide (NO) levels when administered into the common carotid artery of rabbits, and potentiated selectively, when infused together with histamine (HIST) or serotonin (5-HT), their effects on both CBF and jugular NO levels (but not vice versa).	Histamine	216-220	kininogen 1	Homo sapiens	0-10
10604529-1	1999	Bradykinin (BK) increased carotid blood flow (CBF) and jugular nitric oxide (NO) levels when administered into the common carotid artery of rabbits, and potentiated selectively, when infused together with histamine (HIST) or serotonin (5-HT), their effects on both CBF and jugular NO levels (but not vice versa).	Serotonin	225-234	kininogen 1	Homo sapiens	0-10
10604529-1	1999	Bradykinin (BK) increased carotid blood flow (CBF) and jugular nitric oxide (NO) levels when administered into the common carotid artery of rabbits, and potentiated selectively, when infused together with histamine (HIST) or serotonin (5-HT), their effects on both CBF and jugular NO levels (but not vice versa).	Bufotenin	238-240	kininogen 1	Homo sapiens	0-10
10514288-2	1999	The same modification was performed on the potent bradykinin B(2) receptor antagonist HOE 140 (H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg-OH), in which the -D-Tic-Oic- moiety was replaced by D-BT to yield H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-BT-Arg-OH, 1 (JMV1116).	Glycine	114-118	kininogen 1	Homo sapiens	50-60
10514288-0	1999	Design and synthesis of potent bradykinin agonists containing a benzothiazepine moiety.	benzothiazepine	64-79	kininogen 1	Homo sapiens	31-41
10514288-1	1999	A bradykinin analogue (H-Arg-Pro-Pro-Gly-Phe-Ser-D-BT-Arg-OH, 3) in which the Pro-Phe dipeptide was replaced by the (3S)[amino]-5-(carbonylmethyl)-2,3-dihydro-1, 5-benzothiazepin-4(5H)-one (D-BT) moiety has been synthesized.	h-arg-pro-pro-gly-phe-ser-d-bt-arg-oh	23-60	kininogen 1	Homo sapiens	2-12
10514288-1	1999	A bradykinin analogue (H-Arg-Pro-Pro-Gly-Phe-Ser-D-BT-Arg-OH, 3) in which the Pro-Phe dipeptide was replaced by the (3S)[amino]-5-(carbonylmethyl)-2,3-dihydro-1, 5-benzothiazepin-4(5H)-one (D-BT) moiety has been synthesized.	pro-phe dipeptide	78-95	kininogen 1	Homo sapiens	2-12
10514288-1	1999	A bradykinin analogue (H-Arg-Pro-Pro-Gly-Phe-Ser-D-BT-Arg-OH, 3) in which the Pro-Phe dipeptide was replaced by the (3S)[amino]-5-(carbonylmethyl)-2,3-dihydro-1, 5-benzothiazepin-4(5H)-one (D-BT) moiety has been synthesized.	(3s)[amino]-5-(carbonylmethyl)-2,3-dihydro-1, 5-benzothiazepin-4(5h)-one	116-188	kininogen 1	Homo sapiens	2-12
10514288-1	1999	A bradykinin analogue (H-Arg-Pro-Pro-Gly-Phe-Ser-D-BT-Arg-OH, 3) in which the Pro-Phe dipeptide was replaced by the (3S)[amino]-5-(carbonylmethyl)-2,3-dihydro-1, 5-benzothiazepin-4(5H)-one (D-BT) moiety has been synthesized.	d-bt	49-53	kininogen 1	Homo sapiens	2-12
10514288-2	1999	The same modification was performed on the potent bradykinin B(2) receptor antagonist HOE 140 (H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg-OH), in which the -D-Tic-Oic- moiety was replaced by D-BT to yield H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-BT-Arg-OH, 1 (JMV1116).	4-hydroxy-2-octenal	86-89	kininogen 1	Homo sapiens	50-60
10514288-2	1999	The same modification was performed on the potent bradykinin B(2) receptor antagonist HOE 140 (H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg-OH), in which the -D-Tic-Oic- moiety was replaced by D-BT to yield H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-BT-Arg-OH, 1 (JMV1116).	h-d-arg-arg	95-106	kininogen 1	Homo sapiens	50-60
10514288-2	1999	The same modification was performed on the potent bradykinin B(2) receptor antagonist HOE 140 (H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg-OH), in which the -D-Tic-Oic- moiety was replaced by D-BT to yield H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-BT-Arg-OH, 1 (JMV1116).	Glycine	115-118	kininogen 1	Homo sapiens	50-60
10514288-2	1999	The same modification was performed on the potent bradykinin B(2) receptor antagonist HOE 140 (H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg-OH), in which the -D-Tic-Oic- moiety was replaced by D-BT to yield H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-BT-Arg-OH, 1 (JMV1116).	Serine	123-126	kininogen 1	Homo sapiens	50-60
10514288-2	1999	The same modification was performed on the potent bradykinin B(2) receptor antagonist HOE 140 (H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg-OH), in which the -D-Tic-Oic- moiety was replaced by D-BT to yield H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-BT-Arg-OH, 1 (JMV1116).	Dacarbazine	127-132	kininogen 1	Homo sapiens	50-60
10514288-2	1999	The same modification was performed on the potent bradykinin B(2) receptor antagonist HOE 140 (H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg-OH), in which the -D-Tic-Oic- moiety was replaced by D-BT to yield H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-BT-Arg-OH, 1 (JMV1116).	h-d-arg	95-102	kininogen 1	Homo sapiens	50-60
10514288-2	1999	The same modification was performed on the potent bradykinin B(2) receptor antagonist HOE 140 (H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg-OH), in which the -D-Tic-Oic- moiety was replaced by D-BT to yield H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-BT-Arg-OH, 1 (JMV1116).	Arginine	99-102	kininogen 1	Homo sapiens	50-60
10514288-2	1999	The same modification was performed on the potent bradykinin B(2) receptor antagonist HOE 140 (H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Tic-Oic-Arg-OH), in which the -D-Tic-Oic- moiety was replaced by D-BT to yield H-D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-BT-Arg-OH, 1 (JMV1116).	2-acetyl-4(5)-tetrahydroxybutylimidazole	119-122	kininogen 1	Homo sapiens	50-60
10514288-7	1999	These data provide evidence for a bioactive conformation of bradykinin constrained at the dipeptide Pro-Phe.	Dipeptides	90-99	kininogen 1	Homo sapiens	60-70
10514288-7	1999	These data provide evidence for a bioactive conformation of bradykinin constrained at the dipeptide Pro-Phe.	H-Pro-Phe-OH	100-107	kininogen 1	Homo sapiens	60-70
10514289-0	1999	Synthesis and characterization of bradykinin B(2) receptor agonists containing constrained dipeptide mimics.	Dipeptides	91-100	kininogen 1	Homo sapiens	34-44
10514289-6	1999	Substitution of the D-arginine residue by a L-lysine residue led to a 10-fold more potent bradykinin B(2) ligand [compound 22 (JMV1465) (K(i) 0.07 nM)], retaining full agonist activity on human umbilical vein.	D-Arginine	20-30	kininogen 1	Homo sapiens	90-100
10514289-6	1999	Substitution of the D-arginine residue by a L-lysine residue led to a 10-fold more potent bradykinin B(2) ligand [compound 22 (JMV1465) (K(i) 0.07 nM)], retaining full agonist activity on human umbilical vein.	Lysine	44-52	kininogen 1	Homo sapiens	90-100
10511133-0	1999	Reactive oxygen species: role in the relaxation induced by bradykinin or arachidonic acid via EDHF in isolated porcine coronary arteries.	Reactive Oxygen Species	0-23	kininogen 1	Homo sapiens	59-69
10549414-6	1999	At 1 nmol/L, testosterone impaired relaxations to BK and A23187, while the same concentration of 17 beta-oestradiol potentiated levcromakalim- and SNP-induced relaxations.	Testosterone	13-25	kininogen 1	Homo sapiens	50-52
10511133-0	1999	Reactive oxygen species: role in the relaxation induced by bradykinin or arachidonic acid via EDHF in isolated porcine coronary arteries.	edhf	94-98	kininogen 1	Homo sapiens	59-69
10501190-6	1999	The effect of bradykinin was blocked by KN-93, an inhibitor of Ca2+/calmodulin-dependent protein kinases, and by bisindolylmaleimide I, an inhibitor of protein kinase C, suggesting the involvement of these protein kinases.	KN 93	40-45	kininogen 1	Homo sapiens	14-24
10501190-6	1999	The effect of bradykinin was blocked by KN-93, an inhibitor of Ca2+/calmodulin-dependent protein kinases, and by bisindolylmaleimide I, an inhibitor of protein kinase C, suggesting the involvement of these protein kinases.	bisindolylmaleimide I	113-134	kininogen 1	Homo sapiens	14-24
10535387-2	1999	In the present study, we measured plasma levels of nitric oxide (NO) and the related vasoactive factors bradykinin, 6-keto prostaglandin F1alpha (6-keto PGF1alpha) a stable metabolite of prostacyclin, and cyclic guanosine-3",5"-monophosphate (cGMP) before and after a 4-week treatment with the ACE inhibitor lisinopril in 17 patients with essential hypertension.	6-Ketoprostaglandin F1 alpha	146-162	kininogen 1	Homo sapiens	104-114
10535387-2	1999	In the present study, we measured plasma levels of nitric oxide (NO) and the related vasoactive factors bradykinin, 6-keto prostaglandin F1alpha (6-keto PGF1alpha) a stable metabolite of prostacyclin, and cyclic guanosine-3",5"-monophosphate (cGMP) before and after a 4-week treatment with the ACE inhibitor lisinopril in 17 patients with essential hypertension.	Epoprostenol	187-199	kininogen 1	Homo sapiens	104-114
10535387-2	1999	In the present study, we measured plasma levels of nitric oxide (NO) and the related vasoactive factors bradykinin, 6-keto prostaglandin F1alpha (6-keto PGF1alpha) a stable metabolite of prostacyclin, and cyclic guanosine-3",5"-monophosphate (cGMP) before and after a 4-week treatment with the ACE inhibitor lisinopril in 17 patients with essential hypertension.	Cyclic GMP	205-241	kininogen 1	Homo sapiens	104-114
10535387-2	1999	In the present study, we measured plasma levels of nitric oxide (NO) and the related vasoactive factors bradykinin, 6-keto prostaglandin F1alpha (6-keto PGF1alpha) a stable metabolite of prostacyclin, and cyclic guanosine-3",5"-monophosphate (cGMP) before and after a 4-week treatment with the ACE inhibitor lisinopril in 17 patients with essential hypertension.	Cyclic GMP	243-247	kininogen 1	Homo sapiens	104-114
10535387-2	1999	In the present study, we measured plasma levels of nitric oxide (NO) and the related vasoactive factors bradykinin, 6-keto prostaglandin F1alpha (6-keto PGF1alpha) a stable metabolite of prostacyclin, and cyclic guanosine-3",5"-monophosphate (cGMP) before and after a 4-week treatment with the ACE inhibitor lisinopril in 17 patients with essential hypertension.	Lisinopril	308-318	kininogen 1	Homo sapiens	104-114
10551272-4	1999	They reach only 70% and 30% of the BK-induced maximal contractions in the hUV and rbJV, respectively.	rbjv	82-86	kininogen 1	Homo sapiens	35-37
10551272-7	1999	When tested as an antagonist, FR 190997 inhibits also the contractile effects of BK in the hUV (pK(B) 7.8) and in the rbJV (pK(B) 7.6).	FR 190997	30-39	kininogen 1	Homo sapiens	81-83
10655909-5	1999	Propofol and its lipid solvent mixed with blood produced approximately two-fold generation of bradykinin compared with the saline control, and this was inhibited completely by nafamostat and lidocaine.	Propofol	0-8	kininogen 1	Homo sapiens	94-104
10511133-4	1999	Eicosatetraynoic acid (ETYA; 20 microM), which inhibits all AA pathways, slightly affected the response to BK and AA; however, lipoxygenase or cytochrome P-450 inhibitors had no effect, suggesting that relaxation is independent of these enzymatic pathways.	ETYA	0-21	kininogen 1	Homo sapiens	107-109
10511133-4	1999	Eicosatetraynoic acid (ETYA; 20 microM), which inhibits all AA pathways, slightly affected the response to BK and AA; however, lipoxygenase or cytochrome P-450 inhibitors had no effect, suggesting that relaxation is independent of these enzymatic pathways.	ETYA	23-27	kininogen 1	Homo sapiens	107-109
10511133-10	1999	We therefore questioned whether ROS might be involved in BK- and AA-induced relaxation.	Reactive Oxygen Species	32-35	kininogen 1	Homo sapiens	57-59
10511133-11	1999	Because catalase combined with SOD had little or no effect, we concluded that in the PCA, the relaxation induced by BK via EDHF involves some mechanism independent of NO, AA metabolism, or ROS.	edhf	123-127	kininogen 1	Homo sapiens	116-118
10511133-11	1999	Because catalase combined with SOD had little or no effect, we concluded that in the PCA, the relaxation induced by BK via EDHF involves some mechanism independent of NO, AA metabolism, or ROS.	Reactive Oxygen Species	189-192	kininogen 1	Homo sapiens	116-118
10493215-5	1999	Plasma levels of bradykinin increased 12-fold during LDL apheresis with heparin, but did not increase during LDL apheresis with nafamostat mesilate.	Heparin	72-79	kininogen 1	Homo sapiens	17-27
10600483-5	1999	In the absence of extracellular Ca(2+), pretreatment of cells with bradykinin (BK) and thapsigargin completely prevented W-7-stimulated increase in [Ca(2+)](i).	W 7	121-124	kininogen 1	Homo sapiens	67-77
10600483-5	1999	In the absence of extracellular Ca(2+), pretreatment of cells with bradykinin (BK) and thapsigargin completely prevented W-7-stimulated increase in [Ca(2+)](i).	W 7	121-124	kininogen 1	Homo sapiens	79-81
10532602-6	1999	In the presence of ACE inhibition (enalaprilat), the t1/2 of des-Arg9-BK was significantly greater in patients who presented with a severe hypotensive transfusion reaction (1549 +/- 319 sec) than in normal controls (661 +/- 38 sec) (p &lt; 0.001).	Enalaprilat	35-46	kininogen 1	Homo sapiens	70-72
10500040-0	1999	Vasodilation to bradykinin is mediated by an ouabain-sensitive pathway as a compensatory mechanism for impaired nitric oxide availability in essential hypertensive patients.	Nitric Oxide	112-124	kininogen 1	Homo sapiens	16-26
10500040-4	1999	In healthy subjects, vasodilatation to bradykinin was significantly blunted by L-NMMA and unaffected by ouabain.	omega-N-Methylarginine	79-85	kininogen 1	Homo sapiens	39-49
10500040-7	1999	In these patients, L-NMMA-induced inhibition of vasodilation to bradykinin was restored, and ouabain was no longer effective.	omega-N-Methylarginine	19-25	kininogen 1	Homo sapiens	64-74
10485876-3	1999	Stimulation of either Galpha(i)-coupled receptor expressed in COS cells increased the potency and the efficacy of inositol phosphate production by bradykinin or UTP.	Inositol Phosphates	114-132	kininogen 1	Homo sapiens	147-157
10484429-2	1999	Exposure of vascular smooth muscle cells (VSMC) to BK (10(-7) M) produced a rapid and transient rise in intracellular calcium, which preceded an increase in tyrosine phosphorylation of mitogen-activated protein kinase (MAPK).	vsmc	42-46	kininogen 1	Homo sapiens	51-53
10484429-2	1999	Exposure of vascular smooth muscle cells (VSMC) to BK (10(-7) M) produced a rapid and transient rise in intracellular calcium, which preceded an increase in tyrosine phosphorylation of mitogen-activated protein kinase (MAPK).	Calcium	118-125	kininogen 1	Homo sapiens	51-53
10484429-2	1999	Exposure of vascular smooth muscle cells (VSMC) to BK (10(-7) M) produced a rapid and transient rise in intracellular calcium, which preceded an increase in tyrosine phosphorylation of mitogen-activated protein kinase (MAPK).	Tyrosine	157-165	kininogen 1	Homo sapiens	51-53
10484429-4	1999	Treatment of cells with the intracellular calcium chelator EGTA-acetoxymethyl ester inhibited BK-stimulated MAPK activation, suggesting that intracellular calcium mobilization contributes to the activation of MAPK.	Calcium	42-49	kininogen 1	Homo sapiens	94-96
10484429-4	1999	Treatment of cells with the intracellular calcium chelator EGTA-acetoxymethyl ester inhibited BK-stimulated MAPK activation, suggesting that intracellular calcium mobilization contributes to the activation of MAPK.	EGTA acetoxymethyl ester	59-83	kininogen 1	Homo sapiens	94-96
10484429-4	1999	Treatment of cells with the intracellular calcium chelator EGTA-acetoxymethyl ester inhibited BK-stimulated MAPK activation, suggesting that intracellular calcium mobilization contributes to the activation of MAPK.	Calcium	155-162	kininogen 1	Homo sapiens	94-96
10484429-5	1999	The calmodulin inhibitor W-7 also markedly inhibited BK-induced MAPK phosphorylation in the cytoplasm as well as in the nucleus.	W 7	25-28	kininogen 1	Homo sapiens	53-55
10655909-5	1999	Propofol and its lipid solvent mixed with blood produced approximately two-fold generation of bradykinin compared with the saline control, and this was inhibited completely by nafamostat and lidocaine.	nafamostat	176-186	kininogen 1	Homo sapiens	94-104
10655909-5	1999	Propofol and its lipid solvent mixed with blood produced approximately two-fold generation of bradykinin compared with the saline control, and this was inhibited completely by nafamostat and lidocaine.	Lidocaine	191-200	kininogen 1	Homo sapiens	94-104
10655909-7	1999	These results suggest that the lipid solvent for propofol activates the plasma kallikrein-kinin system and produces bradykinin which modifies the injected local vein.	Propofol	49-57	kininogen 1	Homo sapiens	116-126
10395480-0	1999	Apstatin analogue inhibitors of aminopeptidase P, a bradykinin-degrading enzyme.	apstatin	0-8	kininogen 1	Homo sapiens	52-62
10498848-13	1999	In the same everted segment contracted with PGF2alpha, the concentration-response relationship for bradykinin was not different under isometric and isobaric conditions.	Dinoprost	44-53	kininogen 1	Homo sapiens	99-109
10596866-7	1999	The preincubation of sera with enalaprilat at a concentration inhibiting ACE significantly prevented the rapid degradation of BK and des-Arg9-BK in these four subgroups.	Enalaprilat	31-42	kininogen 1	Homo sapiens	126-128
10596866-7	1999	The preincubation of sera with enalaprilat at a concentration inhibiting ACE significantly prevented the rapid degradation of BK and des-Arg9-BK in these four subgroups.	Enalaprilat	31-42	kininogen 1	Homo sapiens	142-144
10484595-1	1999	The purpose of this study was to verify the possible appearance in the blood of bradykinin (BK) and des-Arg(9)-bradykinin (des-Arg(9)-BK) after eccentric exercise in 13 male subjects.	des-arg	100-107	kininogen 1	Homo sapiens	111-121
10484595-1	1999	The purpose of this study was to verify the possible appearance in the blood of bradykinin (BK) and des-Arg(9)-bradykinin (des-Arg(9)-BK) after eccentric exercise in 13 male subjects.	des-arg	100-107	kininogen 1	Homo sapiens	134-136
10484595-1	1999	The purpose of this study was to verify the possible appearance in the blood of bradykinin (BK) and des-Arg(9)-bradykinin (des-Arg(9)-BK) after eccentric exercise in 13 male subjects.	des-arg	123-130	kininogen 1	Homo sapiens	111-121
10484595-1	1999	The purpose of this study was to verify the possible appearance in the blood of bradykinin (BK) and des-Arg(9)-bradykinin (des-Arg(9)-BK) after eccentric exercise in 13 male subjects.	des-arg	123-130	kininogen 1	Homo sapiens	134-136
10470994-0	1999	Improvement of bradykinin endothelium-mediated vasodilation of forearm resistance circulation by quinaprilat in patients with coronary artery disease with or without left ventricular dysfunction.	quinaprilat	97-108	kininogen 1	Homo sapiens	15-25
10470994-6	1999	Then quinaprilat was infused alone at the rate of 50 microg/min and then coinfused with acetylcholine and bradykinin.	quinaprilat	5-16	kininogen 1	Homo sapiens	106-116
10470994-10	1999	Quinaprilat significantly enhanced the vasodilator response to acetylcholine only in subjects of the reference group, whereas it enhanced the vasodilator response to each dose of bradykinin, both in subjects of the reference group and in patients.	quinaprilat	0-11	kininogen 1	Homo sapiens	179-189
10470994-12	1999	In healthy persons, quinaprilat had no effect on its own on forearm blood flow but enhanced the response to bradykinin and even acetylcholine.	quinaprilat	20-31	kininogen 1	Homo sapiens	108-118
10470994-13	1999	In patients with coronary disease, short-term administration of quinaprilat was able to improve the impaired response to bradykinin.	quinaprilat	64-75	kininogen 1	Homo sapiens	121-131
10458930-0	1999	A role of protein kinase C in the regulation of cytosolic phospholipase A(2) in bradykinin-induced PGI(2) synthesis by human vascular endothelial cells.	Epoprostenol	99-105	kininogen 1	Homo sapiens	80-90
10458930-1	1999	The purpose of this study was to elucidate the mechanism by which bradykinin (BK) enhances prostacyclin (PGI(2)) production in human umbilical vein endothelial cells (HUVEC).	Epoprostenol	91-103	kininogen 1	Homo sapiens	66-76
10458930-1	1999	The purpose of this study was to elucidate the mechanism by which bradykinin (BK) enhances prostacyclin (PGI(2)) production in human umbilical vein endothelial cells (HUVEC).	Epoprostenol	91-103	kininogen 1	Homo sapiens	78-80
10458930-1	1999	The purpose of this study was to elucidate the mechanism by which bradykinin (BK) enhances prostacyclin (PGI(2)) production in human umbilical vein endothelial cells (HUVEC).	Epoprostenol	105-111	kininogen 1	Homo sapiens	66-76
10458930-1	1999	The purpose of this study was to elucidate the mechanism by which bradykinin (BK) enhances prostacyclin (PGI(2)) production in human umbilical vein endothelial cells (HUVEC).	Epoprostenol	105-111	kininogen 1	Homo sapiens	78-80
10458930-2	1999	BK-induced enhancement of PGI(2) synthesis was observed in a dose- and time-dependent manner, and it also increased [Ca(2+)](i) followed by enhancement of cytosolic phospholipase A(2) (cPLA(2)) activity.	Epoprostenol	26-32	kininogen 1	Homo sapiens	0-2
10458930-3	1999	The PKC inhibitors GF109203X and H7 attenuated the BK-induced increase in [Ca(2+)](i) and inhibited the BK-induced PGI(2) synthesis.	Epoprostenol	115-121	kininogen 1	Homo sapiens	104-106
10458930-7	1999	These results suggest that BK stimulates PGI(2) synthesis in HUVEC by activation of cPLA(2) by dual mechanisms: an elevation of [Ca(2+)](i) and a PKC-dependent pathway.	Epoprostenol	41-47	kininogen 1	Homo sapiens	27-29
10458930-8	1999	Moreover, changes in calcium kinetics and expression of cPLA(2) mRNA may underlie the BK-induced PGI(2) enhancement in these cells.	Calcium	21-28	kininogen 1	Homo sapiens	86-88
10458930-8	1999	Moreover, changes in calcium kinetics and expression of cPLA(2) mRNA may underlie the BK-induced PGI(2) enhancement in these cells.	Epoprostenol	97-103	kininogen 1	Homo sapiens	86-88
10464023-1	1999	The conformational features of H-Lys-Arg-Ado-Ser-Pro-Phe-OH (Ado = 12-aminododecanoic acid), a des-Arg(9) analogue of Lys-bradykinin, have been determined by high-resolution NMR in the presence of a zwitterionic lipid environment.	h-lys-arg-ado-ser-pro-phe-oh	31-59	kininogen 1	Homo sapiens	122-132
10464023-1	1999	The conformational features of H-Lys-Arg-Ado-Ser-Pro-Phe-OH (Ado = 12-aminododecanoic acid), a des-Arg(9) analogue of Lys-bradykinin, have been determined by high-resolution NMR in the presence of a zwitterionic lipid environment.	beta-apocarotenoid-14',13'-dioxygenase	41-44	kininogen 1	Homo sapiens	122-132
10464023-1	1999	The conformational features of H-Lys-Arg-Ado-Ser-Pro-Phe-OH (Ado = 12-aminododecanoic acid), a des-Arg(9) analogue of Lys-bradykinin, have been determined by high-resolution NMR in the presence of a zwitterionic lipid environment.	12-aminododecanoic acid	67-90	kininogen 1	Homo sapiens	122-132
10464023-1	1999	The conformational features of H-Lys-Arg-Ado-Ser-Pro-Phe-OH (Ado = 12-aminododecanoic acid), a des-Arg(9) analogue of Lys-bradykinin, have been determined by high-resolution NMR in the presence of a zwitterionic lipid environment.	des-arg	95-102	kininogen 1	Homo sapiens	122-132
10464023-8	1999	Although removed from a standard beta-turn, required for activity at the B2 kinin receptor, the topological orientation of the side chains of the des-Arg(9) compound are surprisingly similar to those previously observed for beta-turn-containing bradykinin analogues.	des-arg	146-153	kininogen 1	Homo sapiens	245-255
10464023-9	1999	Therefore, we attribute the high B1 receptor selectivity, observed upon removal of Arg(9) from bradykinin, solely to the loss of a charged amino acid and not to altered structural features.	Arginine	83-86	kininogen 1	Homo sapiens	95-105
10444401-5	1999	Addition of 10(-10)-10(-7) M BK to VSMC resulted in a rapid and concentration-dependent increase in tyrosine phosphorylation of several 144- to 40-kDa proteins.	vsmc	35-39	kininogen 1	Homo sapiens	29-31
10444401-5	1999	Addition of 10(-10)-10(-7) M BK to VSMC resulted in a rapid and concentration-dependent increase in tyrosine phosphorylation of several 144- to 40-kDa proteins.	Tyrosine	100-108	kininogen 1	Homo sapiens	29-31
10444401-7	1999	Immunoprecipitation with anti-phosphotyrosine antibodies followed by immunoblot revealed that 10(-9) M BK induced tyrosine phosphorylation of focal adhesion kinase (p125(FAK)).	Phosphotyrosine	30-45	kininogen 1	Homo sapiens	103-105
10444401-7	1999	Immunoprecipitation with anti-phosphotyrosine antibodies followed by immunoblot revealed that 10(-9) M BK induced tyrosine phosphorylation of focal adhesion kinase (p125(FAK)).	Tyrosine	37-45	kininogen 1	Homo sapiens	103-105
10444401-10	1999	Protein kinase C downregulation by phorbol 12-myristate 13-acetate and/or inhibitors to protein kinase C, p60(src) kinase, and MAPK kinase inhibited BK-induced MAPK tyrosine phosphorylation.	Tetradecanoylphorbol Acetate	35-66	kininogen 1	Homo sapiens	149-151
10444401-10	1999	Protein kinase C downregulation by phorbol 12-myristate 13-acetate and/or inhibitors to protein kinase C, p60(src) kinase, and MAPK kinase inhibited BK-induced MAPK tyrosine phosphorylation.	Tyrosine	165-173	kininogen 1	Homo sapiens	149-151
10444513-5	1999	The decrease in perfusion pressure observed with bradykinin was potentiated by captopril and was significantly attenuated in the presence of HOE-140, the B(2)-receptor antagonist, or by pretreatment with an inhibitor of nitric oxide synthase, but not by an inhibitor of cyclooxygenase.	Captopril	79-88	kininogen 1	Homo sapiens	49-59
10444513-7	1999	It is concluded that endothelium-dependent vasodilation can be demonstrated with histamine and bradykinin in the fetoplacental vessels, and at least for bradykinin, this is partly mediated by release of nitric oxide.	Nitric Oxide	203-215	kininogen 1	Homo sapiens	153-163
10536676-11	1999	Endothelium-dependent relaxations to serotonin and to the alpha 2-adrenergic agonist UK14304 (which both activate receptors coupled to Gi-proteins) and to sodium fluoride (a direct activator of G-proteins) were decreased 30 days after transplantation, while those to the calcium ionophore, A23187, and bradykinin were shifted to the right and those to ADP were normal.	Brimonidine Tartrate	85-92	kininogen 1	Homo sapiens	302-312
10536676-11	1999	Endothelium-dependent relaxations to serotonin and to the alpha 2-adrenergic agonist UK14304 (which both activate receptors coupled to Gi-proteins) and to sodium fluoride (a direct activator of G-proteins) were decreased 30 days after transplantation, while those to the calcium ionophore, A23187, and bradykinin were shifted to the right and those to ADP were normal.	Sodium Fluoride	155-170	kininogen 1	Homo sapiens	302-312
10439510-1	1999	Hydrogen/deuterium (H/D) exchange chemistry monitored by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry is used to study solution phase conformational changes of bradykinin, alpha-melanocyte stimulating hormone, and melittin as water is added to methanol-d4, acetonitrile, and isopropanol-d8 solutions.	Hydrogen	0-8	kininogen 1	Homo sapiens	204-214
10439510-1	1999	Hydrogen/deuterium (H/D) exchange chemistry monitored by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry is used to study solution phase conformational changes of bradykinin, alpha-melanocyte stimulating hormone, and melittin as water is added to methanol-d4, acetonitrile, and isopropanol-d8 solutions.	Deuterium	9-18	kininogen 1	Homo sapiens	204-214
10439510-1	1999	Hydrogen/deuterium (H/D) exchange chemistry monitored by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry is used to study solution phase conformational changes of bradykinin, alpha-melanocyte stimulating hormone, and melittin as water is added to methanol-d4, acetonitrile, and isopropanol-d8 solutions.	Water	270-275	kininogen 1	Homo sapiens	204-214
10439510-1	1999	Hydrogen/deuterium (H/D) exchange chemistry monitored by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry is used to study solution phase conformational changes of bradykinin, alpha-melanocyte stimulating hormone, and melittin as water is added to methanol-d4, acetonitrile, and isopropanol-d8 solutions.	Methanol-d4	288-299	kininogen 1	Homo sapiens	204-214
10439510-1	1999	Hydrogen/deuterium (H/D) exchange chemistry monitored by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry is used to study solution phase conformational changes of bradykinin, alpha-melanocyte stimulating hormone, and melittin as water is added to methanol-d4, acetonitrile, and isopropanol-d8 solutions.	acetonitrile	301-313	kininogen 1	Homo sapiens	204-214
10439510-1	1999	Hydrogen/deuterium (H/D) exchange chemistry monitored by matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry is used to study solution phase conformational changes of bradykinin, alpha-melanocyte stimulating hormone, and melittin as water is added to methanol-d4, acetonitrile, and isopropanol-d8 solutions.	2-Propanol-d8	319-333	kininogen 1	Homo sapiens	204-214
10499558-8	1999	Beyond inhibiting the renin-angiotensin system, angiotensin-converting enzyme (ACE) inhibitors diminish the inactivation of bradykinin, thus leading to an augmentation of nitric oxide release.	Nitric Oxide	171-183	kininogen 1	Homo sapiens	124-134
10478565-3	1999	A low concentration of progesterone (1 nM), with no effects of its own, shifted the relaxation curves of bradykinin and calcium ionophore A23187 to the right while not affecting those of sodium nitroprusside and levcromakalim.	Progesterone	23-35	kininogen 1	Homo sapiens	105-115
10478565-4	1999	The negative influence that 1 nM progesterone exerted on bradykinin- and A23187-mediated relaxation was diminished when 1 nM 17beta-estradiol was concomitantly added to the bathing medium.	Estradiol	125-141	kininogen 1	Homo sapiens	57-67
10411851-0	1999	Role of bradykinin in the vasodilator effects of losartan and enalapril in patients with heart failure.	Losartan	49-57	kininogen 1	Homo sapiens	8-18
10411851-0	1999	Role of bradykinin in the vasodilator effects of losartan and enalapril in patients with heart failure.	Enalapril	62-71	kininogen 1	Homo sapiens	8-18
10411851-5	1999	Bradykinin caused profound vasodilatation after enalapril (peak, 357+/-67%) and less after losartan (peak, 230+/-46%).	Enalapril	48-57	kininogen 1	Homo sapiens	0-10
10411851-5	1999	Bradykinin caused profound vasodilatation after enalapril (peak, 357+/-67%) and less after losartan (peak, 230+/-46%).	Losartan	91-99	kininogen 1	Homo sapiens	0-10
10411851-7	1999	Similarly, this was despite the finding that Hoe-140 significantly reduced vasodilatation to bradykinin after enalapril (peak, 192+/-35%) and losartan (peak, 66+/-13%).	Enalapril	110-119	kininogen 1	Homo sapiens	93-103
10404842-8	1999	Enalaprilat did not alter femoral vascular tone at rest or vasodilation with sodium nitroprusside, but potentiated bradykinin-mediated vasodilation in patients (p&lt;0.001) and controls (p = 0.02).	Enalaprilat	0-11	kininogen 1	Homo sapiens	115-125
10404842-10	1999	L-NMMA inhibited the potentiation by enalaprilat of acetylcholine and bradykinin responses.	N(G)-monomethylarginine acetate	0-6	kininogen 1	Homo sapiens	70-80
10498858-8	1999	Indomethacin (a cyclo-oxygenase inhibitor) completely and ONO-3708 (a TXA2/prostaglandin H2 receptor antagonist) partially inhibited BK-induced contraction, whereas OKY-046 (a TXA2 synthase inhibitor) and nordihydroguaiaretic acid (a lipoxygenase inhibitor) did not.	ONO 3708	58-66	kininogen 1	Homo sapiens	133-135
10498858-10	1999	In the presence of L-NA, the contractile response to BK was inhibited by indomethacin or ONO-3708 and was competitively antagonized by [Thi5,8, D-Phe7]-BK (pA2=7.50).	Indomethacin	73-85	kininogen 1	Homo sapiens	53-55
10498858-10	1999	In the presence of L-NA, the contractile response to BK was inhibited by indomethacin or ONO-3708 and was competitively antagonized by [Thi5,8, D-Phe7]-BK (pA2=7.50).	ONO 3708	89-97	kininogen 1	Homo sapiens	53-55
10498858-11	1999	In the presence of indomethacin, the relaxant response to BK was inhibited by L-NA and was competitively antagonized by [Thi5,8, D-Phe7]-BK (pA2=7.59).	Indomethacin	19-31	kininogen 1	Homo sapiens	58-60
10498858-11	1999	In the presence of indomethacin, the relaxant response to BK was inhibited by L-NA and was competitively antagonized by [Thi5,8, D-Phe7]-BK (pA2=7.59).	Indomethacin	19-31	kininogen 1	Homo sapiens	137-139
10596847-0	1999	Increased adsorption of high molecular weight kininogen to heparin-coated artificial surfaces and correlation to hemocompatibility.	Heparin	59-66	kininogen 1	Homo sapiens	24-55
10596847-6	1999	However, high amounts of HMWK were only found on the heparin-bonded surfaces.	Heparin	53-60	kininogen 1	Homo sapiens	25-29
10596847-8	1999	We presume that adsorption of HMWK to heparin-coated surfaces contributes to the improved hemocompatibility of these bondings.	Heparin	38-45	kininogen 1	Homo sapiens	30-34
10596858-2	1999	In this model, bradykinin (BK) increases the release of arachidonic acid (AA), the precursor of labor-promoting prostaglandins.	Arachidonic Acid	56-72	kininogen 1	Homo sapiens	15-25
10596858-2	1999	In this model, bradykinin (BK) increases the release of arachidonic acid (AA), the precursor of labor-promoting prostaglandins.	Arachidonic Acid	56-72	kininogen 1	Homo sapiens	27-29
10596858-2	1999	In this model, bradykinin (BK) increases the release of arachidonic acid (AA), the precursor of labor-promoting prostaglandins.	Prostaglandins	112-126	kininogen 1	Homo sapiens	15-25
10596858-2	1999	In this model, bradykinin (BK) increases the release of arachidonic acid (AA), the precursor of labor-promoting prostaglandins.	Prostaglandins	112-126	kininogen 1	Homo sapiens	27-29
10381803-6	1999	Pretreatment with either tetraethylammonium (360 micromol/kg) or 4-aminopyridine (4-AP; 1 micromol/kg) did not alter the effects of phenylephrine or bradykinin in control animals, but prevented SNP-induced changes in responsiveness to phenylephrine or bradykinin.	Tetraethylammonium	25-43	kininogen 1	Homo sapiens	252-262
10400014-0	1999	Effect of acetylsalicylate on cardiac and muscular pain induced by intracoronary and intra-arterial infusion of bradykinin in humans.	Aspirin	10-26	kininogen 1	Homo sapiens	112-122
10400014-1	1999	OBJECTIVES: This study assessed the algesic activity of bradykinin (BK) in humans and the effects of acetylsalicylate on muscular and cardiac BK-induced pain.	Aspirin	101-117	kininogen 1	Homo sapiens	142-144
10400014-13	1999	The BK-induced pain is abolished or reduced by acetylsalicylate, thus suggesting that acetylsalicylate-sensitive mediators, such as prostaglandins, are involved in its pathogenesis.	Aspirin	47-63	kininogen 1	Homo sapiens	4-6
10400014-13	1999	The BK-induced pain is abolished or reduced by acetylsalicylate, thus suggesting that acetylsalicylate-sensitive mediators, such as prostaglandins, are involved in its pathogenesis.	Aspirin	86-102	kininogen 1	Homo sapiens	4-6
10400014-13	1999	The BK-induced pain is abolished or reduced by acetylsalicylate, thus suggesting that acetylsalicylate-sensitive mediators, such as prostaglandins, are involved in its pathogenesis.	Prostaglandins	132-146	kininogen 1	Homo sapiens	4-6
10384200-4	1999	The endothelium-derived hyperpolarizing factor-mediated relaxation to bradykinin was studied when endothelium-derived nitric oxide and prostaglandin I2 were inhibited with the presence of 7 micromol/L indomethacin and 300 micromol/L NG-nitro-L -arginine.	Nitric Oxide	118-130	kininogen 1	Homo sapiens	70-80
10384200-4	1999	The endothelium-derived hyperpolarizing factor-mediated relaxation to bradykinin was studied when endothelium-derived nitric oxide and prostaglandin I2 were inhibited with the presence of 7 micromol/L indomethacin and 300 micromol/L NG-nitro-L -arginine.	Epoprostenol	135-151	kininogen 1	Homo sapiens	70-80
10384200-4	1999	The endothelium-derived hyperpolarizing factor-mediated relaxation to bradykinin was studied when endothelium-derived nitric oxide and prostaglandin I2 were inhibited with the presence of 7 micromol/L indomethacin and 300 micromol/L NG-nitro-L -arginine.	Indomethacin	201-213	kininogen 1	Homo sapiens	70-80
10381803-6	1999	Pretreatment with either tetraethylammonium (360 micromol/kg) or 4-aminopyridine (4-AP; 1 micromol/kg) did not alter the effects of phenylephrine or bradykinin in control animals, but prevented SNP-induced changes in responsiveness to phenylephrine or bradykinin.	4-Aminopyridine	65-80	kininogen 1	Homo sapiens	252-262
10422653-11	1999	However, the combination of 5-HT and BKN (10 nmol) produced: (1) significantly higher VAS scores (P &lt; 0.05) compared with all other combinations; (2) significantly longer pain offset (P &lt; 0.05) compared with the combinations of isotonic saline and BKN; (3) significantly lower PPTs at 5, 20, and 40 min post-infusion (P &lt; 0.05) compared with baseline PPT and PPTs after all other combinations.	Serotonin	28-32	kininogen 1	Homo sapiens	254-257
10422653-11	1999	However, the combination of 5-HT and BKN (10 nmol) produced: (1) significantly higher VAS scores (P &lt; 0.05) compared with all other combinations; (2) significantly longer pain offset (P &lt; 0.05) compared with the combinations of isotonic saline and BKN; (3) significantly lower PPTs at 5, 20, and 40 min post-infusion (P &lt; 0.05) compared with baseline PPT and PPTs after all other combinations.	Sodium Chloride	243-249	kininogen 1	Homo sapiens	37-40
10422653-11	1999	However, the combination of 5-HT and BKN (10 nmol) produced: (1) significantly higher VAS scores (P &lt; 0.05) compared with all other combinations; (2) significantly longer pain offset (P &lt; 0.05) compared with the combinations of isotonic saline and BKN; (3) significantly lower PPTs at 5, 20, and 40 min post-infusion (P &lt; 0.05) compared with baseline PPT and PPTs after all other combinations.	Pyridinium p-toluenesulfonate	283-287	kininogen 1	Homo sapiens	37-40
10422653-11	1999	However, the combination of 5-HT and BKN (10 nmol) produced: (1) significantly higher VAS scores (P &lt; 0.05) compared with all other combinations; (2) significantly longer pain offset (P &lt; 0.05) compared with the combinations of isotonic saline and BKN; (3) significantly lower PPTs at 5, 20, and 40 min post-infusion (P &lt; 0.05) compared with baseline PPT and PPTs after all other combinations.	Pyridinium p-toluenesulfonate	368-372	kininogen 1	Homo sapiens	37-40
10422653-14	1999	Pre-treatment with serotonin may enhance the effect of bradykinin in the generation of muscle pain and muscular hyperalgesia in humans.	Serotonin	19-28	kininogen 1	Homo sapiens	55-65
10422659-10	1999	Moreover, we demonstrated that PLGA/bupivacaine has a prolonged inhibitory effect on the tissue levels of substance P and bradykinin in the inflamed hindpaws.	Bupivacaine	36-47	kininogen 1	Homo sapiens	122-132
10415540-0	1999	Interaction of bradykinin with angiotensin, prostacyclin, and nitric oxide in myocardial preservation.	Epoprostenol	44-56	kininogen 1	Homo sapiens	15-25
10415540-0	1999	Interaction of bradykinin with angiotensin, prostacyclin, and nitric oxide in myocardial preservation.	Nitric Oxide	62-74	kininogen 1	Homo sapiens	15-25
10415540-3	1999	Bradykinin appears to function as a signaling molecule by controlling the release of other intracellular modulators, such as prostacyclins and nitric oxide, which also exert beneficial effects on the ischemic myocardium.	Prostaglandins I	125-138	kininogen 1	Homo sapiens	0-10
10415540-3	1999	Bradykinin appears to function as a signaling molecule by controlling the release of other intracellular modulators, such as prostacyclins and nitric oxide, which also exert beneficial effects on the ischemic myocardium.	Nitric Oxide	143-155	kininogen 1	Homo sapiens	0-10
10377076-0	1999	Human coronary arteriolar dilation to bradykinin depends on membrane hyperpolarization: contribution of nitric oxide and Ca2+-activated K+ channels.	Nitric Oxide	104-116	kininogen 1	Homo sapiens	38-48
10444401-4	1999	In the present study we characterized the signal transduction pathway leading to mitogen-activated protein kinase (MAPK) activation in response to bradykinin (BK) in VSMC.	vsmc	166-170	kininogen 1	Homo sapiens	147-157
10444401-4	1999	In the present study we characterized the signal transduction pathway leading to mitogen-activated protein kinase (MAPK) activation in response to bradykinin (BK) in VSMC.	vsmc	166-170	kininogen 1	Homo sapiens	159-161
10377076-8	1999	In vessels constricted and depolarized (Em; -50+/-3 to -28+/-2 mV) with endothelin-1 (ET), dilation to BK was associated with greater membrane hyperpolarization (-48+/-3 mV at 10(-6) mol/L) than dilation to sodium nitroprusside (SNP) (-34+/-2 mV at 10(-4) mol/L) for similar degrees of dilation.	Nitroprusside	207-227	kininogen 1	Homo sapiens	103-105
10377076-9	1999	Treatment with Nomega-nitro-L-arginine methyl ester (L-NAME; 10(-4) mol/L), an NO synthase inhibitor, partially decreased dilation to BK (maximum dilation 61+/-10% versus control 92+/-4%; P&lt;0.05).	NG-Nitroarginine Methyl Ester	15-51	kininogen 1	Homo sapiens	134-136
10377076-9	1999	Treatment with Nomega-nitro-L-arginine methyl ester (L-NAME; 10(-4) mol/L), an NO synthase inhibitor, partially decreased dilation to BK (maximum dilation 61+/-10% versus control 92+/-4%; P&lt;0.05).	NG-Nitroarginine Methyl Ester	53-59	kininogen 1	Homo sapiens	134-136
10336607-0	1999	Calcium-binding properties and molecular organization of bradykinin A solution 1H-NMR study.	Calcium	0-7	kininogen 1	Homo sapiens	57-67
10750596-8	1999	Bradykinin and SNAP caused dose-dependent reductions in myocardial oxygen consumption (p &lt;0.05).	Oxygen	67-73	kininogen 1	Homo sapiens	0-10
10401557-8	1999	Moreover, rolipram significantly potentiated hyperalgesia induced by carrageenan, bradykinin, TNF alpha, IL-1 beta, IL-6 and IL-8.	Rolipram	10-18	kininogen 1	Homo sapiens	82-92
10401557-15	1999	The ODQ potentiated hyperalgesia induced by carrageenan, bradykinin, TNF alpha, IL-1 beta, IL-6 and IL-8.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	4-7	kininogen 1	Homo sapiens	57-67
10336607-0	1999	Calcium-binding properties and molecular organization of bradykinin A solution 1H-NMR study.	Hydrogen	79-81	kininogen 1	Homo sapiens	57-67
10336607-1	1999	The NMR features of bradykinin were investigated in dimethylsulfoxide containing 1% water.	Dimethyl Sulfoxide	52-69	kininogen 1	Homo sapiens	20-30
10336607-1	1999	The NMR features of bradykinin were investigated in dimethylsulfoxide containing 1% water.	Water	84-89	kininogen 1	Homo sapiens	20-30
10336607-7	1999	In light of conformational changes experienced by the peptide upon interaction with calcium, a role for the metal was hypothesized in the process of conformational selection from the free to the receptor-bound state of bradykinin.	Calcium	84-91	kininogen 1	Homo sapiens	219-229
10336607-7	1999	In light of conformational changes experienced by the peptide upon interaction with calcium, a role for the metal was hypothesized in the process of conformational selection from the free to the receptor-bound state of bradykinin.	Metals	108-113	kininogen 1	Homo sapiens	219-229
10378100-5	1999	For nonciliated HNE cells maintained 4-5 days in culture, ATP (10(-4) M) increased cytosolic Ca2+ in all cells tested, but only 85% of the cells responded to bradykinin (10(-5) M) addition, and 65% to histamine (10(-4) M) stimulation.	Adenosine Triphosphate	58-61	kininogen 1	Homo sapiens	158-168
10412558-7	1999	The participation of BK in this response was investigated in subjects given the BK-potentiating drug captopril prior to food intake.	Captopril	101-110	kininogen 1	Homo sapiens	80-82
10378100-6	1999	In terms of the absolute change of Ca2+i (delta Ca2+i, peak-basal value), the efficacy was ATP &gt; bradykinin &gt; histamine for the 3 HNE cell preparations.	Adenosine Triphosphate	91-94	kininogen 1	Homo sapiens	100-110
10378100-6	1999	In terms of the absolute change of Ca2+i (delta Ca2+i, peak-basal value), the efficacy was ATP &gt; bradykinin &gt; histamine for the 3 HNE cell preparations.	Histamine	116-125	kininogen 1	Homo sapiens	100-110
10392553-7	1999	Diphenylamine-2-carboxylate or 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid, Cl- channel blockers, significantly blocked the I(sc) responses to lys-BK or histamine.	fenamic acid	0-27	kininogen 1	Homo sapiens	152-154
10392553-7	1999	Diphenylamine-2-carboxylate or 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid, Cl- channel blockers, significantly blocked the I(sc) responses to lys-BK or histamine.	4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid	31-79	kininogen 1	Homo sapiens	152-154
10392553-10	1999	1,2-Bis-(2-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid-acetoxymethyl ester, a calcium chelator, greatly reduced the increase in the I(sc) responses to lys-BK or histamine.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	0-77	kininogen 1	Homo sapiens	158-160
10367598-0	1999	Nitric oxide decreases microvascular permeability in bradykinin stimulated and nonstimulated conditions.	Nitric Oxide	0-12	kininogen 1	Homo sapiens	53-63
10359890-8	1999	RESULTS: Eicosanoid output was largely confined to prostaglandins with values of 5 +/- 2 and 82 +/- 35 ng PGE2/10(6) cells for basal- and BK stimulation, respectively (n = 8).	Eicosanoids	9-19	kininogen 1	Homo sapiens	138-140
10359890-9	1999	All 3 corticosteroids inhibited basal- and BK-induced PGE2 output in a dose- and time-dependent manner.	Dinoprostone	54-58	kininogen 1	Homo sapiens	43-45
10370087-3	1999	In T84 cells grown on impermeable supports, BK stimulated a transient increase in [Ca2+]i as assessed by fura-2 ratio imaging.	Fura-2	105-111	kininogen 1	Homo sapiens	44-46
10350623-8	1999	In the presence of 25 microM mergetpa, an inhibitor of kininase I, the increase in bradykinin concentration from 10-12 to 10-10 M promoted similar inhibition of the Na+-ATPase activity of both cortex homogenates and basolateral membrane preparations.	2-mercaptomethyl-3-guanidinoethylthiopropionic acid	29-37	kininogen 1	Homo sapiens	83-93
10397075-0	1999	The role of nitric oxide in bradykinin-induced dilation of coronary resistance vessels in patients with hypercholesterolemia.	Nitric Oxide	12-24	kininogen 1	Homo sapiens	28-38
10397075-10	1999	Bradykinin-induced dilation was similar in hypercholesterolemic patients and control patients after inhibition of nitric oxide.	Nitric Oxide	114-126	kininogen 1	Homo sapiens	0-10
10397075-11	1999	CONCLUSION: These results suggest that the bradykinin-mediated endothelium-dependent dilation of coronary resistance vessels may be impaired due to depressed nitric oxide production in patients with hypercholesterolemia.	Nitric Oxide	158-170	kininogen 1	Homo sapiens	43-53
10403610-2	1999	DESIGN: We synthesized internally quenched fluorogenic bradykinin-related peptides introducing Abz (ortho-aminobenzoic acid) and EDDnp (N-[2,4-dinitrophenyl]-ethylenediamine) at their N- and C-terminal groups, respectively, and these were assayed as ACE substrates.	ortho-Aminobenzoates	100-123	kininogen 1	Homo sapiens	55-65
10403610-2	1999	DESIGN: We synthesized internally quenched fluorogenic bradykinin-related peptides introducing Abz (ortho-aminobenzoic acid) and EDDnp (N-[2,4-dinitrophenyl]-ethylenediamine) at their N- and C-terminal groups, respectively, and these were assayed as ACE substrates.	n1-(2,4-dinitrophenyl)ethane-1,2-diamine	129-134	kininogen 1	Homo sapiens	55-65
10403610-2	1999	DESIGN: We synthesized internally quenched fluorogenic bradykinin-related peptides introducing Abz (ortho-aminobenzoic acid) and EDDnp (N-[2,4-dinitrophenyl]-ethylenediamine) at their N- and C-terminal groups, respectively, and these were assayed as ACE substrates.	N-(2,4-dinitrophenyl)ethylenediamine	136-173	kininogen 1	Homo sapiens	55-65
10370087-13	1999	When, however, the monolayers were pre-stimulated by forskolin (1 microM), BK further enhanced Cl-secretion (DeltaIsc=21+/-5 microA/cm2, n=10) transiently and biphasically.	Colforsin	53-62	kininogen 1	Homo sapiens	75-77
10370087-14	1999	In conclusion, BK enhances cyclic adenosine monophosphate-stimulated Cl- secretion in T84 cells, probably via basolateral, Ca2+-liganded activation of low-conductance hSK4-type K+ channels.	Cyclic AMP	27-57	kininogen 1	Homo sapiens	15-17
10212257-0	1999	Bradykinin-induced internalization of the human B2 receptor requires phosphorylation of three serine and two threonine residues at its carboxyl tail.	Serine	94-100	kininogen 1	Homo sapiens	0-10
10361449-3	1999	On the other hand, ACEIs can increase bradykinin, and thus, nitric oxide, which may cause potent cardioprotection.	Nitric Oxide	60-72	kininogen 1	Homo sapiens	38-48
10212257-0	1999	Bradykinin-induced internalization of the human B2 receptor requires phosphorylation of three serine and two threonine residues at its carboxyl tail.	Threonine	109-118	kininogen 1	Homo sapiens	0-10
10199886-7	1999	Proinflammatory mediators reduced the synthesis of EDHF assessed as hyperpolarization of vascular smooth muscle cells elicited by the effluent from bradykinin-stimulated coronary arteries.	edhf	51-55	kininogen 1	Homo sapiens	148-158
10187765-4	1999	Pre-treatment with the PI 3-kinase-specific inhibitors, wortmannin, and LY294002 effectively blocked BK-induced PI 3-kinase activity.	Wortmannin	56-66	kininogen 1	Homo sapiens	101-103
10187765-4	1999	Pre-treatment with the PI 3-kinase-specific inhibitors, wortmannin, and LY294002 effectively blocked BK-induced PI 3-kinase activity.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	72-80	kininogen 1	Homo sapiens	101-103
10187765-5	1999	Wortmannin and LY294002 also abolished BK-induced NF-kappaB activation, as did transient transfection with a dominant negative mutant of the p85 subunit.	Wortmannin	0-10	kininogen 1	Homo sapiens	39-41
10187765-5	1999	Wortmannin and LY294002 also abolished BK-induced NF-kappaB activation, as did transient transfection with a dominant negative mutant of the p85 subunit.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	15-23	kininogen 1	Homo sapiens	39-41
10198354-4	1999	Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect.	Carbachol	0-9	kininogen 1	Homo sapiens	265-275
10209009-4	1999	Effects of bradykinin and ramiprilat on intracellular signaling were determined by monitoring the activation of the extracellularly regulated kinases Erk1 and Erk2 as well as [Ca2+]i increases in fura 2-loaded endothelial cells.	Fura-2	196-202	kininogen 1	Homo sapiens	11-21
10209009-8	1999	Ramiprilat also decreased [3H]bradykinin binding to CR membranes when applied either before or after bradykinin stimulation.	ramiprilat	0-10	kininogen 1	Homo sapiens	30-40
10209009-8	1999	Ramiprilat also decreased [3H]bradykinin binding to CR membranes when applied either before or after bradykinin stimulation.	ramiprilat	0-10	kininogen 1	Homo sapiens	101-111
10209009-8	1999	Ramiprilat also decreased [3H]bradykinin binding to CR membranes when applied either before or after bradykinin stimulation.	Tritium	27-29	kininogen 1	Homo sapiens	30-40
10209009-8	1999	Ramiprilat also decreased [3H]bradykinin binding to CR membranes when applied either before or after bradykinin stimulation.	Chromium	52-54	kininogen 1	Homo sapiens	30-40
10209009-9	1999	Moreover, ramiprilat resulted in reactivation of the B2 receptor in bradykinin-stimulated cells and induced a second peak in [Ca2+]i and reactivation of Erk1/2.	ramiprilat	10-20	kininogen 1	Homo sapiens	68-78
10199815-1	1999	The effect of chronic exposure to transforming growth factor-alpha (TGF-alpha) on bradykinin-stimulated acute prostanoid production and ion secretion in monolayers of HCA-7 colony 29 colonic epithelial cells has been studied.	Prostaglandins	110-120	kininogen 1	Homo sapiens	82-92
10199815-4	1999	min-1 over 24 h. Bradykinin (10(-8)-10(-5) M) dose dependently increased acute PGE2 release by three orders of magnitude.	Dinoprostone	79-83	kininogen 1	Homo sapiens	17-27
10199815-10	1999	Priming with PGE2 (10(-8)-10(-6) M) over 24 h mimicked the effect of TGF-alpha on bradykinin-induced changes in cAMP and SCC.	Dinoprostone	13-17	kininogen 1	Homo sapiens	82-92
10199815-10	1999	Priming with PGE2 (10(-8)-10(-6) M) over 24 h mimicked the effect of TGF-alpha on bradykinin-induced changes in cAMP and SCC.	Cyclic AMP	112-116	kininogen 1	Homo sapiens	82-92
10199815-11	1999	These data suggest that enhanced chronic release of prostaglandins in response to stimulation with TGF-alpha may downregulate acute responses to bradykinin.	Prostaglandins	52-66	kininogen 1	Homo sapiens	145-155
10323587-5	1999	This study examined the effects of differentiating SH-SY5Y cells on muscarinic- and bradykinin-receptor-mediated phosphoinositide and Ca2+ signalling.	Phosphatidylinositols	113-129	kininogen 1	Homo sapiens	84-94
10323587-9	1999	Bradykinin receptor-mediated Ins(1,4,5)P3 signalling was also potentiated following differentiation.	Inositol 1,4,5-Trisphosphate	29-41	kininogen 1	Homo sapiens	0-10
10323587-10	1999	Determination of agonist-evoked accumulation of [3H]-inositol phosphates under lithium-block demonstrated these changes reflected enhanced phospholipase C activity which is consistent with observed increases in the expression of muscarinic and bradykinin receptors.	[3h]-inositol phosphates	48-72	kininogen 1	Homo sapiens	244-254
10323587-10	1999	Determination of agonist-evoked accumulation of [3H]-inositol phosphates under lithium-block demonstrated these changes reflected enhanced phospholipase C activity which is consistent with observed increases in the expression of muscarinic and bradykinin receptors.	Lithium	79-86	kininogen 1	Homo sapiens	244-254
10412158-6	1999	It appears that the tone of brain microvessels is controlled towards dilation by cholinergic innervation originating from the nucleus basalis of Meynert, glutamatergic or GABAergic mediated GABAA receptor, and by a mediator such as NO, bradykinin, PGs.	Phosphatidylglycerols	248-251	kininogen 1	Homo sapiens	236-246
10066772-10	1999	Biotin-HK specifically bound to rCK128 and rCK131 in the presence of Zn2+ but not to Deleted1-6rCK131.	Biotin	0-6	kininogen 1	Homo sapiens	7-9
10066772-10	1999	Biotin-HK specifically bound to rCK128 and rCK131 in the presence of Zn2+ but not to Deleted1-6rCK131.	Zinc	69-73	kininogen 1	Homo sapiens	7-9
10066772-11	1999	Recombinant CK128 and rCK131 also inhibited biotin-HK binding to HUVEC with IC50 of 0.4 and 0.5 microM, respectively.	Biotin	44-50	kininogen 1	Homo sapiens	51-53
10066772-16	1999	A sequence scrambled peptide of PGG15 did not block binding to HUVEC and biotin-GPV20 specifically bound to HK.	Biotin	73-79	kininogen 1	Homo sapiens	108-110
10066772-18	1999	However, inhibition of PK activation by peptide PGG15 occurred at 10-fold lower concentration (IC50 = 1 microM) than inhibition of biotin-HK binding to HUVEC (IC50 = 10 microM).	Biotin	131-137	kininogen 1	Homo sapiens	138-140
10066772-19	1999	These studies indicate that HK binds to a region of 20 amino acids coded by exon 1 on CK1 which is carboxyl-terminal to its glycine-rich amino-terminal globular domain.	Glycine	124-131	kininogen 1	Homo sapiens	28-30
10403610-2	1999	DESIGN: We synthesized internally quenched fluorogenic bradykinin-related peptides introducing Abz (ortho-aminobenzoic acid) and EDDnp (N-[2,4-dinitrophenyl]-ethylenediamine) at their N- and C-terminal groups, respectively, and these were assayed as ACE substrates.	ortho-Aminobenzoates	95-98	kininogen 1	Homo sapiens	55-65
10435013-8	1999	CONCLUSION: In ITA relaxations to carbachol and bradykinin were mediated via nitric oxide.	Nitric Oxide	77-89	kininogen 1	Homo sapiens	48-58
10202208-3	1999	After local tissue injury, the release of chemical mediators such as potassium ions, ATP, bradykinin and prostaglandin E2 directly activate nerve endings and indirectly trigger the release of algesic mediators such as histamine, 5-hydroxytryptamine and nerve growth factor from other cells, which, in turn, stimulate proximal afferent nerve endings and silent nociceptors.	Histamine	218-227	kininogen 1	Homo sapiens	90-100
10202208-3	1999	After local tissue injury, the release of chemical mediators such as potassium ions, ATP, bradykinin and prostaglandin E2 directly activate nerve endings and indirectly trigger the release of algesic mediators such as histamine, 5-hydroxytryptamine and nerve growth factor from other cells, which, in turn, stimulate proximal afferent nerve endings and silent nociceptors.	Serotonin	229-248	kininogen 1	Homo sapiens	90-100
10096262-1	1999	OBJECTIVE: In arteries and veins smoking is associated with impaired nitric oxide-mediated relaxation to endothelium-dependent agonists such as bradykinin.	Nitric Oxide	69-81	kininogen 1	Homo sapiens	144-154
10096262-2	1999	We investigated whether acute local angiotensin-converting enzyme (ACE) inhibition, achieved by enalaprilat, could influence bradykinin-induced vasodilation in veins of smokers.	Enalaprilat	96-107	kininogen 1	Homo sapiens	125-135
10082496-3	1999	Administration of bradykinin or its ACE-resistant analogue desensitized the receptor, but it was resensitized (arachidonic acid release or [Ca2+]i mobilization) by agents such as enalaprilat (1 micromol/L).	Arachidonic Acid	111-127	kininogen 1	Homo sapiens	18-28
10082496-3	1999	Administration of bradykinin or its ACE-resistant analogue desensitized the receptor, but it was resensitized (arachidonic acid release or [Ca2+]i mobilization) by agents such as enalaprilat (1 micromol/L).	Enalaprilat	179-190	kininogen 1	Homo sapiens	18-28
10082496-6	1999	Enalaprilat resensitized the receptor via ACE to release arachidonic acid by bradykinin at a lower concentration (5 nmol/L) than required to mobilize [Ca2+]i (1 micromol/L).	Enalaprilat	0-11	kininogen 1	Homo sapiens	77-87
10082496-6	1999	Enalaprilat resensitized the receptor via ACE to release arachidonic acid by bradykinin at a lower concentration (5 nmol/L) than required to mobilize [Ca2+]i (1 micromol/L).	Arachidonic Acid	57-73	kininogen 1	Homo sapiens	77-87
10080484-7	1999	RESULTS: Enalaprilat did not alter either resting coronary vascular tone or dilation with sodium nitroprusside, but potentiated BK-mediated dilation.	Enalaprilat	9-20	kininogen 1	Homo sapiens	128-130
10027827-0	1999	Bradykinin promotes ischemic norepinephrine release in guinea pig and human hearts.	Norepinephrine	29-43	kininogen 1	Homo sapiens	0-10
10027827-1	1999	We previously reported that bradykinin (BK; 1-1000 nM) facilitates norepinephrine (NE) release from cardiac sympathetic nerves.	Norepinephrine	67-81	kininogen 1	Homo sapiens	28-38
10027827-1	1999	We previously reported that bradykinin (BK; 1-1000 nM) facilitates norepinephrine (NE) release from cardiac sympathetic nerves.	Norepinephrine	67-81	kininogen 1	Homo sapiens	40-42
10027827-8	1999	In contrast, when kininase I and II inhibitors (DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid and enalaprilat, each 1 microM) were used to prevent the degradation of endogenous BK, NE overflow and reperfusion arrhythmias were enhanced.	2-mercaptomethyl-3-guanidinoethylthiopropionic acid	48-102	kininogen 1	Homo sapiens	186-188
10027827-8	1999	In contrast, when kininase I and II inhibitors (DL-2-mercaptomethyl-3-guanidinoethylthiopropanoic acid and enalaprilat, each 1 microM) were used to prevent the degradation of endogenous BK, NE overflow and reperfusion arrhythmias were enhanced.	Enalaprilat	107-118	kininogen 1	Homo sapiens	186-188
10027847-7	1999	In addition, we show that the release of PGE2 stimulated by either bradykinin, A23187, or arachidonic acid was inhibited by the phospholipase A2 inhibitor arachidonate trifluoromethyl ketone.	Dinoprostone	41-45	kininogen 1	Homo sapiens	67-77
10027847-7	1999	In addition, we show that the release of PGE2 stimulated by either bradykinin, A23187, or arachidonic acid was inhibited by the phospholipase A2 inhibitor arachidonate trifluoromethyl ketone.	arachidonate trifluoromethyl ketone	155-190	kininogen 1	Homo sapiens	67-77
10198354-4	1999	Carbachol and endothelin-1 increased GTP-bound p21(ras) in a pertussis toxin-sensitive manner [ratio of [32P]GTP to ([32P]GTP + [32P]GDP): control, 30 +/- 1.7; 3 min of 1 microM carbachol, 39 +/- 1.1; 3 min of 1 microM endothelin-1, 40 +/- 1.2], whereas histamine, bradykinin, and KCl were without effect.	Guanosine Triphosphate	37-40	kininogen 1	Homo sapiens	265-275
9933251-7	1999	DEX alone (10(-8) mol/L for 48 hours) caused a 93% fall in basal PGI2 production, and bradykinin- and A23187-stimulated PGI2 were diminished 96% and 94%, respectively.	Epoprostenol	120-124	kininogen 1	Homo sapiens	86-96
9918895-9	1999	Endothelial function assessed using the endothelium-dependent agonists acetylcholine and bradykinin showed a significantly impaired relaxation response to acetylcholine but not to bradykinin in the ischaemic vessels, and acetylcholine-induced relaxation was not improved after incubation with indomethacin.	Acetylcholine	155-168	kininogen 1	Homo sapiens	89-99
9918895-9	1999	Endothelial function assessed using the endothelium-dependent agonists acetylcholine and bradykinin showed a significantly impaired relaxation response to acetylcholine but not to bradykinin in the ischaemic vessels, and acetylcholine-induced relaxation was not improved after incubation with indomethacin.	Acetylcholine	155-168	kininogen 1	Homo sapiens	89-99
9918895-9	1999	Endothelial function assessed using the endothelium-dependent agonists acetylcholine and bradykinin showed a significantly impaired relaxation response to acetylcholine but not to bradykinin in the ischaemic vessels, and acetylcholine-induced relaxation was not improved after incubation with indomethacin.	Indomethacin	293-305	kininogen 1	Homo sapiens	89-99
10102747-3	1999	These potentiated effects of captopril and bradykinin were suppressed by Hoe-140, a kinin B2 receptor antagonist, or by concomitant addition of N(G)-nitro arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, and aspirin, a cyclooxygenase inhibitor.	NG-Nitroarginine Methyl Ester	144-176	kininogen 1	Homo sapiens	43-53
10102747-3	1999	These potentiated effects of captopril and bradykinin were suppressed by Hoe-140, a kinin B2 receptor antagonist, or by concomitant addition of N(G)-nitro arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, and aspirin, a cyclooxygenase inhibitor.	NG-Nitroarginine Methyl Ester	178-184	kininogen 1	Homo sapiens	43-53
10102747-3	1999	These potentiated effects of captopril and bradykinin were suppressed by Hoe-140, a kinin B2 receptor antagonist, or by concomitant addition of N(G)-nitro arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, and aspirin, a cyclooxygenase inhibitor.	Aspirin	226-233	kininogen 1	Homo sapiens	43-53
10102747-4	1999	It appears that captopril potentiates chorda tympani-induced salivation through endogenously accumulated bradykinin, which acts on kinin B2 receptors, mediating production of nitric oxide and cyclooxygenase products.	Captopril	16-25	kininogen 1	Homo sapiens	105-115
10102747-4	1999	It appears that captopril potentiates chorda tympani-induced salivation through endogenously accumulated bradykinin, which acts on kinin B2 receptors, mediating production of nitric oxide and cyclooxygenase products.	Nitric Oxide	175-187	kininogen 1	Homo sapiens	105-115
9973312-4	1999	Thus, only after intravenous injection of bradykinin or exogenous arachidonic acid was a marked increase in prostanoid formation seen.	Prostaglandins	108-118	kininogen 1	Homo sapiens	42-52
10188626-1	1999	The elevation of intracellular [Ca2+] induced by bradykinin (Bk) was monitored with fura-2 fluorescence in human skin fibroblasts.	Fura-2	84-90	kininogen 1	Homo sapiens	49-59
10093057-4	1999	The NO synthase inhibitor L-NAME attenuated the reduction observed in fibronectin and collagen mRNA levels in response to bradykinin.	NG-Nitroarginine Methyl Ester	26-32	kininogen 1	Homo sapiens	122-132
10093057-5	1999	The NO donor DETA NONOate (100 microM) mimicked the effects of bradykinin on ECM mRNA levels.	2,2'-(hydroxynitrosohydrazono)bis-ethanamine	13-25	kininogen 1	Homo sapiens	63-73
10093057-7	1999	Bradykinin stimulated intracellular cGMP accumulation 73.7 +/- 10.3% after 10 min of treatment.	Cyclic GMP	36-40	kininogen 1	Homo sapiens	0-10
10093057-9	1999	These data indicate that bradykinin downregulates ECM protein production in cardiac fibroblasts and suggest that NO and the related signaling molecule cGMP may play an important role in mediating this response.	Cyclic GMP	151-155	kininogen 1	Homo sapiens	25-35
10093213-0	1999	Conformations of protonated gas-phase bradykinin ions: evidence for intramolecular hydrogen bonding.	Hydrogen	83-91	kininogen 1	Homo sapiens	38-48
10093213-2	1999	Fragment ions corresponding to the elimination of H2O and HN=C=NH are observed in the product ion mass spectra of Lys1-bradykinin and des-Arg1-bradykinin but not in the spectra of bradykinin or des-Arg9-bradykinin.	Water	50-53	kininogen 1	Homo sapiens	119-129
10093213-2	1999	Fragment ions corresponding to the elimination of H2O and HN=C=NH are observed in the product ion mass spectra of Lys1-bradykinin and des-Arg1-bradykinin but not in the spectra of bradykinin or des-Arg9-bradykinin.	Water	50-53	kininogen 1	Homo sapiens	143-153
10093213-2	1999	Fragment ions corresponding to the elimination of H2O and HN=C=NH are observed in the product ion mass spectra of Lys1-bradykinin and des-Arg1-bradykinin but not in the spectra of bradykinin or des-Arg9-bradykinin.	Water	50-53	kininogen 1	Homo sapiens	143-153
10093213-2	1999	Fragment ions corresponding to the elimination of H2O and HN=C=NH are observed in the product ion mass spectra of Lys1-bradykinin and des-Arg1-bradykinin but not in the spectra of bradykinin or des-Arg9-bradykinin.	Water	50-53	kininogen 1	Homo sapiens	143-153
10093213-5	1999	The strongest intramolecular interaction appears to be a proton bridge between the guanidino groups of the N- and C-terminal arginines in bradykinin.	guanidino	83-92	kininogen 1	Homo sapiens	138-148
10093213-5	1999	The strongest intramolecular interaction appears to be a proton bridge between the guanidino groups of the N- and C-terminal arginines in bradykinin.	Arginine	125-134	kininogen 1	Homo sapiens	138-148
10408151-0	1999	Possible role of bradykinin on stimulus-secretion coupling in adrenal chromaffin cells.	chromaffin	70-80	kininogen 1	Homo sapiens	17-27
10408151-3	1999	In this article, the role of bradykinin on catecholamine biosynthesis, secretion and Ca2+ movement in adrenal chromaffin cells as a model for catecholamine-containing neurons are examined.	Catecholamines	43-56	kininogen 1	Homo sapiens	29-39
10408151-6	1999	Bradykinin increases the influx of Ca2+ and the turnover of phosphoinositide through the stimulation of bradykinin B2 receptor.	Phosphatidylinositols	60-76	kininogen 1	Homo sapiens	0-10
10408151-6	1999	Bradykinin increases the influx of Ca2+ and the turnover of phosphoinositide through the stimulation of bradykinin B2 receptor.	Phosphatidylinositols	60-76	kininogen 1	Homo sapiens	104-114
10408151-12	1999	It is interesting that bradykinin, which stimulates the biosynthesis and secretion of catecholamine in adrenal chromaffin cells, plays a role in the termination of calcium-signal transduction through the stimulation of Ca2+ efflux from the cells.	Catecholamines	86-99	kininogen 1	Homo sapiens	23-33
10408151-12	1999	It is interesting that bradykinin, which stimulates the biosynthesis and secretion of catecholamine in adrenal chromaffin cells, plays a role in the termination of calcium-signal transduction through the stimulation of Ca2+ efflux from the cells.	chromaffin	111-121	kininogen 1	Homo sapiens	23-33
10408151-12	1999	It is interesting that bradykinin, which stimulates the biosynthesis and secretion of catecholamine in adrenal chromaffin cells, plays a role in the termination of calcium-signal transduction through the stimulation of Ca2+ efflux from the cells.	Calcium	164-171	kininogen 1	Homo sapiens	23-33
10191623-10	1999	In allergic patients, captopril enhanced BK-induced vascular permeability, but not glandular secretion.	Captopril	22-31	kininogen 1	Homo sapiens	41-43
10883320-1	1999	Vasopressin and bradykinin are two of the most important peptides in regulating vascular tone, water, and ionic balance in the body, and thus they play a key role in controlling blood pressure.	Water	95-100	kininogen 1	Homo sapiens	16-26
10073745-5	1999	L-NMMA inhibited relaxation to bradykinin by 64% (P=0.014) but did not influence relaxation induced by isoprenaline.	omega-N-Methylarginine	0-6	kininogen 1	Homo sapiens	31-41
10464000-7	1999	The addition of L-NMMA significantly, but only partially, reduced the relaxation to bradykinin in the presence of indomethacin (p = 0.03).	omega-N-Methylarginine	16-22	kininogen 1	Homo sapiens	84-94
10464000-7	1999	The addition of L-NMMA significantly, but only partially, reduced the relaxation to bradykinin in the presence of indomethacin (p = 0.03).	Indomethacin	114-126	kininogen 1	Homo sapiens	84-94
27093744-8	1999	The mechanism involved in the decrease of IOP and blood pressure with captopril could be due to inhibition in the formation of angiotensin-II and sparing of bradykinin.	Captopril	70-79	kininogen 1	Homo sapiens	157-167
10082496-10	1999	Enalaprilat potentiated the bradykinin effect in cells expressing a mutant ACE with a single N-domain active site.	Enalaprilat	0-11	kininogen 1	Homo sapiens	28-38
10803488-1	1999	Angiotensin-converting enzyme inhibitors (ACEI) block degradation of bradykinin, and bradykinin stimulates prostacyclin synthesis.	Epoprostenol	107-119	kininogen 1	Homo sapiens	85-95
9951431-5	1999	Enalaprilat and captopril increased the sensitivity to bradykinin, decreasing the dose producing half-maximal response (ED50) of bradykinin 18-fold and 5-fold, respectively, without changing the maximal venodilatory response.	Enalaprilat	0-11	kininogen 1	Homo sapiens	55-65
9951431-5	1999	Enalaprilat and captopril increased the sensitivity to bradykinin, decreasing the dose producing half-maximal response (ED50) of bradykinin 18-fold and 5-fold, respectively, without changing the maximal venodilatory response.	Enalaprilat	0-11	kininogen 1	Homo sapiens	129-139
9951431-5	1999	Enalaprilat and captopril increased the sensitivity to bradykinin, decreasing the dose producing half-maximal response (ED50) of bradykinin 18-fold and 5-fold, respectively, without changing the maximal venodilatory response.	Captopril	16-25	kininogen 1	Homo sapiens	55-65
9951431-5	1999	Enalaprilat and captopril increased the sensitivity to bradykinin, decreasing the dose producing half-maximal response (ED50) of bradykinin 18-fold and 5-fold, respectively, without changing the maximal venodilatory response.	Captopril	16-25	kininogen 1	Homo sapiens	129-139
9887113-2	1999	PA rings exposed to BK resulted in contraction in the GBS group and a decrease in resting tension in the Control group (P = 0.034) at a concentration of 10(-5) M. GBS-treated PA rings contracted more to des-Arg9-BK than did Controls (P &lt; 0.001).	gbs	54-57	kininogen 1	Homo sapiens	20-22
9887113-2	1999	PA rings exposed to BK resulted in contraction in the GBS group and a decrease in resting tension in the Control group (P = 0.034) at a concentration of 10(-5) M. GBS-treated PA rings contracted more to des-Arg9-BK than did Controls (P &lt; 0.001).	gbs	163-166	kininogen 1	Homo sapiens	20-22
9887113-3	1999	BK (10(-6) M) relaxed preconstricted PA rings incubated in GBS less than BK relaxed Controls (P &lt; 0.001), and preincubation with L-NAME decreased relaxation in both.	gbs	59-62	kininogen 1	Homo sapiens	0-2
9887113-3	1999	BK (10(-6) M) relaxed preconstricted PA rings incubated in GBS less than BK relaxed Controls (P &lt; 0.001), and preincubation with L-NAME decreased relaxation in both.	NG-Nitroarginine Methyl Ester	132-138	kininogen 1	Homo sapiens	0-2
9887113-3	1999	BK (10(-6) M) relaxed preconstricted PA rings incubated in GBS less than BK relaxed Controls (P &lt; 0.001), and preincubation with L-NAME decreased relaxation in both.	NG-Nitroarginine Methyl Ester	132-138	kininogen 1	Homo sapiens	73-75
9887113-4	1999	These results suggest that GBS decreased endothelium-dependent BK relaxation and increased contractile response to des-Arg9-BK.	gbs	27-30	kininogen 1	Homo sapiens	63-65
10458510-5	1999	Preincubation of the sera with an ACE inhibitor (enalaprilat) significantly increased the t1/2 of both BK and des-Arg9-BK in both groups.	Enalaprilat	49-60	kininogen 1	Homo sapiens	103-105
10458510-5	1999	Preincubation of the sera with an ACE inhibitor (enalaprilat) significantly increased the t1/2 of both BK and des-Arg9-BK in both groups.	Enalaprilat	49-60	kininogen 1	Homo sapiens	119-121
10458510-6	1999	There was no significant difference between the groups with respect to the t1/2 of BK, but there was a significantly greater increase (3.8-fold) in the t1/2 of des-Arg9-BK in HSR+ patients compared to HSR-subjects.	des-arg9	160-168	kininogen 1	Homo sapiens	169-171
10188626-1	1999	The elevation of intracellular [Ca2+] induced by bradykinin (Bk) was monitored with fura-2 fluorescence in human skin fibroblasts.	Fura-2	84-90	kininogen 1	Homo sapiens	61-63
10390859-4	1999	For bradykinin and kemptide, a significant mobility difference between protonated and sodiated species (where sodium replaced a proton in singly and doubly charged peptides) was demonstrated.	Sodium	110-116	kininogen 1	Homo sapiens	4-14
9893159-4	1999	Ca2+ store depletion by thapsigargin, endothelin-1, or bradykinin activated calcium entry pathways.	Calcium	76-83	kininogen 1	Homo sapiens	55-65
10632476-4	1999	In cultured decidua-derived cells, bradykinin stimulates the release of arachidonic acid, interleukin-6 (IL-6), and interleukin-8 (IL-8).	Arachidonic Acid	72-88	kininogen 1	Homo sapiens	35-45
10458523-3	1999	Acylation of the amino-terminus of bradykinin (BK) and a B2a-selective antagonist produced ligands derivatized with biotinamidocaproate or 7-Amino-4-methylcoumarin-3-acetate.	biotinamidocaproate	116-135	kininogen 1	Homo sapiens	35-45
10458523-3	1999	Acylation of the amino-terminus of bradykinin (BK) and a B2a-selective antagonist produced ligands derivatized with biotinamidocaproate or 7-Amino-4-methylcoumarin-3-acetate.	biotinamidocaproate	116-135	kininogen 1	Homo sapiens	47-49
10458523-3	1999	Acylation of the amino-terminus of bradykinin (BK) and a B2a-selective antagonist produced ligands derivatized with biotinamidocaproate or 7-Amino-4-methylcoumarin-3-acetate.	7-amino-4-methylcoumarin-3-acetic acid	139-173	kininogen 1	Homo sapiens	35-45
10458523-3	1999	Acylation of the amino-terminus of bradykinin (BK) and a B2a-selective antagonist produced ligands derivatized with biotinamidocaproate or 7-Amino-4-methylcoumarin-3-acetate.	7-amino-4-methylcoumarin-3-acetic acid	139-173	kininogen 1	Homo sapiens	47-49
10216428-4	1999	LPS (100 ng/ml, for 3 to 6 h) or IL-1 beta potentiated bradykinin and the tachykinin NK-1 selective receptor agonist [Sar9, Met-O2] SP -induced human isolated bronchi contraction in vitro (IL-1 beta 3 10(-10) M, at 37 degrees C for 1 to 3 h for bradykinin or at 21 degrees C for 15 h for [Sar9, Met-O2] SP in Krebs-Henseleit solution).	TFF2 protein, human	132-134	kininogen 1	Homo sapiens	245-255
10216428-4	1999	LPS (100 ng/ml, for 3 to 6 h) or IL-1 beta potentiated bradykinin and the tachykinin NK-1 selective receptor agonist [Sar9, Met-O2] SP -induced human isolated bronchi contraction in vitro (IL-1 beta 3 10(-10) M, at 37 degrees C for 1 to 3 h for bradykinin or at 21 degrees C for 15 h for [Sar9, Met-O2] SP in Krebs-Henseleit solution).	TFF2 protein, human	303-305	kininogen 1	Homo sapiens	55-65
10216428-4	1999	LPS (100 ng/ml, for 3 to 6 h) or IL-1 beta potentiated bradykinin and the tachykinin NK-1 selective receptor agonist [Sar9, Met-O2] SP -induced human isolated bronchi contraction in vitro (IL-1 beta 3 10(-10) M, at 37 degrees C for 1 to 3 h for bradykinin or at 21 degrees C for 15 h for [Sar9, Met-O2] SP in Krebs-Henseleit solution).	krebs	309-314	kininogen 1	Homo sapiens	55-65
10216428-5	1999	As in control bronchi, the effects of bradykinin and of [Sar9, Met-O2] SP after interleukin 1 beta pre-treatment were abolished by indomethacin (10(-6) M), the thromboxane A2 receptor antagonist GR 32191 suggesting that prostanoids remain involved under these experimental conditions.	Indomethacin	131-143	kininogen 1	Homo sapiens	38-48
10216428-5	1999	As in control bronchi, the effects of bradykinin and of [Sar9, Met-O2] SP after interleukin 1 beta pre-treatment were abolished by indomethacin (10(-6) M), the thromboxane A2 receptor antagonist GR 32191 suggesting that prostanoids remain involved under these experimental conditions.	Prostaglandins	220-231	kininogen 1	Homo sapiens	38-48
10216428-9	1999	Bradykinin-induced release of 6 keto prostaglandin F1 alpha (the stable metabolite of prostaglandin I2) was not enhanced by IL-1 beta.	6-Ketoprostaglandin F1 alpha	30-59	kininogen 1	Homo sapiens	0-10
10216428-9	1999	Bradykinin-induced release of 6 keto prostaglandin F1 alpha (the stable metabolite of prostaglandin I2) was not enhanced by IL-1 beta.	Epoprostenol	86-102	kininogen 1	Homo sapiens	0-10
9837936-9	1998	Importantly, the pattern of BK-activated arachidonate release differed markedly in the mutant receptors.	Arachidonic Acid	41-53	kininogen 1	Homo sapiens	28-30
10390859-4	1999	For bradykinin and kemptide, a significant mobility difference between protonated and sodiated species (where sodium replaced a proton in singly and doubly charged peptides) was demonstrated.	Peptides	164-172	kininogen 1	Homo sapiens	4-14
9865533-0	1998	17Beta-estradiol acutely improves endothelium-dependent relaxation to bradykinin in isolated human coronary arteries.	Estradiol	0-16	kininogen 1	Homo sapiens	70-80
9877481-6	1998	In the presence of GR 32191 (10(-6) M), bradykinin induced a prostanoid dependent relaxation that was not significantly modified by IL-1beta pretreatment.	Prostaglandins	61-71	kininogen 1	Homo sapiens	40-50
9877481-7	1998	Determination of prostanoids in the organ bath fluid showed that bradykinin induced TxB2, the stable metabolite of TxA2, and 6-keto prostaglandin F1alpha, the stable metabolite of PGI2, release.	Prostaglandins	17-28	kininogen 1	Homo sapiens	65-75
9877481-7	1998	Determination of prostanoids in the organ bath fluid showed that bradykinin induced TxB2, the stable metabolite of TxA2, and 6-keto prostaglandin F1alpha, the stable metabolite of PGI2, release.	6-Ketoprostaglandin F1 alpha	125-153	kininogen 1	Homo sapiens	65-75
9877481-7	1998	Determination of prostanoids in the organ bath fluid showed that bradykinin induced TxB2, the stable metabolite of TxA2, and 6-keto prostaglandin F1alpha, the stable metabolite of PGI2, release.	Epoprostenol	180-184	kininogen 1	Homo sapiens	65-75
9877481-9	1998	Taken together our results suggest that interleukin-1beta (1-3 h)-induced potentiation of the effect of bradykinin is linked to an increased activity of thromboxane synthase and, in turn, to increased thromboxane synthesis.	Thromboxanes	153-164	kininogen 1	Homo sapiens	104-114
9893038-7	1998	Phorbol 12-myristate 13-acetate pretreatment diminished the ability of BK to stimulate IL-8 production.	Tetradecanoylphorbol Acetate	0-31	kininogen 1	Homo sapiens	71-73
9893038-8	1998	In addition, GF109203X, a selective protein kinase C inhibitor, blocked BK-induced IL-8 production.	bisindolylmaleimide I	13-22	kininogen 1	Homo sapiens	72-74
9822674-3	1998	Both BK-induced stimulation of DNA synthesis and activation of MAPK in response to BK were abolished by two different inhibitors of phosphatidylinositol 3-kinase (PI3K), wortmannin and LY 294002, as well as by two different inhibitors of protein kinase C (PKC), bisindolylmaleimide and Ro 31-8220.	Wortmannin	170-180	kininogen 1	Homo sapiens	5-7
9822674-3	1998	Both BK-induced stimulation of DNA synthesis and activation of MAPK in response to BK were abolished by two different inhibitors of phosphatidylinositol 3-kinase (PI3K), wortmannin and LY 294002, as well as by two different inhibitors of protein kinase C (PKC), bisindolylmaleimide and Ro 31-8220.	Wortmannin	170-180	kininogen 1	Homo sapiens	83-85
9822674-3	1998	Both BK-induced stimulation of DNA synthesis and activation of MAPK in response to BK were abolished by two different inhibitors of phosphatidylinositol 3-kinase (PI3K), wortmannin and LY 294002, as well as by two different inhibitors of protein kinase C (PKC), bisindolylmaleimide and Ro 31-8220.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	185-194	kininogen 1	Homo sapiens	5-7
9822674-3	1998	Both BK-induced stimulation of DNA synthesis and activation of MAPK in response to BK were abolished by two different inhibitors of phosphatidylinositol 3-kinase (PI3K), wortmannin and LY 294002, as well as by two different inhibitors of protein kinase C (PKC), bisindolylmaleimide and Ro 31-8220.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	185-194	kininogen 1	Homo sapiens	83-85
9822674-3	1998	Both BK-induced stimulation of DNA synthesis and activation of MAPK in response to BK were abolished by two different inhibitors of phosphatidylinositol 3-kinase (PI3K), wortmannin and LY 294002, as well as by two different inhibitors of protein kinase C (PKC), bisindolylmaleimide and Ro 31-8220.	bisindolylmaleimide	262-281	kininogen 1	Homo sapiens	5-7
9822674-3	1998	Both BK-induced stimulation of DNA synthesis and activation of MAPK in response to BK were abolished by two different inhibitors of phosphatidylinositol 3-kinase (PI3K), wortmannin and LY 294002, as well as by two different inhibitors of protein kinase C (PKC), bisindolylmaleimide and Ro 31-8220.	bisindolylmaleimide	262-281	kininogen 1	Homo sapiens	83-85
9822674-4	1998	Stimulation of SW-480 cells by BK led to increased formation of PI3K lipid products (phosphatidylinositol 3,4,5-trisphosphate and phosphatidylinositol 3, 4-bisphosphate) and to enhanced translocation of the PKCepsilon isoform from the cytosol to the membrane.	phosphatidylinositol 3,4,5-triphosphate	85-125	kininogen 1	Homo sapiens	31-33
9822674-4	1998	Stimulation of SW-480 cells by BK led to increased formation of PI3K lipid products (phosphatidylinositol 3,4,5-trisphosphate and phosphatidylinositol 3, 4-bisphosphate) and to enhanced translocation of the PKCepsilon isoform from the cytosol to the membrane.	phosphatidylinositol 3,4-diphosphate	130-168	kininogen 1	Homo sapiens	31-33
9822674-5	1998	Both effects of BK were inhibited by wortmannin, too.	Wortmannin	37-47	kininogen 1	Homo sapiens	16-18
9865533-4	1998	Incubation with 17beta-estradiol enhanced relaxations to bradykinin (from 43 +/- 6 to 83 +/- 3%, P &lt; 0.0001) but not those to nitroglycerine (n.s.).	Estradiol	16-32	kininogen 1	Homo sapiens	57-67
9865533-2	1998	In isolated human coronary arteries, we investigated whether 17beta-estradiol affects endothelium-dependent responses to bradykinin, an endothelium-derived vasodilator locally produced by endothelial cells.	Estradiol	61-77	kininogen 1	Homo sapiens	121-131
9814974-1	1998	In cultured porcine aortic smooth muscle cells, sphingosylphosphorylcholine (SPC), ATP, or bradykinin (BK) induced a rapid dose-dependent increase in the cytosolic Ca2+ concentration ([Ca2+]i) and also stimulated inositol 1,4,5-trisphosphate (IP3) generation.	sphingosine phosphorylcholine	48-75	kininogen 1	Homo sapiens	103-105
9814974-1	1998	In cultured porcine aortic smooth muscle cells, sphingosylphosphorylcholine (SPC), ATP, or bradykinin (BK) induced a rapid dose-dependent increase in the cytosolic Ca2+ concentration ([Ca2+]i) and also stimulated inositol 1,4,5-trisphosphate (IP3) generation.	1,4,5-trisphosphate	222-241	kininogen 1	Homo sapiens	91-101
9814974-1	1998	In cultured porcine aortic smooth muscle cells, sphingosylphosphorylcholine (SPC), ATP, or bradykinin (BK) induced a rapid dose-dependent increase in the cytosolic Ca2+ concentration ([Ca2+]i) and also stimulated inositol 1,4,5-trisphosphate (IP3) generation.	1,4,5-trisphosphate	222-241	kininogen 1	Homo sapiens	103-105
9814974-1	1998	In cultured porcine aortic smooth muscle cells, sphingosylphosphorylcholine (SPC), ATP, or bradykinin (BK) induced a rapid dose-dependent increase in the cytosolic Ca2+ concentration ([Ca2+]i) and also stimulated inositol 1,4,5-trisphosphate (IP3) generation.	Inositol 1,4,5-Trisphosphate	243-246	kininogen 1	Homo sapiens	91-101
9814974-1	1998	In cultured porcine aortic smooth muscle cells, sphingosylphosphorylcholine (SPC), ATP, or bradykinin (BK) induced a rapid dose-dependent increase in the cytosolic Ca2+ concentration ([Ca2+]i) and also stimulated inositol 1,4,5-trisphosphate (IP3) generation.	Inositol 1,4,5-Trisphosphate	243-246	kininogen 1	Homo sapiens	103-105
9823712-1	1998	Ion abundances in the MALDI TOF mass spectra of the model peptides (bradykinin, alpha-melanocyte stimulating hormone, and melittin) change significantly as water is added to the solution used for dried droplet sample preparation.	Water	156-161	kininogen 1	Homo sapiens	68-78
9890715-2	1998	There is general agreement that the initial contact phase in the coagulation pathway may be activated by a negatively charged surface such as dextran sulfate cellulose, resulting in the generation of bradykinin.	dextran sulfate cellulose	142-167	kininogen 1	Homo sapiens	200-210
10227759-7	1998	We speculate that bradykinin could be responsible for the hypotension occurring in patients during tryptophan column immunoabsorption therapy and that the metabolism of bradykinin could be caused by the decreased activity of CPR.	Tryptophan	99-109	kininogen 1	Homo sapiens	18-28
9860207-7	1998	After 240 min PGI-2 production was stimulated by 10 microM bradykinin.	Epoprostenol	14-19	kininogen 1	Homo sapiens	59-69
10227752-1	1998	The negative charges of dextran sulfate (DS) used for low-density lipoprotein (LDL) apheresis activate the intrinsic coagulation pathway, accompanied by the production of bradykinin.	Dextran Sulfate	24-39	kininogen 1	Homo sapiens	171-181
10227752-1	1998	The negative charges of dextran sulfate (DS) used for low-density lipoprotein (LDL) apheresis activate the intrinsic coagulation pathway, accompanied by the production of bradykinin.	Dextran Sulfate	41-43	kininogen 1	Homo sapiens	171-181
9765266-7	1998	The bradykinin-induced internalization of eNOS is completely abrogated by the intracellular Ca2+ chelator BAPTA; conversely, Ca2+-mobilizing drugs and agonists promote eNOS translocation.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	106-111	kininogen 1	Homo sapiens	4-14
10227752-3	1998	Previously, we showed the rise in plasma levels of prostaglandins and nitric oxide derivatives accompanied by the rise in bradykinin levels.	Prostaglandins	51-65	kininogen 1	Homo sapiens	122-132
10227752-3	1998	Previously, we showed the rise in plasma levels of prostaglandins and nitric oxide derivatives accompanied by the rise in bradykinin levels.	Nitric Oxide	70-82	kininogen 1	Homo sapiens	122-132
10227759-0	1998	Elevated bradykinin and decreased carboxypeptidase R as a cause of hypotension during tryptophan column immunoabsorption therapy.	Tryptophan	86-96	kininogen 1	Homo sapiens	9-19
10227759-3	1998	In regards to this shock state, it has been reported that plasma bradykinin levels increase during tryptophan column immunoabsorption therapy.	Tryptophan	99-109	kininogen 1	Homo sapiens	65-75
9800827-4	1998	Endothelium-derived hyperpolarizing factor-mediated relaxation (percentage of 30 nmol/L U46619 precontraction) was induced by calcium ionophore A23187 and bradykinin in the presence of indomethacin (7 micromol/L) and Nomega-nitro-L-arginine (300 micromol/L).	Indomethacin	185-197	kininogen 1	Homo sapiens	155-165
9822888-3	1998	The anti-inflammatory steroid, dexamethasone, produced a rightward shift of the concentration-response curve to des-Arg9-bradykinin, without affecting the maximal response.	Steroids	22-29	kininogen 1	Homo sapiens	121-131
9822888-3	1998	The anti-inflammatory steroid, dexamethasone, produced a rightward shift of the concentration-response curve to des-Arg9-bradykinin, without affecting the maximal response.	Dexamethasone	31-44	kininogen 1	Homo sapiens	121-131
9822888-3	1998	The anti-inflammatory steroid, dexamethasone, produced a rightward shift of the concentration-response curve to des-Arg9-bradykinin, without affecting the maximal response.	des-arg9	112-120	kininogen 1	Homo sapiens	121-131
9822888-8	1998	The inhibitory effect of dexamethasone and the potentiating actions of lipopolysaccharide and exogenous human recombinant interleukin-1 beta on des-Arg9-bradykinin-mediated responses, suggest the possible role of interleukin-1 beta in the bradykinin B1 receptor up-regulation phenomenon in human umbilical vein.	Dexamethasone	25-38	kininogen 1	Homo sapiens	153-163
9781934-5	1998	When the experiment was performed in the presence of 10 microM indomethacin and 30 microM N(G)-nitro-L-arginine (L-NNA), which block the generation of prostaglandin I2 (PGI2) and NO, respectively, K(Ca) channel activity was stimulated by bradykinin, indicating the direct involvement of EDHF in K(Ca) channel stimulation.	Indomethacin	63-75	kininogen 1	Homo sapiens	238-248
9781934-5	1998	When the experiment was performed in the presence of 10 microM indomethacin and 30 microM N(G)-nitro-L-arginine (L-NNA), which block the generation of prostaglandin I2 (PGI2) and NO, respectively, K(Ca) channel activity was stimulated by bradykinin, indicating the direct involvement of EDHF in K(Ca) channel stimulation.	Nitroarginine	90-111	kininogen 1	Homo sapiens	238-248
9781934-5	1998	When the experiment was performed in the presence of 10 microM indomethacin and 30 microM N(G)-nitro-L-arginine (L-NNA), which block the generation of prostaglandin I2 (PGI2) and NO, respectively, K(Ca) channel activity was stimulated by bradykinin, indicating the direct involvement of EDHF in K(Ca) channel stimulation.	Nitroarginine	113-118	kininogen 1	Homo sapiens	238-248
9781934-5	1998	When the experiment was performed in the presence of 10 microM indomethacin and 30 microM N(G)-nitro-L-arginine (L-NNA), which block the generation of prostaglandin I2 (PGI2) and NO, respectively, K(Ca) channel activity was stimulated by bradykinin, indicating the direct involvement of EDHF in K(Ca) channel stimulation.	Epoprostenol	169-173	kininogen 1	Homo sapiens	238-248
9781934-8	1998	However, in the presence of 0.5 mM guanosine triphosphate (GTP) and 1.0 mM adenosine triphosphate (ATP) in the bath solution, K(Ca) channels was activated by bradykinin.	Guanosine Triphosphate	35-57	kininogen 1	Homo sapiens	158-168
9781934-8	1998	However, in the presence of 0.5 mM guanosine triphosphate (GTP) and 1.0 mM adenosine triphosphate (ATP) in the bath solution, K(Ca) channels was activated by bradykinin.	Guanosine Triphosphate	59-62	kininogen 1	Homo sapiens	158-168
9781934-8	1998	However, in the presence of 0.5 mM guanosine triphosphate (GTP) and 1.0 mM adenosine triphosphate (ATP) in the bath solution, K(Ca) channels was activated by bradykinin.	Adenosine Triphosphate	75-97	kininogen 1	Homo sapiens	158-168
9781934-8	1998	However, in the presence of 0.5 mM guanosine triphosphate (GTP) and 1.0 mM adenosine triphosphate (ATP) in the bath solution, K(Ca) channels was activated by bradykinin.	Adenosine Triphosphate	99-102	kininogen 1	Homo sapiens	158-168
9781934-9	1998	In outside-out patches, the addition of bradykinin also increased K(Ca) channel activity, when GTP and ATP were added to the pipette solution.	Guanosine Triphosphate	95-98	kininogen 1	Homo sapiens	40-50
9781934-9	1998	In outside-out patches, the addition of bradykinin also increased K(Ca) channel activity, when GTP and ATP were added to the pipette solution.	Adenosine Triphosphate	103-106	kininogen 1	Homo sapiens	40-50
9781934-10	1998	The addition of GDP-beta-S (100 microM) in the cytosolic solution completely blocked the activation K(Ca) channels induced by bradykinin in inside-out and outside-out patches.	guanosine 5'-O-(2-thiodiphosphate)	16-26	kininogen 1	Homo sapiens	126-136
9781934-13	1998	These results suggest that EDHF, released from endothelial cells in response to bradykinin, hyperpolarizes smooth muscle cells by opening K(Ca) channels.	edhf	27-31	kininogen 1	Homo sapiens	80-90
9784925-10	1998	The endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation to A23187, bradykinin, and substance P in arteries contracted by either U46619 (10 nmol/L) or K+ (25 mmol/L) was reduced after exposure to either high K+ or UW solution, but was maximally preserved after exposure to aprikalim.	endothelium-derived hyperpolarizing factor	4-46	kininogen 1	Homo sapiens	85-95
9784925-10	1998	The endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation to A23187, bradykinin, and substance P in arteries contracted by either U46619 (10 nmol/L) or K+ (25 mmol/L) was reduced after exposure to either high K+ or UW solution, but was maximally preserved after exposure to aprikalim.	edhf	48-52	kininogen 1	Homo sapiens	85-95
9766316-7	1998	After bradykinin treatment, there was minimal change in delivery of methotrexate or dextran 70 to tumor and brain around tumor, with the greatest increase less than 60% over controls.	Methotrexate	68-80	kininogen 1	Homo sapiens	6-16
9724311-6	1998	Coinfusion of L-arginine (0.33 mg/min) markedly improved the bradykinin-induced venodilation in smokers (52 +/- 7 to 90 +/- 9%; P &lt; 0.01).	Arginine	14-24	kininogen 1	Homo sapiens	61-71
9743237-6	1998	Increased Ca2+ release in response to bradykinin in XO/HX-pretreated cells might be due to enhanced formation of inositol-1,4,5-trisphosphate (+140%).	Inositol 1,4,5-Trisphosphate	113-141	kininogen 1	Homo sapiens	38-48
9876291-4	1998	Although in some cases the action of bradykinin is entirely mediated by the endothelial release of nitric oxide (NO) and/or prostacyclin (PGI2), a large amount of evidence has been accumulated during the last 10 years indicating that a non-NO/PGI2 factor accounts for bradykinin-induced vasodilation in a wide variety of perfused vascular beds and isolated small arteries from several species including humans.	Nitric Oxide	99-111	kininogen 1	Homo sapiens	37-47
9876291-4	1998	Although in some cases the action of bradykinin is entirely mediated by the endothelial release of nitric oxide (NO) and/or prostacyclin (PGI2), a large amount of evidence has been accumulated during the last 10 years indicating that a non-NO/PGI2 factor accounts for bradykinin-induced vasodilation in a wide variety of perfused vascular beds and isolated small arteries from several species including humans.	Epoprostenol	124-136	kininogen 1	Homo sapiens	37-47
9876291-4	1998	Although in some cases the action of bradykinin is entirely mediated by the endothelial release of nitric oxide (NO) and/or prostacyclin (PGI2), a large amount of evidence has been accumulated during the last 10 years indicating that a non-NO/PGI2 factor accounts for bradykinin-induced vasodilation in a wide variety of perfused vascular beds and isolated small arteries from several species including humans.	Epoprostenol	138-142	kininogen 1	Homo sapiens	37-47
9876291-4	1998	Although in some cases the action of bradykinin is entirely mediated by the endothelial release of nitric oxide (NO) and/or prostacyclin (PGI2), a large amount of evidence has been accumulated during the last 10 years indicating that a non-NO/PGI2 factor accounts for bradykinin-induced vasodilation in a wide variety of perfused vascular beds and isolated small arteries from several species including humans.	Epoprostenol	243-247	kininogen 1	Homo sapiens	37-47
9762778-9	1998	In subjects with mild-to-moderate asthma, airway responsiveness to bradykinin is more strongly associated with the magnitude of eosinophilic inflammation in the airways than methacholine.	Methacholine Chloride	174-186	kininogen 1	Homo sapiens	67-77
9725250-9	1998	The nonselective COX inhibitor indomethacin and the selective COX-2 inhibitor NS-398 strongly inhibited BK-stimulated PGE2 and IL-8 production.	Indomethacin	31-43	kininogen 1	Homo sapiens	104-106
9725250-9	1998	The nonselective COX inhibitor indomethacin and the selective COX-2 inhibitor NS-398 strongly inhibited BK-stimulated PGE2 and IL-8 production.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	78-84	kininogen 1	Homo sapiens	104-106
9725250-9	1998	The nonselective COX inhibitor indomethacin and the selective COX-2 inhibitor NS-398 strongly inhibited BK-stimulated PGE2 and IL-8 production.	Dinoprostone	118-122	kininogen 1	Homo sapiens	104-106
9725250-11	1998	Both the BK- and arachidonic acid-induced IL-8 production was inhibited by the protein synthesis inhibitors cycloheximide and actinomycin D and by the steroid dexamethasone.	Cycloheximide	108-121	kininogen 1	Homo sapiens	9-11
9725250-11	1998	Both the BK- and arachidonic acid-induced IL-8 production was inhibited by the protein synthesis inhibitors cycloheximide and actinomycin D and by the steroid dexamethasone.	Dactinomycin	126-139	kininogen 1	Homo sapiens	9-11
9725250-11	1998	Both the BK- and arachidonic acid-induced IL-8 production was inhibited by the protein synthesis inhibitors cycloheximide and actinomycin D and by the steroid dexamethasone.	Steroids	151-158	kininogen 1	Homo sapiens	9-11
9725250-11	1998	Both the BK- and arachidonic acid-induced IL-8 production was inhibited by the protein synthesis inhibitors cycloheximide and actinomycin D and by the steroid dexamethasone.	Dexamethasone	159-172	kininogen 1	Homo sapiens	9-11
9725250-13	1998	BK-induced IL-8 release was mimicked by the BK B2 receptor agonist (Tyr(Me)8)-BK and was potently inhibited by the selective B2 receptor antagonist HOE-140.	tyr(me)8	68-76	kininogen 1	Homo sapiens	0-2
9725250-13	1998	BK-induced IL-8 release was mimicked by the BK B2 receptor agonist (Tyr(Me)8)-BK and was potently inhibited by the selective B2 receptor antagonist HOE-140.	tyr(me)8	68-76	kininogen 1	Homo sapiens	44-46
9725250-13	1998	BK-induced IL-8 release was mimicked by the BK B2 receptor agonist (Tyr(Me)8)-BK and was potently inhibited by the selective B2 receptor antagonist HOE-140.	4-hydroxy-2-octenal	148-151	kininogen 1	Homo sapiens	0-2
9725250-14	1998	These results suggest that human ASM can be a source of IL-8 and also that endogenous prostanoids, involving both COX-1 and COX-2, have a novel role in mediating BK-induced IL-8 production.	Prostaglandins	86-97	kininogen 1	Homo sapiens	162-164
9785759-4	1998	In this vascular bed the ACh sensitive path cannot be triggered by bradykinin (BK).	Acetylcholine	25-28	kininogen 1	Homo sapiens	79-81
9713849-0	1998	Nitric oxide and cyclic GMP attenuate sensitivity of the blood-tumor barrier permeability to bradykinin.	Nitric Oxide	0-12	kininogen 1	Homo sapiens	93-103
9712847-2	1998	We report here that depletion of cellular cholesterol leads to the inhibition of epidermal growth factor- and bradykinin-stimulated PtdIns turnover in A431 cells.	Cholesterol	42-53	kininogen 1	Homo sapiens	110-120
9712847-2	1998	We report here that depletion of cellular cholesterol leads to the inhibition of epidermal growth factor- and bradykinin-stimulated PtdIns turnover in A431 cells.	Phosphatidylinositols	132-138	kininogen 1	Homo sapiens	110-120
9761428-1	1998	In Swiss 3T3 fibroblasts, changing the culture medium prior to stimulation resulted in an augmentation of bradykinin-induced prostaglandin E2 synthesis.	Dinoprostone	125-141	kininogen 1	Homo sapiens	106-116
9761428-3	1998	The medium change slightly augmented the bradykinin-induced increase in intracellular free Ca2+ concentration and phosphoinositide hydrolysis with a different time course from that for prostaglandin E2 synthesis.	Phosphatidylinositols	114-130	kininogen 1	Homo sapiens	41-51
9761428-3	1998	The medium change slightly augmented the bradykinin-induced increase in intracellular free Ca2+ concentration and phosphoinositide hydrolysis with a different time course from that for prostaglandin E2 synthesis.	Dinoprostone	185-201	kininogen 1	Homo sapiens	41-51
9700093-0	1998	Impaired cAMP production in human airway smooth muscle cells by bradykinin: role of cyclooxygenase products.	Cyclic AMP	9-13	kininogen 1	Homo sapiens	64-74
9700093-2	1998	We investigated if bradykinin (BK) could cause a similar effect and the role of cyclooxygenase (COX) products in this event, since we have recently reported that BK, like IL-1beta, also causes COX-2 induction and prostanoid release in human ASM cells.	Prostaglandins	213-223	kininogen 1	Homo sapiens	162-164
9765948-0	1998	Effects of sphingosine 1-phosphate and bradykinin on phospholipid signalling in human epithelial A549 cells.	Phospholipids	53-65	kininogen 1	Homo sapiens	39-49
9713849-0	1998	Nitric oxide and cyclic GMP attenuate sensitivity of the blood-tumor barrier permeability to bradykinin.	Cyclic GMP	17-27	kininogen 1	Homo sapiens	93-103
9713849-1	1998	Intracarotid infusion of bradykinin and its analogue, RMP-7, selectively increase the permeability of brain tumor capillaries though the nitrix oxide (NO) and cyclic GMP pathway.	nitrix oxide	137-149	kininogen 1	Homo sapiens	25-35
9713849-1	1998	Intracarotid infusion of bradykinin and its analogue, RMP-7, selectively increase the permeability of brain tumor capillaries though the nitrix oxide (NO) and cyclic GMP pathway.	Cyclic GMP	159-169	kininogen 1	Homo sapiens	25-35
9713849-7	1998	At 30 min of bradykinin infusion, BTB permeability was significantly lower compared to 15 min of bradykinin infusion (3.79 +/- 0.99 vs. 16.20 +/- 3.43 microliters g-1 min-1, p &lt; 0.001).	btb	34-37	kininogen 1	Homo sapiens	13-23
9713849-8	1998	Pretreatment with an NO donor significantly decreased BTB permeability in bradykinin infused rats (5.09 +/- 2.61 vs. 13.51 +/- 4.19 microliters g-1 min-1, p &lt; 0.001), as did pretreatment with a cyclic GMP analogue (4.48 +/- 0.95 vs. 12.31 +/- 3.90 microliters g-1 min-1, p &lt; 0.001).	btb	54-57	kininogen 1	Homo sapiens	74-84
9713849-10	1998	Increased tumor permeability by bradykinin appears to be regulated by NO and cyclic GMP which are second messengers involved in the bradykinin B2 receptor mediated cascade.	Cyclic GMP	77-87	kininogen 1	Homo sapiens	32-42
9713849-10	1998	Increased tumor permeability by bradykinin appears to be regulated by NO and cyclic GMP which are second messengers involved in the bradykinin B2 receptor mediated cascade.	Cyclic GMP	77-87	kininogen 1	Homo sapiens	132-142
9719163-0	1998	Bradykinin stimulates the intracellular calcium activity in human mesothelial cells.	Calcium	40-47	kininogen 1	Homo sapiens	0-10
9719163-1	1998	AIM: The aim of this study was to investigate the influence of bradykinin on the intracellular calcium activity ([Ca2+]i) in human mesothelial cells in culture.	Calcium	95-102	kininogen 1	Homo sapiens	63-73
9719163-5	1998	Flufenamate (&gt; or = 10 micromol/l), an inhibitor of non-selective ion channels abolished the bradykinin-mediated increase of [Ca2+], whereas the L-type Ca2+ channel blocker nicardipine (10 micromol/l) had no effect (n = 3-5).	Flufenamic Acid	0-11	kininogen 1	Homo sapiens	96-106
9719163-6	1998	The [Ca2+]i response to bradykinin was inhibited by the BK2 antagonist Hoe 140 (IC50 +/- k7 nmol/l, n = 30).	4-hydroxy-2-octenal	71-74	kininogen 1	Homo sapiens	24-34
9726641-1	1998	We studied the effect of the glucocorticoids, dexamethasone and budesonide, on the interleukin-1beta-induced increase of bradykinin B2 receptors in cultured human bronchial smooth muscle cells, a cellular model of bronchial hyperreactivity.	Dexamethasone	46-59	kininogen 1	Homo sapiens	121-131
9726641-1	1998	We studied the effect of the glucocorticoids, dexamethasone and budesonide, on the interleukin-1beta-induced increase of bradykinin B2 receptors in cultured human bronchial smooth muscle cells, a cellular model of bronchial hyperreactivity.	Budesonide	64-74	kininogen 1	Homo sapiens	121-131
9726641-2	1998	Both compounds prevented the increase of the bradykinin B2 mRNA and the bradykinin-induced inositol phosphate accumulation.	Inositol Phosphates	91-109	kininogen 1	Homo sapiens	72-82
9707267-5	1998	ACE inhibition of kininase II inhibits the breakdown of bradykinin, a direct stimulant of nitric oxide release from the intact endothelial cell.	Nitric Oxide	90-102	kininogen 1	Homo sapiens	56-66
9816408-8	1998	Epsilon-aminocaproic acid and tranexamic acid inhibit the formation of plasmin and fragments of the Hageman factor, thus inhibiting kallikrein and bradykinin production.	Aminocaproic Acid	0-25	kininogen 1	Homo sapiens	147-157
9816408-8	1998	Epsilon-aminocaproic acid and tranexamic acid inhibit the formation of plasmin and fragments of the Hageman factor, thus inhibiting kallikrein and bradykinin production.	Tranexamic Acid	30-45	kininogen 1	Homo sapiens	147-157
9688841-0	1998	Extracellular ATP and bradykinin increase cGMP in vascular endothelial cells via activation of PKC.	Cyclic GMP	42-46	kininogen 1	Homo sapiens	22-32
9688841-1	1998	Vasodilation by agents such as bradykinin and ATP is dependent on nitric oxide, the endothelium-dependent relaxing factor (EDRF).	Nitric Oxide	66-78	kininogen 1	Homo sapiens	31-41
9688841-4	1998	The role of protein kinase C (PKC) in the elevation of cGMP induced by ATP and bradykinin was studied in cultured porcine aortic endothelial cells, by measuring PKC phosphorylation of a substrate and by measuring cGMP levels by radioimmunoassay.	Cyclic GMP	55-59	kininogen 1	Homo sapiens	79-89
9688841-5	1998	Extracellular ATP and bradykinin simultaneously elevated cGMP levels and PKC activity.	Cyclic GMP	57-61	kininogen 1	Homo sapiens	22-32
9688841-12	1998	159: 1359-1367, 1989) prevented the elevation of cGMP elicited by ATP and reduced that produced by bradykinin.	Cyclic GMP	49-53	kininogen 1	Homo sapiens	99-109
9688907-5	1998	Two contiguous peptides from D5 in the histidine-glycine-rich region, Gly442-Lys458 and Phe459-Lys478, each inhibit the binding of HK to PMN.	Histidine	39-48	kininogen 1	Homo sapiens	131-133
9688907-5	1998	Two contiguous peptides from D5 in the histidine-glycine-rich region, Gly442-Lys458 and Phe459-Lys478, each inhibit the binding of HK to PMN.	Glycine	49-56	kininogen 1	Homo sapiens	131-133
9689009-13	1998	It is concluded that the stimulation of the renin-angiotensin system on a low-NaCl diet is associated with a decrease in pKKS (bradykinin and plasma kallikrein) but not in tissue and renal KKS.	Sodium Chloride	78-82	kininogen 1	Homo sapiens	127-137
9717055-4	1998	Bradykinin is a vasodilator that increases the activity of constitutive nitric oxide.	Nitric Oxide	72-84	kininogen 1	Homo sapiens	0-10
9649571-6	1998	E2beta treatment (10(-)8 M for 48 h) also caused a threefold increase in COX-1 protein expression and a threefold increase in PGI2 synthesis stimulated by bradykinin, the calcium ionophore A23187, or arachidonic acid.	Epoprostenol	126-130	kininogen 1	Homo sapiens	155-165
9767830-4	1998	NO SYNTHESIS: Nitric oxide is synthesized from L-arginine by NO-synthetase whose activity is regulated by intracellular calcium concentration and modulated by pharmacological compounds such as acetylcholine, 5-hydroxytryptamine, bradykinin and ADP as well as the sheer forces produced by blood flow.	Nitric Oxide	14-26	kininogen 1	Homo sapiens	229-239
9767830-4	1998	NO SYNTHESIS: Nitric oxide is synthesized from L-arginine by NO-synthetase whose activity is regulated by intracellular calcium concentration and modulated by pharmacological compounds such as acetylcholine, 5-hydroxytryptamine, bradykinin and ADP as well as the sheer forces produced by blood flow.	Arginine	47-57	kininogen 1	Homo sapiens	229-239
9767830-4	1998	NO SYNTHESIS: Nitric oxide is synthesized from L-arginine by NO-synthetase whose activity is regulated by intracellular calcium concentration and modulated by pharmacological compounds such as acetylcholine, 5-hydroxytryptamine, bradykinin and ADP as well as the sheer forces produced by blood flow.	Calcium	120-127	kininogen 1	Homo sapiens	229-239
9767830-4	1998	NO SYNTHESIS: Nitric oxide is synthesized from L-arginine by NO-synthetase whose activity is regulated by intracellular calcium concentration and modulated by pharmacological compounds such as acetylcholine, 5-hydroxytryptamine, bradykinin and ADP as well as the sheer forces produced by blood flow.	Serotonin	208-227	kininogen 1	Homo sapiens	229-239
9767830-4	1998	NO SYNTHESIS: Nitric oxide is synthesized from L-arginine by NO-synthetase whose activity is regulated by intracellular calcium concentration and modulated by pharmacological compounds such as acetylcholine, 5-hydroxytryptamine, bradykinin and ADP as well as the sheer forces produced by blood flow.	Adenosine Diphosphate	244-247	kininogen 1	Homo sapiens	229-239
9734886-11	1998	In the patient receiving the ACE-inhibitor captopril, bradykinin concentration was very high at 47 fmol/mL during an acute attack of angio-oedema, but normal at 3.2 fmol/mL in remission after withdrawal of the drug.	Captopril	43-52	kininogen 1	Homo sapiens	54-64
9734886-13	1998	Although the differences between patients in remission and healthy controls did not reach statistical significance, there were substantial rises in bradykinin during acute attacks of hereditary, acquired, or captopril-induced angio-oedema.	Captopril	208-217	kininogen 1	Homo sapiens	148-158
9680062-0	1998	Synthesis and activity of dimeric bradykinin antagonists containing diaminodicarboxylic acid bridge residues.	diaminodicarboxylic acid	68-92	kininogen 1	Homo sapiens	34-44
9680062-4	1998	Using suitably modified standard solid-phase peptide synthesis protocols, dimeric bradykinin antagonist peptides [H-(D-Arg)-Arg-Pro-Hyp-Gly-Phe]2-X-[(D-Phe)-Leu-Arg-OH]2 were synthesized where X corresponds to a L,L-2,7-diaminosuberic or L,L-2,9-diaminosebacic acid residue, respectively.	h-(d-arg)-arg-pro-hyp-gly-phe	114-143	kininogen 1	Homo sapiens	82-92
9680062-4	1998	Using suitably modified standard solid-phase peptide synthesis protocols, dimeric bradykinin antagonist peptides [H-(D-Arg)-Arg-Pro-Hyp-Gly-Phe]2-X-[(D-Phe)-Leu-Arg-OH]2 were synthesized where X corresponds to a L,L-2,7-diaminosuberic or L,L-2,9-diaminosebacic acid residue, respectively.	(d-phe)-leu-arg-oh	149-167	kininogen 1	Homo sapiens	82-92
9680062-4	1998	Using suitably modified standard solid-phase peptide synthesis protocols, dimeric bradykinin antagonist peptides [H-(D-Arg)-Arg-Pro-Hyp-Gly-Phe]2-X-[(D-Phe)-Leu-Arg-OH]2 were synthesized where X corresponds to a L,L-2,7-diaminosuberic or L,L-2,9-diaminosebacic acid residue, respectively.	diaminosuberic	220-234	kininogen 1	Homo sapiens	82-92
9680062-4	1998	Using suitably modified standard solid-phase peptide synthesis protocols, dimeric bradykinin antagonist peptides [H-(D-Arg)-Arg-Pro-Hyp-Gly-Phe]2-X-[(D-Phe)-Leu-Arg-OH]2 were synthesized where X corresponds to a L,L-2,7-diaminosuberic or L,L-2,9-diaminosebacic acid residue, respectively.	l,l-2,9-diaminosebacic acid	238-265	kininogen 1	Homo sapiens	82-92
9680062-5	1998	The biological activity of these peptides was comparable to that of conventional dimeric bradykinin antagonists cross-linked through cystine or bis(succinimido)alkyl bridges.	Cystine	133-140	kininogen 1	Homo sapiens	89-99
9680062-5	1998	The biological activity of these peptides was comparable to that of conventional dimeric bradykinin antagonists cross-linked through cystine or bis(succinimido)alkyl bridges.	bis(succinimido)alkyl bridges	144-173	kininogen 1	Homo sapiens	89-99
9614202-0	1998	Interleukin-1beta induces bradykinin B2 receptor gene expression through a prostanoid cyclic AMP-dependent pathway in human bronchial smooth muscle cells.	prostanoid cyclic amp	75-96	kininogen 1	Homo sapiens	26-36
9614202-3	1998	The increase in B2 receptors was correlated to an enhancement of inositol phosphate formation elicited by bradykinin, indicating its relevance to the contractile response of smooth muscle cells to bradykinin.	Inositol Phosphates	65-83	kininogen 1	Homo sapiens	106-116
9614202-3	1998	The increase in B2 receptors was correlated to an enhancement of inositol phosphate formation elicited by bradykinin, indicating its relevance to the contractile response of smooth muscle cells to bradykinin.	Inositol Phosphates	65-83	kininogen 1	Homo sapiens	197-207
9671906-6	1998	Under both normothermia and hypothermia, after the incubation, the relaxation mediated by EDHF significantly decreased (under normothermia: from 68.7% +/- 10.2% to 32.1% +/- 8%, n = 7, p = 0.001, for bradykinin and from 79.9% +/- 8.4% to 56.9% +/- 8.5%, n = 7, p = 0.01, for A23187; under hypothermia and hypoxia: to 18.9% +/- 5.6%, n = 9, p = 0.0005, for bradykinin and 52.7% +/- 7.5%, n = 9, p = 0.03, for A23187).	edhf	90-94	kininogen 1	Homo sapiens	200-210
9671906-6	1998	Under both normothermia and hypothermia, after the incubation, the relaxation mediated by EDHF significantly decreased (under normothermia: from 68.7% +/- 10.2% to 32.1% +/- 8%, n = 7, p = 0.001, for bradykinin and from 79.9% +/- 8.4% to 56.9% +/- 8.5%, n = 7, p = 0.01, for A23187; under hypothermia and hypoxia: to 18.9% +/- 5.6%, n = 9, p = 0.0005, for bradykinin and 52.7% +/- 7.5%, n = 9, p = 0.03, for A23187).	edhf	90-94	kininogen 1	Homo sapiens	356-366
9701712-1	1998	An endothelium-derived hyperpolarizing factor (EDHF) mediates a part of the vasodilatory action of bradykinin.	endothelium-derived hyperpolarizing factor	3-45	kininogen 1	Homo sapiens	99-109
9701712-1	1998	An endothelium-derived hyperpolarizing factor (EDHF) mediates a part of the vasodilatory action of bradykinin.	edhf	47-51	kininogen 1	Homo sapiens	99-109
17013240-5	1998	In clinical practice, ACE inhibitors may be preferred to angiotensin II receptor antagonists since the former, besides reducing angiotensin II synthesis, also lead to an accumulation of kinins (e.g. bradykinin), which have important cardio- and renal protective effects through liberation of prostacyclin and nitric oxide in endothelial cells and through stimulation of guanylate cyclase to form cyclic GMP.	Epoprostenol	292-304	kininogen 1	Homo sapiens	199-209
17013240-5	1998	In clinical practice, ACE inhibitors may be preferred to angiotensin II receptor antagonists since the former, besides reducing angiotensin II synthesis, also lead to an accumulation of kinins (e.g. bradykinin), which have important cardio- and renal protective effects through liberation of prostacyclin and nitric oxide in endothelial cells and through stimulation of guanylate cyclase to form cyclic GMP.	Nitric Oxide	309-321	kininogen 1	Homo sapiens	199-209
17013240-5	1998	In clinical practice, ACE inhibitors may be preferred to angiotensin II receptor antagonists since the former, besides reducing angiotensin II synthesis, also lead to an accumulation of kinins (e.g. bradykinin), which have important cardio- and renal protective effects through liberation of prostacyclin and nitric oxide in endothelial cells and through stimulation of guanylate cyclase to form cyclic GMP.	Cyclic GMP	396-406	kininogen 1	Homo sapiens	199-209
9754910-3	1998	Analysis of specific [3H]-bradykinin binding revealed that IFNgamma-treated cells had a two- to threefold increase in bradykinin receptor number compared to the controls with no effect on receptor affinity.	Tritium	22-24	kininogen 1	Homo sapiens	26-36
9754910-4	1998	The ability of IFNgamma to stimulate increased bradykinin receptor expression was abrogated by treatment with either the transcription inhibitor actinomycin D or the protein synthesis inhibitor cycloheximide.	Dactinomycin	145-158	kininogen 1	Homo sapiens	47-57
9754910-4	1998	The ability of IFNgamma to stimulate increased bradykinin receptor expression was abrogated by treatment with either the transcription inhibitor actinomycin D or the protein synthesis inhibitor cycloheximide.	Cycloheximide	194-207	kininogen 1	Homo sapiens	47-57
9754910-6	1998	B2 bradykinin receptor mRNA expression was increased as early as 1 h following IFNgamma stimulation, and continued to accumulate for 24 h. Bradykinin-stimulated intracellular calcium mobilization was also increased in IFNgamma-treated T24 cells compared to controls.	Calcium	175-182	kininogen 1	Homo sapiens	139-149
10434255-0	1998	Similarity studies on guanidinium, imidazolinium, and imidazolium cations: toward new bradykinin antagonists.	Guanidine	22-33	kininogen 1	Homo sapiens	86-96
10434255-0	1998	Similarity studies on guanidinium, imidazolinium, and imidazolium cations: toward new bradykinin antagonists.	imidazolinium	35-48	kininogen 1	Homo sapiens	86-96
10434255-0	1998	Similarity studies on guanidinium, imidazolinium, and imidazolium cations: toward new bradykinin antagonists.	imidazolium	54-65	kininogen 1	Homo sapiens	86-96
10434255-3	1998	Among these new antagonists, the guanidinium cations, which appear not only in the terminal arginine residues of BK but also in several nonpeptidic antagonists, will be substituted by groups with characteristics similar in terms of electrostatic potential, electron density, shape, etc.	Guanidine	33-44	kininogen 1	Homo sapiens	113-115
10434255-3	1998	Among these new antagonists, the guanidinium cations, which appear not only in the terminal arginine residues of BK but also in several nonpeptidic antagonists, will be substituted by groups with characteristics similar in terms of electrostatic potential, electron density, shape, etc.	Arginine	92-100	kininogen 1	Homo sapiens	113-115
10434255-4	1998	Several similarity indexes have been calculated for guanidinium, 2-aminoimidazolinium, and 2-aminoimidazolium cations and their corresponding neutral species to design new nonpeptidic BK antagonists.	Guanidine	52-63	kininogen 1	Homo sapiens	184-186
10434255-4	1998	Several similarity indexes have been calculated for guanidinium, 2-aminoimidazolinium, and 2-aminoimidazolium cations and their corresponding neutral species to design new nonpeptidic BK antagonists.	2-aminoimidazolinium	65-85	kininogen 1	Homo sapiens	184-186
10434255-4	1998	Several similarity indexes have been calculated for guanidinium, 2-aminoimidazolinium, and 2-aminoimidazolium cations and their corresponding neutral species to design new nonpeptidic BK antagonists.	2-aminoimidazolium	91-109	kininogen 1	Homo sapiens	184-186
9600070-0	1998	Bradykinin stimulates the tyrosine phosphorylation and bradykinin B2 receptor association of phospholipase C gamma 1 in vascular endothelial cells.	Tyrosine	26-34	kininogen 1	Homo sapiens	0-10
9600070-4	1998	In the present study, however, we have found that BK stimulation of IP3 production and the Ca2+ signal in endothelial cells is dependent on tyrosine phosphorylation.	Inositol 1,4,5-Trisphosphate	68-71	kininogen 1	Homo sapiens	50-52
9600070-4	1998	In the present study, however, we have found that BK stimulation of IP3 production and the Ca2+ signal in endothelial cells is dependent on tyrosine phosphorylation.	Tyrosine	140-148	kininogen 1	Homo sapiens	50-52
9717056-6	1998	Bradykinin is a very potent vasodilator that exerts its vasodilatory actions by causing endothelial release of nitric oxide, prostacyclin and/or endothelium-derived hyperpolarizing factor.	Nitric Oxide	111-123	kininogen 1	Homo sapiens	0-10
9717056-6	1998	Bradykinin is a very potent vasodilator that exerts its vasodilatory actions by causing endothelial release of nitric oxide, prostacyclin and/or endothelium-derived hyperpolarizing factor.	Epoprostenol	125-137	kininogen 1	Homo sapiens	0-10
9666826-4	1998	To address this we have used two relatively new techniques, scanning laser Doppler imaging (LDI) and dermal microdialysis to measure changes in skin blood flow and the release of histamine within the weal and flare, following intradermal injection of histamine or bradykinin.	Histamine	251-260	kininogen 1	Homo sapiens	264-274
9643615-5	1998	Furthermore, we investigated the effects of the ET(A)-selective antagonist PD147953 on bradykinin-induced vasodilation.	et(a)	48-53	kininogen 1	Homo sapiens	87-97
9666826-7	1998	The development of the flare and the weal response to both histamine and bradykinin was significantly reduced by cetirizine but not by loratadine.	Cetirizine	113-123	kininogen 1	Homo sapiens	73-83
9666826-9	1998	Bradykinin-induced inflammatory responses were similarly reduced by cetirizine, the weal by 60 +/- 16% (P &lt; 0.02) and the flare by 61 +/- 4% (P &lt; 0.005).	Cetirizine	68-78	kininogen 1	Homo sapiens	0-10
9666826-11	1998	Histamine levels also rose following bradykinin injection in some subjects (mean 147 +/- 46 nmol/L, range 18-336).	Histamine	0-9	kininogen 1	Homo sapiens	37-47
10684491-10	1998	In the presence of bradykinin and 27% cyclic strain, production of nitrogen oxides and endothelial NO synthase activity were increased by 110 +/- 37% and 135 +/- 7%, respectively (P &lt;.05 compared with control); however, we observed no significant increase in cell number (5 +/- 5%), despite an 86 +/- 7% increase in [(3)H]thymidine incorporation (P &lt;.05).	Nitrogen Oxides	67-82	kininogen 1	Homo sapiens	19-29
9650825-7	1998	A second generation of antagonists, represented by D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE 140) has been found resistant to degradation, long-acting in vivo, selective and specific for the B2 receptor and potent in all species tested.	D-Arginine	51-56	kininogen 1	Homo sapiens	79-89
9650825-7	1998	A second generation of antagonists, represented by D-Arg[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE 140) has been found resistant to degradation, long-acting in vivo, selective and specific for the B2 receptor and potent in all species tested.	thi5	62-66	kininogen 1	Homo sapiens	79-89
9650825-12	1998	Progress has been made with AcLys-[D-betaNal7, Ile8]desArg9-bradykinin (R 715) and Lys-Lys-[Hyp3, Cpg5, D-Tic7,Cpg8]desArg9-bradykinin (B 9958) which are pure B1 antagonists in humans and rabbits; both peptides have shown resistance to degradation by peptidases and have little if any, residual agonistic activity on mouse and rat B1 receptors.	Deuterium	35-36	kininogen 1	Homo sapiens	60-70
9650825-12	1998	Progress has been made with AcLys-[D-betaNal7, Ile8]desArg9-bradykinin (R 715) and Lys-Lys-[Hyp3, Cpg5, D-Tic7,Cpg8]desArg9-bradykinin (B 9958) which are pure B1 antagonists in humans and rabbits; both peptides have shown resistance to degradation by peptidases and have little if any, residual agonistic activity on mouse and rat B1 receptors.	Lysine	30-33	kininogen 1	Homo sapiens	60-70
9657256-0	1998	Bradykinin increases intracellular calcium levels in a human bronchial epithelial cell line via the B2 receptor subtype.	Calcium	35-42	kininogen 1	Homo sapiens	0-10
9681679-2	1998	Application of ATP, bradykinin and formyl-Met-Leu-Phe (fMLP) resulted in a transient increase in intracellular calcium concentration ([Ca2+]i) with an average half-width of 40+/-21 s and a decay time constant of 15+/-10 s (mean +/- SD, n = 108), irrespective of the agonist applied.	Calcium	111-118	kininogen 1	Homo sapiens	20-30
9571146-1	1998	We analyzed the effect of isoprenoid depletion by fluvastatin on bradykinin (BK)- and epidermal growth factor (EGF)-mediated Ca2+ mobilization and prostaglandin E2 production, in the human keratinocyte cell line HaCaT.	Terpenes	26-36	kininogen 1	Homo sapiens	65-75
9571146-1	1998	We analyzed the effect of isoprenoid depletion by fluvastatin on bradykinin (BK)- and epidermal growth factor (EGF)-mediated Ca2+ mobilization and prostaglandin E2 production, in the human keratinocyte cell line HaCaT.	Terpenes	26-36	kininogen 1	Homo sapiens	77-79
9571146-1	1998	We analyzed the effect of isoprenoid depletion by fluvastatin on bradykinin (BK)- and epidermal growth factor (EGF)-mediated Ca2+ mobilization and prostaglandin E2 production, in the human keratinocyte cell line HaCaT.	Fluvastatin	50-61	kininogen 1	Homo sapiens	65-75
9571146-1	1998	We analyzed the effect of isoprenoid depletion by fluvastatin on bradykinin (BK)- and epidermal growth factor (EGF)-mediated Ca2+ mobilization and prostaglandin E2 production, in the human keratinocyte cell line HaCaT.	Fluvastatin	50-61	kininogen 1	Homo sapiens	77-79
9571146-3	1998	The synthesis of prostaglandin E2 paralleled the level of Ca2+ mobilization induced by BK and EGF.	Dinoprostone	17-33	kininogen 1	Homo sapiens	87-89
9546378-6	1998	In contrast to the bradykinin-induced release of EDHF, the EDHF synthesized in response to pulsatile stretch did not exhibit any tachyphylaxis.	edhf	49-53	kininogen 1	Homo sapiens	19-29
9564911-9	1998	Vascular relaxation in response to bradykinin (10[-9] to 10[-6] mol/L), which was found to induce endothelium-dependent vasodilation independent of nitric oxide production, was unaffected by magnesium removal (n=10).	Nitric Oxide	148-160	kininogen 1	Homo sapiens	35-45
9839700-0	1998	Synergistic interactions of bradykinin, thrombin, interleukin 1 and tumor necrosis factor on prostanoid biosynthesis in human periodontal-ligament cells.	Prostaglandins	93-103	kininogen 1	Homo sapiens	28-38
9839700-2	1998	Bradykinin (BK) and thrombin are known to cause a significant time- and concentration-dependent burst of prostanoid biosynthesis in cultured human periodontal-ligament (PDL) cells.	Prostaglandins	105-115	kininogen 1	Homo sapiens	0-10
9839700-2	1998	Bradykinin (BK) and thrombin are known to cause a significant time- and concentration-dependent burst of prostanoid biosynthesis in cultured human periodontal-ligament (PDL) cells.	Prostaglandins	105-115	kininogen 1	Homo sapiens	12-14
9839700-8	1998	These data suggest that the synergistic effect of BK and IL-1 beta on prostanoid biosynthesis is not due to interactions at the receptor level nor to enhanced release of arachidonic acid, but may be due to increased activity of cyclo-oxygenase.	Prostaglandins	70-80	kininogen 1	Homo sapiens	50-52
9839700-8	1998	These data suggest that the synergistic effect of BK and IL-1 beta on prostanoid biosynthesis is not due to interactions at the receptor level nor to enhanced release of arachidonic acid, but may be due to increased activity of cyclo-oxygenase.	Arachidonic Acid	170-186	kininogen 1	Homo sapiens	50-52
9839700-12	1998	These experiments demonstrate synergistic interactions between BK, thrombin, IL-1 and TNF on prostaglandin biosynthesis in cultured human PDL cells.	Prostaglandins	93-106	kininogen 1	Homo sapiens	63-65
9597423-7	1998	Bradykinin-induced nitric oxide production is regulated by angiotensin converting enzyme located on the endothelial cell membrane; indeed, the enzyme not only activates angiotensin I into angiotensin II, but also inactivates bradykinin.	Nitric Oxide	19-31	kininogen 1	Homo sapiens	0-10
9597423-7	1998	Bradykinin-induced nitric oxide production is regulated by angiotensin converting enzyme located on the endothelial cell membrane; indeed, the enzyme not only activates angiotensin I into angiotensin II, but also inactivates bradykinin.	Nitric Oxide	19-31	kininogen 1	Homo sapiens	225-235
9597423-12	1998	Nitrates substitute in part for deficient endogenous nitric oxide, while angiotensin converting enzyme inhibitors increase the bradykinin induced nitric oxide and prostacyclin production.	Nitric Oxide	146-158	kininogen 1	Homo sapiens	127-137
9597423-12	1998	Nitrates substitute in part for deficient endogenous nitric oxide, while angiotensin converting enzyme inhibitors increase the bradykinin induced nitric oxide and prostacyclin production.	Epoprostenol	163-175	kininogen 1	Homo sapiens	127-137
9797190-5	1998	RESULTS: Hypertensive patients had blunted (P &lt; 0.01 or less) vasodilatations in response to infusions of acetylcholine (from 3.7 +/- 0.3 to 18.3 +/- 4.9 ml/100 ml per min) and bradykinin (from 3.7 +/- 0.4 to 15.8 +/- 2.6 ml/100 ml per min) compared with those of controls (from 3.6 +/- 0.3 to 25.3 +/- 5.2 ml/100 ml per min for acetylcholine and from 3.7 +/- 0.3 to 26.9 +/- 4.9 ml/100 ml per min for bradykinin) whereas the responses to infusion of sodium nitroprusside were similar (from 3.6 +/- 0.3 to 18.5 +/- 3.9 and from 3.6 +/- 0.3 to 16.4 +/- 1.8 ml/100 ml per min, respectively).	Acetylcholine	109-122	kininogen 1	Homo sapiens	180-190
9797190-5	1998	RESULTS: Hypertensive patients had blunted (P &lt; 0.01 or less) vasodilatations in response to infusions of acetylcholine (from 3.7 +/- 0.3 to 18.3 +/- 4.9 ml/100 ml per min) and bradykinin (from 3.7 +/- 0.4 to 15.8 +/- 2.6 ml/100 ml per min) compared with those of controls (from 3.6 +/- 0.3 to 25.3 +/- 5.2 ml/100 ml per min for acetylcholine and from 3.7 +/- 0.3 to 26.9 +/- 4.9 ml/100 ml per min for bradykinin) whereas the responses to infusion of sodium nitroprusside were similar (from 3.6 +/- 0.3 to 18.5 +/- 3.9 and from 3.6 +/- 0.3 to 16.4 +/- 1.8 ml/100 ml per min, respectively).	Acetylcholine	109-122	kininogen 1	Homo sapiens	405-415
9797190-6	1998	Acute and prolonged lisinopril treatments significantly (P &lt; 0.05 or less) improved vasodilatation in response to infusion of bradykinin (from 3.7 +/- 0.4 to 24.5 +/- 4.9 and from 3.7 +/- 0.3 to 22.1 +/- 4.9 ml/100 ml per min, respectively), but not in response to infusions of acetylcholine and of sodium nitroprusside.	Lisinopril	20-30	kininogen 1	Homo sapiens	129-139
9797190-6	1998	Acute and prolonged lisinopril treatments significantly (P &lt; 0.05 or less) improved vasodilatation in response to infusion of bradykinin (from 3.7 +/- 0.4 to 24.5 +/- 4.9 and from 3.7 +/- 0.3 to 22.1 +/- 4.9 ml/100 ml per min, respectively), but not in response to infusions of acetylcholine and of sodium nitroprusside.	Acetylcholine	281-294	kininogen 1	Homo sapiens	129-139
9797190-6	1998	Acute and prolonged lisinopril treatments significantly (P &lt; 0.05 or less) improved vasodilatation in response to infusion of bradykinin (from 3.7 +/- 0.4 to 24.5 +/- 4.9 and from 3.7 +/- 0.3 to 22.1 +/- 4.9 ml/100 ml per min, respectively), but not in response to infusions of acetylcholine and of sodium nitroprusside.	Nitroprusside	302-322	kininogen 1	Homo sapiens	129-139
9797190-7	1998	Chronic lisinopril treatment increased (P &lt; 0.05) the response to infusions of not only bradykinin (from 3.5 +/- 0.5 to 27.6 +/- 5.3 ml/100 ml per min), but also of acetylcholine (from 3.5 +/- 0.5 to 27.8 +/- 8.0 ml/100 ml per min) and sodium nitroprusside (from 3.4 +/- 0.6 to 25.9 +/- 8.5 ml/100 ml per min).	Lisinopril	8-18	kininogen 1	Homo sapiens	91-101
9797190-7	1998	Chronic lisinopril treatment increased (P &lt; 0.05) the response to infusions of not only bradykinin (from 3.5 +/- 0.5 to 27.6 +/- 5.3 ml/100 ml per min), but also of acetylcholine (from 3.5 +/- 0.5 to 27.8 +/- 8.0 ml/100 ml per min) and sodium nitroprusside (from 3.4 +/- 0.6 to 25.9 +/- 8.5 ml/100 ml per min).	Acetylcholine	168-181	kininogen 1	Homo sapiens	91-101
9797190-7	1998	Chronic lisinopril treatment increased (P &lt; 0.05) the response to infusions of not only bradykinin (from 3.5 +/- 0.5 to 27.6 +/- 5.3 ml/100 ml per min), but also of acetylcholine (from 3.5 +/- 0.5 to 27.8 +/- 8.0 ml/100 ml per min) and sodium nitroprusside (from 3.4 +/- 0.6 to 25.9 +/- 8.5 ml/100 ml per min).	Nitroprusside	239-259	kininogen 1	Homo sapiens	91-101
9797190-8	1998	However, when the responses to infusions of acetylcholine and bradykinin were normalized with respect to that to infusion of sodium nitroprusside, only the vasodilatation in response to infusion of bradykinin was shown to have been increased by lisinopril treatment.	Acetylcholine	44-57	kininogen 1	Homo sapiens	198-208
10684491-10	1998	In the presence of bradykinin and 27% cyclic strain, production of nitrogen oxides and endothelial NO synthase activity were increased by 110 +/- 37% and 135 +/- 7%, respectively (P &lt;.05 compared with control); however, we observed no significant increase in cell number (5 +/- 5%), despite an 86 +/- 7% increase in [(3)H]thymidine incorporation (P &lt;.05).	[(3)h]thymidine	319-334	kininogen 1	Homo sapiens	19-29
9494096-3	1998	The effect of BK on sAPP secretion appears to be dependent on interaction of the ligand with the B2 type of BK receptors but independent of activation of protein kinase C. We also show that sAPP release after BK treatment in fibroblasts from patients with sporadic Alzheimer"s disease is not different from control cells and is paralleled by equivalent levels of inositol trisphosphate production.	inositol 1,2,3-trisphosphate	363-385	kininogen 1	Homo sapiens	14-16
9530092-5	1998	The mitochondrial uncoupling agent carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone blocked the BK-induced [Ca2+]mt increase, although it did not affect the [Ca2+]c transient.	Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone	35-87	kininogen 1	Homo sapiens	100-102
9523665-1	1998	OBJECTIVE: To characterize the kinin receptor subtype involved in the relaxation of human isolated corpus cavernosum (HCC) induced by bradykinin (BK), Lys-bradykinin (Lys-BK), Met-Lys-bradykinin (Met-Lys-BK) and des-Arg9-bradykinin, and to investigate whether the kinin-induced relaxation of HCC results from the stimulation of nonadrenergic, noncholinergic (NANC) neurons supplying the cavernosal tissue.	Lysine	151-154	kininogen 1	Homo sapiens	155-165
9523665-1	1998	OBJECTIVE: To characterize the kinin receptor subtype involved in the relaxation of human isolated corpus cavernosum (HCC) induced by bradykinin (BK), Lys-bradykinin (Lys-BK), Met-Lys-bradykinin (Met-Lys-BK) and des-Arg9-bradykinin, and to investigate whether the kinin-induced relaxation of HCC results from the stimulation of nonadrenergic, noncholinergic (NANC) neurons supplying the cavernosal tissue.	Lysine	151-154	kininogen 1	Homo sapiens	155-165
9523665-1	1998	OBJECTIVE: To characterize the kinin receptor subtype involved in the relaxation of human isolated corpus cavernosum (HCC) induced by bradykinin (BK), Lys-bradykinin (Lys-BK), Met-Lys-bradykinin (Met-Lys-BK) and des-Arg9-bradykinin, and to investigate whether the kinin-induced relaxation of HCC results from the stimulation of nonadrenergic, noncholinergic (NANC) neurons supplying the cavernosal tissue.	Lysine	151-154	kininogen 1	Homo sapiens	155-165
9523665-10	1998	The infusion of the B2 kinin receptor antagonist Hoe 140 (50 nmol/L) virtually abolished the relaxation induced by BK, Lys-BK and Met-Lys-BK without affecting those induced by acetylcholine and histamine.	4-hydroxy-2-octenal	49-52	kininogen 1	Homo sapiens	115-117
9523665-10	1998	The infusion of the B2 kinin receptor antagonist Hoe 140 (50 nmol/L) virtually abolished the relaxation induced by BK, Lys-BK and Met-Lys-BK without affecting those induced by acetylcholine and histamine.	4-hydroxy-2-octenal	49-52	kininogen 1	Homo sapiens	123-125
9523665-10	1998	The infusion of the B2 kinin receptor antagonist Hoe 140 (50 nmol/L) virtually abolished the relaxation induced by BK, Lys-BK and Met-Lys-BK without affecting those induced by acetylcholine and histamine.	4-hydroxy-2-octenal	49-52	kininogen 1	Homo sapiens	123-125
9523665-11	1998	The infusion of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester increased the tone of the HCC tissues and significantly reduced (P &lt; 0.01) the relaxation induced by BK (74%), Lys-BK (90%), Met-Lys-BK (87%) and acetylcholine (89%) without affecting those induced by GTN.	Nitric Oxide	20-32	kininogen 1	Homo sapiens	195-197
9523665-11	1998	The infusion of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester increased the tone of the HCC tissues and significantly reduced (P &lt; 0.01) the relaxation induced by BK (74%), Lys-BK (90%), Met-Lys-BK (87%) and acetylcholine (89%) without affecting those induced by GTN.	Nitric Oxide	20-32	kininogen 1	Homo sapiens	209-211
9519747-4	1998	Using the Fura-2 technique, application of either 1 nmol/l bradykinin or 1 micromol/l ATP to the normoglycemic endothelial cells led to a significant increase in intracellular calcium, whereas the hyperglycemic cells showed significantly less reactivity to both agents.	Fura-2	10-16	kininogen 1	Homo sapiens	59-69
9519747-4	1998	Using the Fura-2 technique, application of either 1 nmol/l bradykinin or 1 micromol/l ATP to the normoglycemic endothelial cells led to a significant increase in intracellular calcium, whereas the hyperglycemic cells showed significantly less reactivity to both agents.	Calcium	176-183	kininogen 1	Homo sapiens	59-69
9506478-5	1998	ML-9 (100 microM), an inhibitor of MLCK, abolished Ca2+ influx and prevented MLC diphosphorylation in BK- and thapsigargin-treated cells, but did not affect Ca2+ mobilization from internal stores.	ML 9	0-4	kininogen 1	Homo sapiens	102-104
9540305-2	1998	PGE2 mediates vasodilatation, increases vascular permeability, enhances pain perception by bradykinin and histamine, alters connective tissue metabolism and enhances osteoclastic bone resorption.	Dinoprostone	0-4	kininogen 1	Homo sapiens	91-101
9621896-0	1998	Adenosine 5"-triphosphate, uridine 5"-triphosphate, bradykinin, and lysophosphatidic acid induce different patterns of calcium responses by human articular chondrocytes.	Calcium	119-126	kininogen 1	Homo sapiens	52-62
9621896-2	1998	Here we demonstrate that bradykinin, adenosine 5"-triphosphate, uridine 5"-triphosphate, and lysophosphatidic acid raise the intracellular calcium concentration ([Ca2+]i) in human articular chondrocytes.	Calcium	139-146	kininogen 1	Homo sapiens	25-35
9621896-3	1998	Heterologous cross-desensitization experiments showed that the uridine 5"-triphosphate response was abolished by prior treatment with adenosine 5"-triphosphate and, conversely, that the adenosine 5"-triphosphate response was abolished by prior treatment with uridine 5"-triphosphate; this indicated competition for the same receptor site, whereas bradykinin and lysophosphatidic acid did not compete with other ligands.	Uridine Triphosphate	63-86	kininogen 1	Homo sapiens	347-357
9621896-3	1998	Heterologous cross-desensitization experiments showed that the uridine 5"-triphosphate response was abolished by prior treatment with adenosine 5"-triphosphate and, conversely, that the adenosine 5"-triphosphate response was abolished by prior treatment with uridine 5"-triphosphate; this indicated competition for the same receptor site, whereas bradykinin and lysophosphatidic acid did not compete with other ligands.	Adenosine Triphosphate	186-211	kininogen 1	Homo sapiens	347-357
9621896-5	1998	Single-cell analysis of Fura-2 acetoxymethyl ester loaded chondrocytes showed mediator-dependent patterns of oscillatory Ca2+ changes in a subset of cells when challenged with submaximal concentrations of bradykinin, adenosine 5"-triphosphate, or uridine 5"-triphosphate in the presence of extracellular Ca2+.	fura-2-am	24-50	kininogen 1	Homo sapiens	205-215
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Phenylalanine	99-102	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Serine	103-106	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Proline	107-110	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Arginine	111-114	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Leucine	115-118	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Glycine	119-122	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Lysine	123-126	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Arginine	127-130	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Phenylalanine	135-138	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Serine	139-142	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Leucine	151-154	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Arginine	127-130	kininogen 1	Homo sapiens	294-304
9461491-7	1998	The low Km and high kcat values (Km 7.3 and 5.0 microM, kcat 226 and 207 s-1 for the hydrolysis of Phe-Ser-Pro-Arg-Leu-Gly-Lys-Arg and Phe-Ser-Pro-Arg-Leu-Gly-Arg-Arg, respectively) obtained for the hydrolysis of these two peptides by insect ACE means that these peptides, along with mammalian bradykinin, are the most favoured in vitro ACE substrates so far identified.	Arginine	127-130	kininogen 1	Homo sapiens	294-304
9797190-8	1998	However, when the responses to infusions of acetylcholine and bradykinin were normalized with respect to that to infusion of sodium nitroprusside, only the vasodilatation in response to infusion of bradykinin was shown to have been increased by lisinopril treatment.	Nitroprusside	125-145	kininogen 1	Homo sapiens	198-208
9797190-8	1998	However, when the responses to infusions of acetylcholine and bradykinin were normalized with respect to that to infusion of sodium nitroprusside, only the vasodilatation in response to infusion of bradykinin was shown to have been increased by lisinopril treatment.	Lisinopril	245-255	kininogen 1	Homo sapiens	198-208
9797190-9	1998	CONCLUSIONS: Administration of lisinopril to patients with essential hypertension can selectively increase vasodilatation in response to infusion of bradykinin.	Lisinopril	31-41	kininogen 1	Homo sapiens	149-159
9547352-1	1998	In primary human umbilical vein endothelial cells (HUVECs), incubation with phorbol-12-myristate-13-acetate (PMA) enhanced basal and bradykinin-stimulated nitric oxide production.	Tetradecanoylphorbol Acetate	76-107	kininogen 1	Homo sapiens	133-143
9547352-1	1998	In primary human umbilical vein endothelial cells (HUVECs), incubation with phorbol-12-myristate-13-acetate (PMA) enhanced basal and bradykinin-stimulated nitric oxide production.	Tetradecanoylphorbol Acetate	109-112	kininogen 1	Homo sapiens	133-143
9547352-1	1998	In primary human umbilical vein endothelial cells (HUVECs), incubation with phorbol-12-myristate-13-acetate (PMA) enhanced basal and bradykinin-stimulated nitric oxide production.	Nitric Oxide	155-167	kininogen 1	Homo sapiens	133-143
9555059-4	1998	BK and thrombin were able to activate phospholipase D (PLD) in vivo as demonstrated by the accumulation of [3H]phosphatidylethanol (PtdEtOH) through the transphoshatidylation reaction catalyzed by the enzyme in the presence of ethanol.	[3h]phosphatidylethanol	107-130	kininogen 1	Homo sapiens	0-2
9555059-4	1998	BK and thrombin were able to activate phospholipase D (PLD) in vivo as demonstrated by the accumulation of [3H]phosphatidylethanol (PtdEtOH) through the transphoshatidylation reaction catalyzed by the enzyme in the presence of ethanol.	ptdetoh	132-139	kininogen 1	Homo sapiens	0-2
9555059-4	1998	BK and thrombin were able to activate phospholipase D (PLD) in vivo as demonstrated by the accumulation of [3H]phosphatidylethanol (PtdEtOH) through the transphoshatidylation reaction catalyzed by the enzyme in the presence of ethanol.	Ethanol	123-130	kininogen 1	Homo sapiens	0-2
9555059-5	1998	The observation that ethanol could significantly reduce [3H]PtdOH formation in myoblasts stimulated with BK and thrombin indicates that stimulation of PLD has a major role.	Ethanol	21-28	kininogen 1	Homo sapiens	105-107
9555059-5	1998	The observation that ethanol could significantly reduce [3H]PtdOH formation in myoblasts stimulated with BK and thrombin indicates that stimulation of PLD has a major role.	Tritium	57-59	kininogen 1	Homo sapiens	105-107
9555059-5	1998	The observation that ethanol could significantly reduce [3H]PtdOH formation in myoblasts stimulated with BK and thrombin indicates that stimulation of PLD has a major role.	ptdoh	60-65	kininogen 1	Homo sapiens	105-107
9555059-7	1998	In addition, BK and thrombin appear able to activate DAG kinase at early times of incubation and also this pathway may contribute to determine the increase in [3H]PtdOH levels.	Tritium	160-162	kininogen 1	Homo sapiens	13-15
9555059-7	1998	In addition, BK and thrombin appear able to activate DAG kinase at early times of incubation and also this pathway may contribute to determine the increase in [3H]PtdOH levels.	ptdoh	163-168	kininogen 1	Homo sapiens	13-15
9523665-11	1998	The infusion of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester increased the tone of the HCC tissues and significantly reduced (P &lt; 0.01) the relaxation induced by BK (74%), Lys-BK (90%), Met-Lys-BK (87%) and acetylcholine (89%) without affecting those induced by GTN.	NG-Nitroarginine Methyl Ester	52-90	kininogen 1	Homo sapiens	195-197
9523665-11	1998	The infusion of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester increased the tone of the HCC tissues and significantly reduced (P &lt; 0.01) the relaxation induced by BK (74%), Lys-BK (90%), Met-Lys-BK (87%) and acetylcholine (89%) without affecting those induced by GTN.	NG-Nitroarginine Methyl Ester	52-90	kininogen 1	Homo sapiens	209-211
9523665-11	1998	The infusion of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester increased the tone of the HCC tissues and significantly reduced (P &lt; 0.01) the relaxation induced by BK (74%), Lys-BK (90%), Met-Lys-BK (87%) and acetylcholine (89%) without affecting those induced by GTN.	Acetylcholine	240-253	kininogen 1	Homo sapiens	195-197
9523665-11	1998	The infusion of the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester increased the tone of the HCC tissues and significantly reduced (P &lt; 0.01) the relaxation induced by BK (74%), Lys-BK (90%), Met-Lys-BK (87%) and acetylcholine (89%) without affecting those induced by GTN.	Nitroglycerin	295-298	kininogen 1	Homo sapiens	195-197
9523665-12	1998	The subsequent infusion of L-arginine (300 micromol/L) partially reversed the increased tone and significantly (P &lt; 0.01) restored the relaxation induced by BK, Lys-BK and Met-Lys-BK.	Arginine	27-37	kininogen 1	Homo sapiens	160-162
9523665-12	1998	The subsequent infusion of L-arginine (300 micromol/L) partially reversed the increased tone and significantly (P &lt; 0.01) restored the relaxation induced by BK, Lys-BK and Met-Lys-BK.	Arginine	27-37	kininogen 1	Homo sapiens	168-170
9523665-12	1998	The subsequent infusion of L-arginine (300 micromol/L) partially reversed the increased tone and significantly (P &lt; 0.01) restored the relaxation induced by BK, Lys-BK and Met-Lys-BK.	Arginine	27-37	kininogen 1	Homo sapiens	168-170
9523665-13	1998	The results were similar with the novel guanylate cyclase inhibitor 1H-[1,2,4] oxadiazolo[4,3,-alquinoxalin-1-one] which reduced by &gt; 95% (P &lt; 0.01) the relaxation induced by BK, Lys-BK, Met-Lys-BK, acetylcholine and GTN.	1h-[1,2,4] oxadiazolo[4,3,-alquinoxalin-1-one	68-113	kininogen 1	Homo sapiens	181-183
9523665-13	1998	The results were similar with the novel guanylate cyclase inhibitor 1H-[1,2,4] oxadiazolo[4,3,-alquinoxalin-1-one] which reduced by &gt; 95% (P &lt; 0.01) the relaxation induced by BK, Lys-BK, Met-Lys-BK, acetylcholine and GTN.	1h-[1,2,4] oxadiazolo[4,3,-alquinoxalin-1-one	68-113	kininogen 1	Homo sapiens	189-191
9523665-13	1998	The results were similar with the novel guanylate cyclase inhibitor 1H-[1,2,4] oxadiazolo[4,3,-alquinoxalin-1-one] which reduced by &gt; 95% (P &lt; 0.01) the relaxation induced by BK, Lys-BK, Met-Lys-BK, acetylcholine and GTN.	1h-[1,2,4] oxadiazolo[4,3,-alquinoxalin-1-one	68-113	kininogen 1	Homo sapiens	189-191
9514182-9	1998	Inhibition of NO synthase partially attenuated, whereas high potassium chloride (30 mM) markedly inhibited relaxations to bradykinin (p &lt; 0.05).	Potassium Chloride	61-79	kininogen 1	Homo sapiens	122-132
9446690-10	1998	Studies with the converting enzyme inhibitor ramiprilat and the bradykinin receptor antagonist icatibant indicate that bradykinin mediates, at least partly, diuretic NPY effects.	ramiprilat	45-55	kininogen 1	Homo sapiens	119-129
9634724-6	1998	The hyperinsulinemic euglycaemic clamping of 7 patients with NIDDM and essential hypertension showed that ACE-inhibitor (Perindopril, 4 mg) prevented bradykinin from destruction and increased the glucose consumption by tissues.	Perindopril	121-132	kininogen 1	Homo sapiens	150-160
9466814-1	1998	In the human keratinocyte cell line HaCaT, reactive oxygen species (ROS) were generated in a dose- and time-dependent manner in response to epidermal growth factor (EGF), bradykinin, thapsigargin, and the Ca(2+)-ionophore A23187, agonists that interact with different primary cell targets.	Reactive Oxygen Species	43-66	kininogen 1	Homo sapiens	171-181
9466814-1	1998	In the human keratinocyte cell line HaCaT, reactive oxygen species (ROS) were generated in a dose- and time-dependent manner in response to epidermal growth factor (EGF), bradykinin, thapsigargin, and the Ca(2+)-ionophore A23187, agonists that interact with different primary cell targets.	Reactive Oxygen Species	68-71	kininogen 1	Homo sapiens	171-181
9466814-3	1998	The ROS evoked by EGF and bradykinin decayed within 8 and 4 min, respectively, this transient effect resulting probably from down-regulation of the specific agonist receptors or dissipation of the secondary signals.	Reactive Oxygen Species	4-7	kininogen 1	Homo sapiens	26-36
9466814-7	1998	Direct measurement of [Ca2+]i using fura fluorescence revealed that EGF and bradykinin evoked a modest, transient [Ca2+]i elevation of less than twofold, whereas with thapsigargin and A23187 there was a sustained two- to fourfold elevation.	fura	36-40	kininogen 1	Homo sapiens	76-86
9466814-7	1998	Direct measurement of [Ca2+]i using fura fluorescence revealed that EGF and bradykinin evoked a modest, transient [Ca2+]i elevation of less than twofold, whereas with thapsigargin and A23187 there was a sustained two- to fourfold elevation.	Calcimycin	184-190	kininogen 1	Homo sapiens	76-86
9635152-4	1998	Bosentan decreased vasoconstrictor responses to lower doses of angiotensin II, whereas responses to higher doses of angiotensin II and responses to vasopressin, U46619, BAY K8644, norepinephrine, acetylcholine, bradykinin, levcromakalim, PGE1, adrenomedullin, and calcitonin gene-related peptide were not altered.	Bosentan	0-8	kininogen 1	Homo sapiens	211-221
9635158-1	1998	We have recently shown that isolated pulmonary resistance arteries of the fetal lamb have prostaglandin (PG) I2 based and nitric oxide (NO) based relaxing mechanisms, which are activated by oxygen (at neonatal levels) and bradykinin.	Epoprostenol	90-111	kininogen 1	Homo sapiens	222-232
9635158-1	1998	We have recently shown that isolated pulmonary resistance arteries of the fetal lamb have prostaglandin (PG) I2 based and nitric oxide (NO) based relaxing mechanisms, which are activated by oxygen (at neonatal levels) and bradykinin.	Nitric Oxide	122-134	kininogen 1	Homo sapiens	222-232
9635158-5	1998	Bradykinin (0.1-100 nM) dose dependently (from 1-3 nM upwards) relaxed endothelium-denuded arteries that had been precontracted with a thromboxane (TX) A2 analog (ONO-11113, 0.1 microM) or excess potassium (5 mM Ca2+ in K(+)-Krebs) at a neonatal Po2.	Thromboxanes	135-146	kininogen 1	Homo sapiens	0-10
9635158-5	1998	Bradykinin (0.1-100 nM) dose dependently (from 1-3 nM upwards) relaxed endothelium-denuded arteries that had been precontracted with a thromboxane (TX) A2 analog (ONO-11113, 0.1 microM) or excess potassium (5 mM Ca2+ in K(+)-Krebs) at a neonatal Po2.	STA 2	163-172	kininogen 1	Homo sapiens	0-10
9635158-5	1998	Bradykinin (0.1-100 nM) dose dependently (from 1-3 nM upwards) relaxed endothelium-denuded arteries that had been precontracted with a thromboxane (TX) A2 analog (ONO-11113, 0.1 microM) or excess potassium (5 mM Ca2+ in K(+)-Krebs) at a neonatal Po2.	Potassium	196-205	kininogen 1	Homo sapiens	0-10
9635158-5	1998	Bradykinin (0.1-100 nM) dose dependently (from 1-3 nM upwards) relaxed endothelium-denuded arteries that had been precontracted with a thromboxane (TX) A2 analog (ONO-11113, 0.1 microM) or excess potassium (5 mM Ca2+ in K(+)-Krebs) at a neonatal Po2.	k(+)-krebs	220-230	kininogen 1	Homo sapiens	0-10
9635158-5	1998	Bradykinin (0.1-100 nM) dose dependently (from 1-3 nM upwards) relaxed endothelium-denuded arteries that had been precontracted with a thromboxane (TX) A2 analog (ONO-11113, 0.1 microM) or excess potassium (5 mM Ca2+ in K(+)-Krebs) at a neonatal Po2.	PO-2	246-249	kininogen 1	Homo sapiens	0-10
9635158-7	1998	Bradykinin relaxation of ONO-11113-contracted arteries was completely or nearly completely inhibited by indomethacin and L-NAME.	STA 2	25-34	kininogen 1	Homo sapiens	0-10
9635158-7	1998	Bradykinin relaxation of ONO-11113-contracted arteries was completely or nearly completely inhibited by indomethacin and L-NAME.	Indomethacin	104-116	kininogen 1	Homo sapiens	0-10
9635158-7	1998	Bradykinin relaxation of ONO-11113-contracted arteries was completely or nearly completely inhibited by indomethacin and L-NAME.	NG-Nitroarginine Methyl Ester	121-127	kininogen 1	Homo sapiens	0-10
9475274-4	1998	Bradykinin-induced relaxation was significantly potentiated by the kininase I carboxypeptidase inhibitor mergepta (10(-6) M).	2-mercaptomethyl-3-guanidinoethylthiopropionic acid	105-113	kininogen 1	Homo sapiens	0-10
9475274-11	1998	The desArg9-bradykinin-induced contraction also was inhibited by the protein-synthesis inhibitor cycloheximide.	Cycloheximide	97-110	kininogen 1	Homo sapiens	12-22
9475274-13	1998	In conclusion, bradykinin-induced relaxation of isolated porcine iliac arteries was mediated by endothelial bradykinin B2 receptors and mainly nitric oxide.	Nitric Oxide	143-155	kininogen 1	Homo sapiens	15-25
9475274-14	1998	Bradykinin-induced contraction was endothelium independent, indomethacin sensitive, and probably mediated by bradykinin B1 (inducible) and B2 receptors located in the vascular smooth-muscle layer.	Indomethacin	60-72	kininogen 1	Homo sapiens	0-10
9514242-1	1998	The AMBER 4.0 force field was used to perform the characterization of the conformational profile of the highly potent bradykinin antagonist Hoe-140 (D-Arg0-Arg1-Pro2-Hyp3-Gly4-Thi5-Ser6-D-++ +Tic7-Oic8-Arg9).	4-hydroxy-2-octenal	140-143	kininogen 1	Homo sapiens	118-128
9514242-1	1998	The AMBER 4.0 force field was used to perform the characterization of the conformational profile of the highly potent bradykinin antagonist Hoe-140 (D-Arg0-Arg1-Pro2-Hyp3-Gly4-Thi5-Ser6-D-++ +Tic7-Oic8-Arg9).	-arg0	150-155	kininogen 1	Homo sapiens	118-128
9518887-4	1998	The presence of the B2 receptor antagonist, HOE-140 (+2.79 microM indomethacin), resulted in a concentration-related rightward displacement of the concentration-effect curves to BK.	Indomethacin	66-78	kininogen 1	Homo sapiens	178-180
9518887-7	1998	The presence of des-Arg9(leu8)BK (+2.79 microM indomethacin) resulted in a concentration-related rightward displacement of the concentration-effect curve to des-Arg9-BK.	des-arg9	16-24	kininogen 1	Homo sapiens	30-32
9518887-7	1998	The presence of des-Arg9(leu8)BK (+2.79 microM indomethacin) resulted in a concentration-related rightward displacement of the concentration-effect curve to des-Arg9-BK.	des-arg9	16-24	kininogen 1	Homo sapiens	166-168
9518887-7	1998	The presence of des-Arg9(leu8)BK (+2.79 microM indomethacin) resulted in a concentration-related rightward displacement of the concentration-effect curve to des-Arg9-BK.	Indomethacin	47-59	kininogen 1	Homo sapiens	30-32
9518887-7	1998	The presence of des-Arg9(leu8)BK (+2.79 microM indomethacin) resulted in a concentration-related rightward displacement of the concentration-effect curve to des-Arg9-BK.	Indomethacin	47-59	kininogen 1	Homo sapiens	166-168
9518887-7	1998	The presence of des-Arg9(leu8)BK (+2.79 microM indomethacin) resulted in a concentration-related rightward displacement of the concentration-effect curve to des-Arg9-BK.	des-arg9	157-165	kininogen 1	Homo sapiens	30-32
9518887-7	1998	The presence of des-Arg9(leu8)BK (+2.79 microM indomethacin) resulted in a concentration-related rightward displacement of the concentration-effect curve to des-Arg9-BK.	des-arg9	157-165	kininogen 1	Homo sapiens	166-168
9518887-8	1998	The antagonism of the response to des-Arg9-BK by des-Arg9(leu8)BK was found to be competitive (pA2 = 5.9).	des-arg9	34-42	kininogen 1	Homo sapiens	43-45
9518887-8	1998	The antagonism of the response to des-Arg9-BK by des-Arg9(leu8)BK was found to be competitive (pA2 = 5.9).	des-arg9	34-42	kininogen 1	Homo sapiens	63-65
9802957-2	1998	Significant augmentation of contraction was evident during responses to histamine or LTC4 but responses to EFS, methacholine, bradykinin and capsaicin were not influenced and allergic bronchospasm was significantly impaired by prior exposure to S-salbutamol.	Albuterol	245-257	kininogen 1	Homo sapiens	126-136
9475508-4	1998	ATP, histamine, bradykinin, and serotonin significantly decreased model BBB transendothelial electrical resistance and manipulations which elevate cyclic AMP enhanced culture resistance.	Cyclic AMP	147-157	kininogen 1	Homo sapiens	16-26
9446627-2	1998	These peptides act as broad spectrum neuropeptide antagonists, blocking calcium mobilization induced by gastrin-releasing peptide, bradykinin, cholecystokinin, and other neuropeptides.	Calcium	72-79	kininogen 1	Homo sapiens	131-141
9446564-2	1998	Incubation of [3H]BK at 37 degrees C with cells expressing wild type B2KR resulted in pronounced and rapid ligand internalization ( approximately 80% after 10 min).	Tritium	15-17	kininogen 1	Homo sapiens	18-20
9446564-7	1998	Truncation of the B2KR up to Lys315 almost completely abolished internalization of [3H]BK (10% after 10 min).	Tritium	84-86	kininogen 1	Homo sapiens	87-89
9446564-8	1998	This additional reduction is apparently not caused by the loss of the potential palmitoylation site at Cys324, since a B2KR with a point mutation of Cys324 to Ala internalized [3H]BK as rapidly as the wild type B2KR.	Tritium	177-179	kininogen 1	Homo sapiens	180-182
9830506-0	1998	Bradykinin-induced tyrosine phosphorylation of proteins in cultured human keratinocytes.	Tyrosine	19-27	kininogen 1	Homo sapiens	0-10
9830506-1	1998	The stimulating effect of bradykinin on phosphorylation of proteins at tyrosine residues was visualized on human keratinocytes in primary culture.	Tyrosine	71-79	kininogen 1	Homo sapiens	26-36
9830506-8	1998	After short-time stimulation with bradykinin tyrosine phosphorylation was confined to distinct bands at 82, 76, 70, 57, 54, 48, 40 and 39 kDa and a diffuse band at 62 kDa.	Tyrosine	45-53	kininogen 1	Homo sapiens	34-44
9830506-10	1998	Among these proteins, MAP kinase, actin, paxillin and the EGF receptor were the most likely candidates for bradykinin-induced tyrosine phosphorylation.	Tyrosine	126-134	kininogen 1	Homo sapiens	107-117
9830516-0	1998	Interactions between bradykinin and ANP in rat kidney in vitro: inhibition of natriuresis and modulation of medullary cyclic GMP.	Cyclic GMP	118-128	kininogen 1	Homo sapiens	21-31
9830516-8	1998	Despite this, ANP-induced cGMP production was significantly enhanced by co-incubation with low concentrations of bradykinin (up to 0.1 nM).	Cyclic GMP	26-30	kininogen 1	Homo sapiens	113-123
9830516-11	1998	These results demonstrate that bradykinin counteracts ANP-stimulated sodium and water excretion, by acting directly on the kidney.	Sodium	69-75	kininogen 1	Homo sapiens	31-41
9451632-5	1998	L-NAME also significantly attenuated bradykinin-, but not adenosine-induced increase in macromolecular efflux from the in situ nasal mucosa.	NG-Nitroarginine Methyl Ester	0-6	kininogen 1	Homo sapiens	37-47
9505142-5	1998	The upregulation of IL-6 production induced by BK was abolished by the anti-inflammatory agent dexamethasone (DEX) and the phospholipase A2 (PLA2) inhibitor 4-bromphenacyl bromide (BPB).	Dexamethasone	95-108	kininogen 1	Homo sapiens	47-49
9505142-5	1998	The upregulation of IL-6 production induced by BK was abolished by the anti-inflammatory agent dexamethasone (DEX) and the phospholipase A2 (PLA2) inhibitor 4-bromphenacyl bromide (BPB).	Dexamethasone	110-113	kininogen 1	Homo sapiens	47-49
9505142-5	1998	The upregulation of IL-6 production induced by BK was abolished by the anti-inflammatory agent dexamethasone (DEX) and the phospholipase A2 (PLA2) inhibitor 4-bromphenacyl bromide (BPB).	4-bromphenacyl bromide	157-179	kininogen 1	Homo sapiens	47-49
9505142-5	1998	The upregulation of IL-6 production induced by BK was abolished by the anti-inflammatory agent dexamethasone (DEX) and the phospholipase A2 (PLA2) inhibitor 4-bromphenacyl bromide (BPB).	bpb	181-184	kininogen 1	Homo sapiens	47-49
9505142-6	1998	Treatment of the cells with the cyclooxygenase (COX) inhibitor flurbiprofen resulted in a minor reduction of the stimulatory effect of BK.	Flurbiprofen	63-75	kininogen 1	Homo sapiens	135-137
9453327-1	1998	In the present study we tested the hypothesis whether an angiotensin AT2 receptor-mediated stimulation of the bradykinin (BK)/nitric oxide (NO) system can account for the effects of AT1 receptor antagonism on aortic cGMP described previously in SHRSP.	Nitric Oxide	126-138	kininogen 1	Homo sapiens	110-120
9453327-1	1998	In the present study we tested the hypothesis whether an angiotensin AT2 receptor-mediated stimulation of the bradykinin (BK)/nitric oxide (NO) system can account for the effects of AT1 receptor antagonism on aortic cGMP described previously in SHRSP.	Nitric Oxide	126-138	kininogen 1	Homo sapiens	122-124
9453327-1	1998	In the present study we tested the hypothesis whether an angiotensin AT2 receptor-mediated stimulation of the bradykinin (BK)/nitric oxide (NO) system can account for the effects of AT1 receptor antagonism on aortic cGMP described previously in SHRSP.	Cyclic GMP	216-220	kininogen 1	Homo sapiens	110-120
9453327-1	1998	In the present study we tested the hypothesis whether an angiotensin AT2 receptor-mediated stimulation of the bradykinin (BK)/nitric oxide (NO) system can account for the effects of AT1 receptor antagonism on aortic cGMP described previously in SHRSP.	Cyclic GMP	216-220	kininogen 1	Homo sapiens	122-124
9605596-8	1998	ACE inhibitors diminish transformation of angiotensin I (Ang I) into angiotensin II (Ang II) and prevent degradation of bradykinin [which stimulates nitric oxide (NO) and prostacyclin formation].	Nitric Oxide	149-161	kininogen 1	Homo sapiens	120-130
9605596-8	1998	ACE inhibitors diminish transformation of angiotensin I (Ang I) into angiotensin II (Ang II) and prevent degradation of bradykinin [which stimulates nitric oxide (NO) and prostacyclin formation].	Epoprostenol	171-183	kininogen 1	Homo sapiens	120-130
9481676-17	1998	Treatment with 10 mumol-1 nocodazole caused the SER to collapse and unmasked Ca2+ release in response to 1 nmol l-1 Bk and 10 mmol l-1 NaF, similar to low-Na+ conditions, while the effect of thapsigargin was not changed.	Nocodazole	26-36	kininogen 1	Homo sapiens	116-118
9481676-12	1998	Thereby, NaF depleted Bk-releasable Ca2+ pools, while mitochondrial Ca2+ content (released with FCCP or oligomycin) and the amount of Ca2+ stored within the cells (released with ionomycin) was increased compared with cells treated with NaF under normal Na+ conditions.	Sodium Fluoride	9-12	kininogen 1	Homo sapiens	22-24
9481676-13	1998	The NaF-initiated increase in [Ca2+]b and depletion of Bk-releasable Ca2+ pool(s) in the low-Na+ condition was diminished by 25 mumol l-1 ryanodine, indicating the involvement of Ca(2+)-induced Ca2+ release (CICR).	Sodium Fluoride	4-7	kininogen 1	Homo sapiens	55-57
9481676-13	1998	The NaF-initiated increase in [Ca2+]b and depletion of Bk-releasable Ca2+ pool(s) in the low-Na+ condition was diminished by 25 mumol l-1 ryanodine, indicating the involvement of Ca(2+)-induced Ca2+ release (CICR).	cicr	208-212	kininogen 1	Homo sapiens	55-57
9481676-15	1998	In simultaneous recordings of [Ca2+]sp (with FFP-18) and [Ca2+]b (with Calcium Green-1), 1 nmol l-1 Bk or 10 mmol l-1 NaF yielded focal [Ca2+] elevation in the subplasmalemmal region with no increase in the perinuclear area.	ca2+]sp	31-38	kininogen 1	Homo sapiens	100-102
9651119-0	1998	Characterization of bradykinin receptors in human lung fibroblasts using the binding of 3[H][Des-Arg10,Leu9]kallidin and [3H]NPC17731.	des-arg10	93-102	kininogen 1	Homo sapiens	20-30
9651119-0	1998	Characterization of bradykinin receptors in human lung fibroblasts using the binding of 3[H][Des-Arg10,Leu9]kallidin and [3H]NPC17731.	Tritium	122-124	kininogen 1	Homo sapiens	20-30
9680670-0	1998	[Effect of anti-atherosclerotic diet with polyunsaturated fatty acids omega-3 from linseed oil on dynamics of natural antibodies to bradykinin and angiotensin II in blood serum of patients with cardiovascular diseases].	Fatty Acids, Unsaturated	42-69	kininogen 1	Homo sapiens	132-142
9680670-0	1998	[Effect of anti-atherosclerotic diet with polyunsaturated fatty acids omega-3 from linseed oil on dynamics of natural antibodies to bradykinin and angiotensin II in blood serum of patients with cardiovascular diseases].	omega-3	70-77	kininogen 1	Homo sapiens	132-142
9680670-0	1998	[Effect of anti-atherosclerotic diet with polyunsaturated fatty acids omega-3 from linseed oil on dynamics of natural antibodies to bradykinin and angiotensin II in blood serum of patients with cardiovascular diseases].	Linseed Oil	83-94	kininogen 1	Homo sapiens	132-142
9680670-2	1998	Besides favorable influence to a clinical picture of the disease universal normalizing influence of antiatherosclerotic diet with addition of linseed oil, consisting in increase of lowered levels of natural antibodies against bradykinin and angiotensin II and decrease of their contents in blood serum under primary increased concentrations.	Linseed Oil	142-153	kininogen 1	Homo sapiens	226-236
9622017-3	1998	The primary structure of sturgeon bradykinin was established as Met-Pro-Pro-Gly-Met-Ser-Pro-Phe-Arg.	Met-Pro-Pro-Gly-Met-Ser-Pro-Phe-Arg	64-99	kininogen 1	Homo sapiens	34-44
9622017-7	1998	Sturgeon bradykinin produced a strong and concentration-dependent (EC50 = 4.7 +/- 0.7 x 10(-10) M) relaxation of rings of vascular tissue from the sturgeon ventral aorta that had been pre-contracted with acetylcholine.	Acetylcholine	204-217	kininogen 1	Homo sapiens	9-19
9481676-17	1998	Treatment with 10 mumol-1 nocodazole caused the SER to collapse and unmasked Ca2+ release in response to 1 nmol l-1 Bk and 10 mmol l-1 NaF, similar to low-Na+ conditions, while the effect of thapsigargin was not changed.	Serine	48-51	kininogen 1	Homo sapiens	116-118
9371732-0	1997	Bradykinin stimulates cAMP synthesis via mitogen-activated protein kinase-dependent regulation of cytosolic phospholipase A2 and prostaglandin E2 release in airway smooth muscle.	Cyclic AMP	22-26	kininogen 1	Homo sapiens	0-10
9371732-0	1997	Bradykinin stimulates cAMP synthesis via mitogen-activated protein kinase-dependent regulation of cytosolic phospholipase A2 and prostaglandin E2 release in airway smooth muscle.	Dinoprostone	129-145	kininogen 1	Homo sapiens	0-10
9371732-1	1997	Bradykinin stimulates cAMP synthesis in cultured airway smooth muscle (ASM) cells.	Cyclic AMP	22-26	kininogen 1	Homo sapiens	0-10
9421294-5	1997	[3H]-BK, a full agonist labelled ligand, was used to demonstrate a single binding site giving a Kd value of 0.51+/-0.02 nM and a Bmax of 24+/-1 fmol mg(-1) protein.	Tritium	1-4	kininogen 1	Homo sapiens	5-7
9435567-0	1997	PGE2 release by bradykinin in human airway smooth muscle cells: involvement of cyclooxygenase-2 induction.	Dinoprostone	0-4	kininogen 1	Homo sapiens	16-26
9435567-1	1997	Prostanoids may be involved in bradykinin (BK)-induced bronchoconstriction in asthma.	Prostaglandins	0-11	kininogen 1	Homo sapiens	31-41
9435567-1	1997	Prostanoids may be involved in bradykinin (BK)-induced bronchoconstriction in asthma.	Prostaglandins	0-11	kininogen 1	Homo sapiens	43-45
9435567-2	1997	We investigated whether cyclooxygenase (COX)-2 induction was involved in prostaglandin (PG) E2 release by BK in cultured human airway smooth muscle (ASM) cells and analyzed the BK receptor subtypes responsible.	Dinoprostone	73-94	kininogen 1	Homo sapiens	106-108
9435567-3	1997	BK stimulated PGE2 release, COX activity, and COX-2 induction in a concentration- and time-dependent manner.	Dinoprostone	14-18	kininogen 1	Homo sapiens	0-2
9435567-5	1997	In short-term (15-min) experiments, BK stimulated PGE2 generation but did not increase COX activity or induce COX-2.	Dinoprostone	50-54	kininogen 1	Homo sapiens	36-38
9435567-6	1997	In long-term (4-h) experiments, BK enhanced PGE2 release and COX activity and induced COX-2.	Dinoprostone	44-48	kininogen 1	Homo sapiens	32-34
9435567-8	1997	The effects of BK were mimicked by the B2-receptor agonist [Tyr(Me)8]BK, whereas the B1 agonist des-Arg9-BK was weakly effective at high concentrations.	tyr(me)8	60-68	kininogen 1	Homo sapiens	15-17
9435567-8	1997	The effects of BK were mimicked by the B2-receptor agonist [Tyr(Me)8]BK, whereas the B1 agonist des-Arg9-BK was weakly effective at high concentrations.	tyr(me)8	60-68	kininogen 1	Homo sapiens	69-71
9435567-8	1997	The effects of BK were mimicked by the B2-receptor agonist [Tyr(Me)8]BK, whereas the B1 agonist des-Arg9-BK was weakly effective at high concentrations.	tyr(me)8	60-68	kininogen 1	Homo sapiens	69-71
9406662-9	1997	Endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation to A23187, bradykinin, and substance P in the presence of either U46619 (10 nmol/L)- or K+ (25 mmol/L)-induced contraction was reduced after exposure to either 20 or 50 mmol/L K+.	endothelium-derived hyperpolarizing factor	0-42	kininogen 1	Homo sapiens	81-91
9406662-9	1997	Endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation to A23187, bradykinin, and substance P in the presence of either U46619 (10 nmol/L)- or K+ (25 mmol/L)-induced contraction was reduced after exposure to either 20 or 50 mmol/L K+.	edhf	44-48	kininogen 1	Homo sapiens	81-91
9406672-7	1997	A reduction in the bradykinin-elicited response was observed in NG-nitro-L-arginine methyl ester (L-NAME; 300 mumol/L)- and ouabain (50 mumol/L)-treated rings.	NG-Nitroarginine Methyl Ester	64-96	kininogen 1	Homo sapiens	19-29
9406672-7	1997	A reduction in the bradykinin-elicited response was observed in NG-nitro-L-arginine methyl ester (L-NAME; 300 mumol/L)- and ouabain (50 mumol/L)-treated rings.	NG-Nitroarginine Methyl Ester	98-104	kininogen 1	Homo sapiens	19-29
9406672-7	1997	A reduction in the bradykinin-elicited response was observed in NG-nitro-L-arginine methyl ester (L-NAME; 300 mumol/L)- and ouabain (50 mumol/L)-treated rings.	Ouabain	124-131	kininogen 1	Homo sapiens	19-29
9403589-3	1997	In porcine coronary artery segments, brefeldin A (35 micromol/L, 90 minutes) did not affect relaxations to sodium nitroprusside or the K+ channel opener cromakalim but elicited a rightward shift in the concentration-response curve to bradykinin without altering the maximum vasodilator response (Rmax).	Brefeldin A	37-48	kininogen 1	Homo sapiens	234-244
9403589-6	1997	The microtubule destabilizer nocodazole also affected both the EC50 and Rmax to bradykinin in porcine coronary arteries.	Nocodazole	29-39	kininogen 1	Homo sapiens	80-90
9403590-7	1997	In essential hypertensive patients, oral treatment with lacidipine increased forearm vasodilation in response to acetylcholine and bradykinin, suggesting that this drug can improve endothelial function in patients with essential hypertension.	lacidipine	56-66	kininogen 1	Homo sapiens	131-141
9423284-1	1997	Modification of arginine residues in bradykinin, [1-5]-bradykinin, splenopentin and two synthetic pentapeptides with acetylacetone (pentane-2,4-dione) significantly increases the relative abundance of sequence-specific fragment ions produced by matrix-assisted laser desorption/ionization (MALDI).	Arginine	16-24	kininogen 1	Homo sapiens	37-47
9423284-1	1997	Modification of arginine residues in bradykinin, [1-5]-bradykinin, splenopentin and two synthetic pentapeptides with acetylacetone (pentane-2,4-dione) significantly increases the relative abundance of sequence-specific fragment ions produced by matrix-assisted laser desorption/ionization (MALDI).	Arginine	16-24	kininogen 1	Homo sapiens	55-65
9423284-1	1997	Modification of arginine residues in bradykinin, [1-5]-bradykinin, splenopentin and two synthetic pentapeptides with acetylacetone (pentane-2,4-dione) significantly increases the relative abundance of sequence-specific fragment ions produced by matrix-assisted laser desorption/ionization (MALDI).	acetylacetone	117-130	kininogen 1	Homo sapiens	37-47
9423284-1	1997	Modification of arginine residues in bradykinin, [1-5]-bradykinin, splenopentin and two synthetic pentapeptides with acetylacetone (pentane-2,4-dione) significantly increases the relative abundance of sequence-specific fragment ions produced by matrix-assisted laser desorption/ionization (MALDI).	acetylacetone	132-149	kininogen 1	Homo sapiens	37-47
9423284-1	1997	Modification of arginine residues in bradykinin, [1-5]-bradykinin, splenopentin and two synthetic pentapeptides with acetylacetone (pentane-2,4-dione) significantly increases the relative abundance of sequence-specific fragment ions produced by matrix-assisted laser desorption/ionization (MALDI).	acetylacetone	132-149	kininogen 1	Homo sapiens	55-65
9469643-8	1997	In addition, M-5011 inhibited [14C]AA release from prelabeled synovial cells stimulated with bradykinin.	2-(4-(3-methyl-2-thienyl)phenyl)propionic acid	13-19	kininogen 1	Homo sapiens	93-103
9469643-8	1997	In addition, M-5011 inhibited [14C]AA release from prelabeled synovial cells stimulated with bradykinin.	Carbon-14	31-34	kininogen 1	Homo sapiens	93-103
9374762-5	1997	Enalaprilat, an ACE inhibitor, significantly prevented the rapid degradation of BK and des-Arg9-BK in all species studied, whereas retrothiorphan, a neutral endopeptidase inhibitor, and losartan, an angiotensin II type I receptor antagonist, did not affect this metabolism.	Enalaprilat	0-11	kininogen 1	Homo sapiens	80-82
9374762-5	1997	Enalaprilat, an ACE inhibitor, significantly prevented the rapid degradation of BK and des-Arg9-BK in all species studied, whereas retrothiorphan, a neutral endopeptidase inhibitor, and losartan, an angiotensin II type I receptor antagonist, did not affect this metabolism.	Enalaprilat	0-11	kininogen 1	Homo sapiens	96-98
9815580-6	1997	CAI also caused a generalized attenuation of receptor-mediated calcium elevation to several calcium mobilization agonists, including epidermal growth factor and bradykinin.	carboxyamido-triazole	0-3	kininogen 1	Homo sapiens	161-171
9415011-0	1997	Bradykinin induced dilatation of human epicardial and resistance coronary arteries in vivo: effect of inhibition of nitric oxide synthesis.	Nitric Oxide	116-128	kininogen 1	Homo sapiens	0-10
9415011-1	1997	OBJECTIVE: To clarify whether endothelium derived nitric oxide contributes to exogenous bradykinin induced dilatation of human epicardial and resistance coronary arteries in vivo.	Nitric Oxide	50-62	kininogen 1	Homo sapiens	88-98
9415011-2	1997	DESIGN: Quantitative coronary angiography and Doppler flow velocity measurements were used to determine the effects of the nitric oxide synthesis inhibitor, NG-monomethyl-L-arginine (L-NMMA), on bradykinin induced dilatation of the epicardial and resistance coronary arteries.	omega-N-Methylarginine	157-181	kininogen 1	Homo sapiens	195-205
9415011-2	1997	DESIGN: Quantitative coronary angiography and Doppler flow velocity measurements were used to determine the effects of the nitric oxide synthesis inhibitor, NG-monomethyl-L-arginine (L-NMMA), on bradykinin induced dilatation of the epicardial and resistance coronary arteries.	omega-N-Methylarginine	183-189	kininogen 1	Homo sapiens	195-205
9415011-7	1997	RESULTS: Bradykinin-induced epicardial coronary vasodilatation after L-NMMA (dilatation by 2.5 micrograms/min, 3.8(1.4)% in the proximal and 5.9(1.8)% in the distal segments, mean (SEM)) was less (p &lt; 0.001, respectively) than before L-NMMA (11.7(2.5)% and 15.1(2.0)%, respectively).	omega-N-Methylarginine	69-75	kininogen 1	Homo sapiens	9-19
9415011-7	1997	RESULTS: Bradykinin-induced epicardial coronary vasodilatation after L-NMMA (dilatation by 2.5 micrograms/min, 3.8(1.4)% in the proximal and 5.9(1.8)% in the distal segments, mean (SEM)) was less (p &lt; 0.001, respectively) than before L-NMMA (11.7(2.5)% and 15.1(2.0)%, respectively).	omega-N-Methylarginine	237-243	kininogen 1	Homo sapiens	9-19
9415011-9	1997	CONCLUSIONS: Endothelium derived nitric oxide contributes to bradykinin induced dilatation of epicardial coronary arteries, but may be less important in coronary resistance vasodilatation.	Nitric Oxide	33-45	kininogen 1	Homo sapiens	61-71
9435680-5	1997	In the present study, we utilized immunofluorescence, immunoprecipitation, and immunoblotting techniques to identify substrates that are tyrosine phosphorylated in response to bradykinin action in mesangial cells.	Tyrosine	137-145	kininogen 1	Homo sapiens	176-186
9435680-6	1997	Immunofluorescence microscopy of mesangial cells stained with anti-phosphotyrosine (anti-PY) antibodies following bradykinin treatment (10(-9)-10(-6) M) revealed a dose-dependent increase in the labeling of cytoplasmic and nuclear proteins.	Phosphotyrosine	67-82	kininogen 1	Homo sapiens	114-124
9435680-7	1997	Immunoprecipitation with anti-PY, followed by immunoblot revealed bradykinin-induced tyrosyl phosphorylation of tubulin and mitogen-activated protein kinase (MAPK).	cyclo(tyrosyl-tyrosyl)	85-92	kininogen 1	Homo sapiens	66-76
9435680-8	1997	Confocal microscopy of mesangial cells stained for MAPK indicated that bradykinin stimulation resulted in translocation of MAPK from the cytoplasm to the nucleus by 2 h. These data demonstrate that bradykinin action results in the tyrosine phosphorylation of cellular proteins in mesangial cells and suggest a role for tubulin and MAPK in the signaling cascade of bradykinin leading to altered mesangial function.	Tyrosine	231-239	kininogen 1	Homo sapiens	71-81
9435680-8	1997	Confocal microscopy of mesangial cells stained for MAPK indicated that bradykinin stimulation resulted in translocation of MAPK from the cytoplasm to the nucleus by 2 h. These data demonstrate that bradykinin action results in the tyrosine phosphorylation of cellular proteins in mesangial cells and suggest a role for tubulin and MAPK in the signaling cascade of bradykinin leading to altered mesangial function.	Tyrosine	231-239	kininogen 1	Homo sapiens	198-208
9435680-8	1997	Confocal microscopy of mesangial cells stained for MAPK indicated that bradykinin stimulation resulted in translocation of MAPK from the cytoplasm to the nucleus by 2 h. These data demonstrate that bradykinin action results in the tyrosine phosphorylation of cellular proteins in mesangial cells and suggest a role for tubulin and MAPK in the signaling cascade of bradykinin leading to altered mesangial function.	Tyrosine	231-239	kininogen 1	Homo sapiens	198-208
9449805-5	1997	The most active peptides show a general structure of Pro-aromatic-Pro, and this pattern resembled the motif displayed by bradykinin-potentiating peptides found in snake venoms.	pro-aromatic-pro	53-69	kininogen 1	Homo sapiens	121-131
9412868-4	1997	The tyrosine kinase inhibitors genistein and herbimycin A attenuated not only Ca2+ influx but also Mn2+ influx from the extracellular space without affecting the release of Ca2+ from internal stores in bradykinin-treated cells.	Genistein	31-40	kininogen 1	Homo sapiens	202-212
9412868-4	1997	The tyrosine kinase inhibitors genistein and herbimycin A attenuated not only Ca2+ influx but also Mn2+ influx from the extracellular space without affecting the release of Ca2+ from internal stores in bradykinin-treated cells.	herbimycin	45-57	kininogen 1	Homo sapiens	202-212
9434142-7	1997	Stimulation of 3H-AA release by EGF (10 nM), IL-1beta (1 ng ml-1) and bradykinin (100 nM) was unaffected by these concentrations of tamoxifen.	3h-aa	15-20	kininogen 1	Homo sapiens	70-80
9374730-3	1997	In human ASM cells loaded with fura 2, TNF-alpha and interleukin (IL)-1 beta significantly enhanced thrombin- and bradykinin-evoked elevations of intracellular Ca2+.	Fura-2	31-37	kininogen 1	Homo sapiens	114-124
9374730-9	1997	We also found that TNF-alpha significantly enhanced increases in phosphoinositide (PI) accumulation induced by bradykinin.	Phosphatidylinositols	65-81	kininogen 1	Homo sapiens	111-121
9383175-1	1997	OBJECTIVE: To investigate the role of angiotensin converting enzyme (ACE) inhibition in bradykinin-mediated modulation of noradrenaline release in human and rat atrium.	Norepinephrine	122-135	kininogen 1	Homo sapiens	88-98
9383175-5	1997	In contrast, 0.001-0.1 micromol/l bradykinin enhanced the release of noradrenaline in rat atrium.	Norepinephrine	69-82	kininogen 1	Homo sapiens	34-44
9383175-6	1997	In the presence of 3 micromol/l of the ACE inhibitor captopril, however, bradykinin significantly enhanced the release of noradrenaline in human atrium.	Captopril	53-62	kininogen 1	Homo sapiens	73-83
9383175-6	1997	In the presence of 3 micromol/l of the ACE inhibitor captopril, however, bradykinin significantly enhanced the release of noradrenaline in human atrium.	Norepinephrine	122-135	kininogen 1	Homo sapiens	73-83
9383175-8	1997	Captopril (3 micromol/l) potentiated the facilitatory effect of bradykinin in rat atrium.	Captopril	0-9	kininogen 1	Homo sapiens	64-74
10225731-1	1997	The negative charges of dextran-sulfate (DS) used for low-density lipoprotein (LDL) apheresis activates the intrinsic coagulation pathway, in which plasma kallikrein acts on high-molecular-weight kininogen (HMWK) to produce large amounts of bradykinin.	Dextran Sulfate	24-39	kininogen 1	Homo sapiens	174-205
10225731-1	1997	The negative charges of dextran-sulfate (DS) used for low-density lipoprotein (LDL) apheresis activates the intrinsic coagulation pathway, in which plasma kallikrein acts on high-molecular-weight kininogen (HMWK) to produce large amounts of bradykinin.	Dextran Sulfate	24-39	kininogen 1	Homo sapiens	207-211
10225731-1	1997	The negative charges of dextran-sulfate (DS) used for low-density lipoprotein (LDL) apheresis activates the intrinsic coagulation pathway, in which plasma kallikrein acts on high-molecular-weight kininogen (HMWK) to produce large amounts of bradykinin.	Dextran Sulfate	24-39	kininogen 1	Homo sapiens	241-251
10225731-1	1997	The negative charges of dextran-sulfate (DS) used for low-density lipoprotein (LDL) apheresis activates the intrinsic coagulation pathway, in which plasma kallikrein acts on high-molecular-weight kininogen (HMWK) to produce large amounts of bradykinin.	Dextran Sulfate	41-43	kininogen 1	Homo sapiens	174-205
10225731-1	1997	The negative charges of dextran-sulfate (DS) used for low-density lipoprotein (LDL) apheresis activates the intrinsic coagulation pathway, in which plasma kallikrein acts on high-molecular-weight kininogen (HMWK) to produce large amounts of bradykinin.	Dextran Sulfate	41-43	kininogen 1	Homo sapiens	207-211
10225731-1	1997	The negative charges of dextran-sulfate (DS) used for low-density lipoprotein (LDL) apheresis activates the intrinsic coagulation pathway, in which plasma kallikrein acts on high-molecular-weight kininogen (HMWK) to produce large amounts of bradykinin.	Dextran Sulfate	41-43	kininogen 1	Homo sapiens	241-251
10225731-5	1997	During apheresis using heparin, the marked increase in bradykinin levels (before apheresis, 18 +/- 3 (mean +/- SE, n = 5) pg/ml; after apheresis 470 +/- 140, p &lt; 0.01) was associated with the increase in NOx (before apheresis 50 +/- 11 pg/ml; after apheresis 66 +/- 15).	Heparin	23-30	kininogen 1	Homo sapiens	55-65
10225731-5	1997	During apheresis using heparin, the marked increase in bradykinin levels (before apheresis, 18 +/- 3 (mean +/- SE, n = 5) pg/ml; after apheresis 470 +/- 140, p &lt; 0.01) was associated with the increase in NOx (before apheresis 50 +/- 11 pg/ml; after apheresis 66 +/- 15).	nox	207-210	kininogen 1	Homo sapiens	55-65
9403589-4	1997	Brefeldin A failed to attenuate the bradykinin-induced, NO-mediated relaxation under depolarizing conditions but inhibited the bradykinin response under conditions of combined cyclooxygenase/NO synthase blockade, suggesting that this agent selectively interferes with the production of EDHF.	Brefeldin A	0-11	kininogen 1	Homo sapiens	127-137
9376123-1	1997	Tracheal epithelial cells and skin fibroblasts from different cystic fibrosis (CF) patients bearing the deltaF508 mutation of cystic fibrosis transmembrane conductance regulator (CFTR) released more arachidonic acid in response to bradykinin than do other CF and normal cells.	Arachidonic Acid	199-215	kininogen 1	Homo sapiens	231-241
9376123-4	1997	The expression of G alpha(q)/11 protein was also increased in deltaF508 cells, with increased stimulation of phosphatidylinositol diphosphate-specific phospholipase C (PLC) by bradykinin, and an early, transient activation of mitogen-activated protein (MAP) kinase.	phosphatidylinositol diphosphate	109-141	kininogen 1	Homo sapiens	176-186
9376123-6	1997	Comparison of the effects of bradykinin to those observed with thapsigargin, an inhibitor of calcium reuptake, suggests that the increase of intracellular calcium is not the only mechanism involved in arachidonic acid release by bradykinin in deltaF508 cells.	Calcium	155-162	kininogen 1	Homo sapiens	29-39
9376123-8	1997	The binding of cPLA2 to membranes after bradykinin stimulation still occurred in CFT2 cells (deltaF508) homogenized in EDTA, suggesting that a membrane component plus increased intracellular calcium influenced cPLA2 anchoring to membranes.	Calcium	191-198	kininogen 1	Homo sapiens	40-50
9376123-9	1997	The defective processing of deltaF508 CFTR seems to increase cPLA2 stimulation by bradykinin, since the bradykinin-stimulated release of arachidonic acid is reversed by growing cells at 28 degrees C for 48 h. The deltaF508 mutation of CFTR appears to increase the stimulation of cPLA2 by Gq-mediated receptors in a PKC-independent and MAP kinase-dependent manner.	Arachidonic Acid	137-153	kininogen 1	Homo sapiens	104-114
9335366-7	1997	We concluded that the SP circuit is superior to the RC one because of the lesser production of BK and thus lesser fluctuation of perfusion pressure.	sp	22-24	kininogen 1	Homo sapiens	95-97
9350335-4	1997	In a competitive binding inhibition assay using neutrophil and PBMC glycerol purified plasma membranes, high affinity binding in the nanomolar range was detected to Lys-BK and BK but with [des-arg9]-BK a 10-100 fold lower order affinity was observed this being indicative of pharmacologically defined B2 characteristics.	Glycerol	68-76	kininogen 1	Homo sapiens	169-171
9350335-4	1997	In a competitive binding inhibition assay using neutrophil and PBMC glycerol purified plasma membranes, high affinity binding in the nanomolar range was detected to Lys-BK and BK but with [des-arg9]-BK a 10-100 fold lower order affinity was observed this being indicative of pharmacologically defined B2 characteristics.	Glycerol	68-76	kininogen 1	Homo sapiens	176-178
9350335-4	1997	In a competitive binding inhibition assay using neutrophil and PBMC glycerol purified plasma membranes, high affinity binding in the nanomolar range was detected to Lys-BK and BK but with [des-arg9]-BK a 10-100 fold lower order affinity was observed this being indicative of pharmacologically defined B2 characteristics.	Glycerol	68-76	kininogen 1	Homo sapiens	176-178
9336392-2	1997	In particular, recently developed ACE inhibitors with tissue-penetrating properties, such as quinaprilat, may exert vascular effects via the bradykinin B2-receptor.	quinaprilat	93-104	kininogen 1	Homo sapiens	141-151
9275066-4	1997	However, ATP and bradykinin increased concentrations of inositol phosphates in both thyroid carcinoma cell lines.	Inositol Phosphates	56-75	kininogen 1	Homo sapiens	17-27
9338651-5	1997	EDHF-mediated relaxation was induced by bradykinin and the calcium ionophore A23187 with the presence of indomethacin (7 micromol/L; INN: indometacin), a cyclooxygenase inhibitor, and N(G)-nitro-L-arginine (300 micromol), a nitric oxide biosynthesis inhibitor in U46619 (30 nmol/L)-induced precontraction.	edhf	0-4	kininogen 1	Homo sapiens	40-50
9338651-7	1997	RESULTS: EDHF-mediated relaxation was significantly impaired in either A23187 or bradykinin studies (80.1% +/- 7.5% vs 24.9% +/- 14.2%, p = 0.004, n = 8 in each group for A23187, and 71.4% +/- 4.7%, n = 13, vs 40.5% +/- 12.9%, n = 7, p = 0.01, for bradykinin).	edhf	9-13	kininogen 1	Homo sapiens	81-91
9338651-7	1997	RESULTS: EDHF-mediated relaxation was significantly impaired in either A23187 or bradykinin studies (80.1% +/- 7.5% vs 24.9% +/- 14.2%, p = 0.004, n = 8 in each group for A23187, and 71.4% +/- 4.7%, n = 13, vs 40.5% +/- 12.9%, n = 7, p = 0.01, for bradykinin).	edhf	9-13	kininogen 1	Homo sapiens	248-258
9338651-7	1997	RESULTS: EDHF-mediated relaxation was significantly impaired in either A23187 or bradykinin studies (80.1% +/- 7.5% vs 24.9% +/- 14.2%, p = 0.004, n = 8 in each group for A23187, and 71.4% +/- 4.7%, n = 13, vs 40.5% +/- 12.9%, n = 7, p = 0.01, for bradykinin).	Calcimycin	171-177	kininogen 1	Homo sapiens	81-91
9338651-9	1997	In contrast, in aprikalim-treated arteries, the EDHF-mediated relaxation induced by either A23187 or bradykinin was unchanged.	edhf	48-52	kininogen 1	Homo sapiens	101-111
9315582-7	1997	However, bradykinin-induced dilation was significantly greater in segments exhibiting acetylcholine-induced vasodilation than in those exhibiting vasoconstriction (p &lt;0.01 in the proximal portion and p &lt;0.02 in the distal portion).	Acetylcholine	86-99	kininogen 1	Homo sapiens	9-19
9330433-5	1997	The BK level in mannitol-containing MAP solutions, but not that in mannitol-free MAP solution, saline or whole blood, increased during storage.	Mannitol	16-24	kininogen 1	Homo sapiens	4-6
9330433-7	1997	These findings suggest that mannitol plays an essential role in the increase in BK level in RC-MAP.	Mannitol	28-36	kininogen 1	Homo sapiens	80-82
9332450-0	1997	Prostaglandin E2 enhances type 2-bradykinin receptor expression in human glomerular podocytes.	Dinoprostone	0-16	kininogen 1	Homo sapiens	33-43
9332450-1	1997	We examined the effect of prostaglandin E2 (PGE2) on bradykinin (BK) binding, BK-dependent intracellular calcium and inositol phosphate (i.p.)	Calcium	105-112	kininogen 1	Homo sapiens	78-80
9332450-3	1997	PGE2 (10 nM) produced a concentration-dependent increase in [3H]-BK specific binding after a lag time of 24 h with a threshold at 0.1 nM.	Dinoprostone	0-4	kininogen 1	Homo sapiens	65-67
9332450-3	1997	PGE2 (10 nM) produced a concentration-dependent increase in [3H]-BK specific binding after a lag time of 24 h with a threshold at 0.1 nM.	Tritium	61-63	kininogen 1	Homo sapiens	65-67
9316414-2	1997	Sphingosine inhibited PKC activity in an isolated airway smooth muscle cell lysate and prevented the activation of mitogen-activated protein kinase (MAPK) by platelet-derived growth factor, bradykinin, and phorbol 12-myristate 13-acetate in intact cells.	Sphingosine	0-11	kininogen 1	Homo sapiens	190-200
9268696-1	1997	In HaCaT keratinocytes bradykinin-triggered actin reorganization was inhibited by quinacrine, a phospholipase A2 inhibitor, and restored by addition of arachidonic acid.	Quinacrine	82-92	kininogen 1	Homo sapiens	23-33
9383175-9	1997	The selective bradykinin B2-receptor antagonist D-Arg[Hyp3,Thi5, D-Tic7,Oic8]-bradykinin (Hoe 140, 0.3 micromol/l) and the cyclo-oxygenase inhibitor indomethacin (10 micromol/l) reduced the facilitatory effect of bradykinin significantly in the presence of captopril in rat and human atrium.	D-Arginine	48-53	kininogen 1	Homo sapiens	14-24
9383175-9	1997	The selective bradykinin B2-receptor antagonist D-Arg[Hyp3,Thi5, D-Tic7,Oic8]-bradykinin (Hoe 140, 0.3 micromol/l) and the cyclo-oxygenase inhibitor indomethacin (10 micromol/l) reduced the facilitatory effect of bradykinin significantly in the presence of captopril in rat and human atrium.	D-Arginine	48-53	kininogen 1	Homo sapiens	78-88
9383175-9	1997	The selective bradykinin B2-receptor antagonist D-Arg[Hyp3,Thi5, D-Tic7,Oic8]-bradykinin (Hoe 140, 0.3 micromol/l) and the cyclo-oxygenase inhibitor indomethacin (10 micromol/l) reduced the facilitatory effect of bradykinin significantly in the presence of captopril in rat and human atrium.	D-Arginine	48-53	kininogen 1	Homo sapiens	78-88
9383175-11	1997	CONCLUSION: These data suggest that bradykinin facilitates the release of noradrenaline in human and rat atrium by activation of bradykinin receptors of the B2-subtype and subsequent release of facilitatory prostaglandins.	Norepinephrine	74-87	kininogen 1	Homo sapiens	36-46
9383175-11	1997	CONCLUSION: These data suggest that bradykinin facilitates the release of noradrenaline in human and rat atrium by activation of bradykinin receptors of the B2-subtype and subsequent release of facilitatory prostaglandins.	Norepinephrine	74-87	kininogen 1	Homo sapiens	129-139
9383175-11	1997	CONCLUSION: These data suggest that bradykinin facilitates the release of noradrenaline in human and rat atrium by activation of bradykinin receptors of the B2-subtype and subsequent release of facilitatory prostaglandins.	Prostaglandins	207-221	kininogen 1	Homo sapiens	36-46
9316832-6	1997	Nimodipine (1 microM), a voltage-dependent Ca++ channel blocker, abolished the BK-induced sustained Ca++ phase and inhibited BK-induced insulin release.	Nimodipine	0-10	kininogen 1	Homo sapiens	79-81
9316832-8	1997	Both the BK-induced insulin secretion and rise in [Ca++]i were inhibited by a selective BK2 receptor antagonist, HOE 140 (3.3-100 nM), in concentration-dependent manners but were not by a BK1 receptor antagonist des-Arg9,Leu8-BK (1 microM).	4-hydroxy-2-octenal	113-116	kininogen 1	Homo sapiens	9-11
9316832-8	1997	Both the BK-induced insulin secretion and rise in [Ca++]i were inhibited by a selective BK2 receptor antagonist, HOE 140 (3.3-100 nM), in concentration-dependent manners but were not by a BK1 receptor antagonist des-Arg9,Leu8-BK (1 microM).	des-arg9	212-220	kininogen 1	Homo sapiens	9-11
9316832-8	1997	Both the BK-induced insulin secretion and rise in [Ca++]i were inhibited by a selective BK2 receptor antagonist, HOE 140 (3.3-100 nM), in concentration-dependent manners but were not by a BK1 receptor antagonist des-Arg9,Leu8-BK (1 microM).	leu8-bk	221-228	kininogen 1	Homo sapiens	9-11
9316832-10	1997	U-73122 (4, 6 and 8 microM), a phospholipase C inhibitor, antagonized both the BK-induced insulin secretion and the increase in [Ca++]i in a concentration-dependent and parallel manner.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	0-7	kininogen 1	Homo sapiens	79-81
9316832-11	1997	BK increased intracellular concentrations of inositol-1,4,5-trisphosphate (IP3).	Inositol 1,4,5-Trisphosphate	45-73	kininogen 1	Homo sapiens	0-2
9316832-11	1997	BK increased intracellular concentrations of inositol-1,4,5-trisphosphate (IP3).	Inositol 1,4,5-Trisphosphate	75-78	kininogen 1	Homo sapiens	0-2
9311664-0	1997	Pharmacological characterization of a novel, orally active, nonpeptide bradykinin B2 receptor antagonist, FR167344.	FR 167344	106-114	kininogen 1	Homo sapiens	71-81
9311664-2	1997	This compound competitively displaced [3H]bradykinin binding to bradykinin B2 receptors present in guinea-pig ileum membrane with an IC50 value of 6.6 X 10(-10) M. In isolated guinea-pig ileum preparations, it also antagonized bradykinin-induced contraction with a pA2 value of 9.3.	Tritium	39-41	kininogen 1	Homo sapiens	42-52
9311664-2	1997	This compound competitively displaced [3H]bradykinin binding to bradykinin B2 receptors present in guinea-pig ileum membrane with an IC50 value of 6.6 X 10(-10) M. In isolated guinea-pig ileum preparations, it also antagonized bradykinin-induced contraction with a pA2 value of 9.3.	Tritium	39-41	kininogen 1	Homo sapiens	64-74
9311664-2	1997	This compound competitively displaced [3H]bradykinin binding to bradykinin B2 receptors present in guinea-pig ileum membrane with an IC50 value of 6.6 X 10(-10) M. In isolated guinea-pig ileum preparations, it also antagonized bradykinin-induced contraction with a pA2 value of 9.3.	Tritium	39-41	kininogen 1	Homo sapiens	64-74
9311664-3	1997	In human lung fibroblast IMR-90 cells, FR167344 displaced [3H]bradykinin binding to human bradykinin B2 receptors with an IC50 value of 1.3 X 10(-8) M, but not [3H]des-Arg10-kallidin binding to human bradykinin B1 receptors.	FR 167344	39-47	kininogen 1	Homo sapiens	62-72
9311664-3	1997	In human lung fibroblast IMR-90 cells, FR167344 displaced [3H]bradykinin binding to human bradykinin B2 receptors with an IC50 value of 1.3 X 10(-8) M, but not [3H]des-Arg10-kallidin binding to human bradykinin B1 receptors.	FR 167344	39-47	kininogen 1	Homo sapiens	90-100
9311664-3	1997	In human lung fibroblast IMR-90 cells, FR167344 displaced [3H]bradykinin binding to human bradykinin B2 receptors with an IC50 value of 1.3 X 10(-8) M, but not [3H]des-Arg10-kallidin binding to human bradykinin B1 receptors.	FR 167344	39-47	kininogen 1	Homo sapiens	90-100
9311664-3	1997	In human lung fibroblast IMR-90 cells, FR167344 displaced [3H]bradykinin binding to human bradykinin B2 receptors with an IC50 value of 1.3 X 10(-8) M, but not [3H]des-Arg10-kallidin binding to human bradykinin B1 receptors.	Tritium	59-61	kininogen 1	Homo sapiens	62-72
9311664-4	1997	In vivo, oral administration of FR167344 inhibited bradykinin-induced bronchoconstriction in guinea pigs and the bradykinin-induced hypotensive response for 6 h in rats.	FR 167344	32-40	kininogen 1	Homo sapiens	51-61
9311664-4	1997	In vivo, oral administration of FR167344 inhibited bradykinin-induced bronchoconstriction in guinea pigs and the bradykinin-induced hypotensive response for 6 h in rats.	FR 167344	32-40	kininogen 1	Homo sapiens	113-123
9311664-5	1997	These results show that FR167344 is a potent, selective, orally active and long acting bradykinin B2 receptor antagonist.	FR 167344	24-32	kininogen 1	Homo sapiens	87-97
9268696-1	1997	In HaCaT keratinocytes bradykinin-triggered actin reorganization was inhibited by quinacrine, a phospholipase A2 inhibitor, and restored by addition of arachidonic acid.	Arachidonic Acid	152-168	kininogen 1	Homo sapiens	23-33
9268696-2	1997	Bradykinin-induced actin breakdown and cortical actin formation were respectively prevented by indomethacin, a cyclooxygenase inhibitor, and nordihydroguaiaretic acid, a lipoxygenase inhibitor.	Indomethacin	95-107	kininogen 1	Homo sapiens	0-10
9268696-2	1997	Bradykinin-induced actin breakdown and cortical actin formation were respectively prevented by indomethacin, a cyclooxygenase inhibitor, and nordihydroguaiaretic acid, a lipoxygenase inhibitor.	Masoprocol	141-166	kininogen 1	Homo sapiens	0-10
9268696-8	1997	In conclusion, bradykinin modulated actin reorganization and cell motility in keratinocytes, probably by a mechanism involving arachidonic acid metabolites and a tyrosine kinase activity.	Arachidonic Acid	127-143	kininogen 1	Homo sapiens	15-25
9293962-1	1997	It is generally accepted that in endothelial cells the occupation of bradykinin B2 receptors, which are linked to the guanine nucleotide-dependent regulatory proteins, Gi and Gq, results in the activation of phospholipase C-beta1 (PLC-beta1), followed by a transient increase in the formation of inositol 1,4,5-trisphosphate (IP3) and diacylglycerol.	Inositol 1,4,5-Trisphosphate	326-329	kininogen 1	Homo sapiens	69-79
9293962-1	1997	It is generally accepted that in endothelial cells the occupation of bradykinin B2 receptors, which are linked to the guanine nucleotide-dependent regulatory proteins, Gi and Gq, results in the activation of phospholipase C-beta1 (PLC-beta1), followed by a transient increase in the formation of inositol 1,4,5-trisphosphate (IP3) and diacylglycerol.	Diglycerides	335-349	kininogen 1	Homo sapiens	69-79
9293962-1	1997	It is generally accepted that in endothelial cells the occupation of bradykinin B2 receptors, which are linked to the guanine nucleotide-dependent regulatory proteins, Gi and Gq, results in the activation of phospholipase C-beta1 (PLC-beta1), followed by a transient increase in the formation of inositol 1,4,5-trisphosphate (IP3) and diacylglycerol.	Inositol 1,4,5-Trisphosphate	296-324	kininogen 1	Homo sapiens	69-79
9293962-3	1997	In cultured human endothelial cells, bradykinin induced a rapid increase in the tyrosine phosphorylation of several Triton-soluble proteins.	Tyrosine	80-88	kininogen 1	Homo sapiens	37-47
9293962-4	1997	Immunoprecipitation of tyrosine-phosphorylated proteins from bradykinin-stimulated cells followed by Western blotting using the respective antibodies facilitated the identification of a 77 kiloDalton (kDa) protein as paxillin, a 130 kDa protein as PLC-gamma1, and a 42/44 kDa doublet as mitogen-activated protein (MAP) kinase.	Tyrosine	23-31	kininogen 1	Homo sapiens	61-71
9293962-5	1997	The bradykinin-induced tyrosine phosphorylation of PLC-gamma1 was relatively transient and was associated with an increase in intracellular levels of IP3.	Tyrosine	23-31	kininogen 1	Homo sapiens	4-14
9293962-5	1997	The bradykinin-induced tyrosine phosphorylation of PLC-gamma1 was relatively transient and was associated with an increase in intracellular levels of IP3.	Inositol 1,4,5-Trisphosphate	150-153	kininogen 1	Homo sapiens	4-14
9293962-6	1997	Bradykinin also induced the rapid and transient activation of phosphotyrosine phosphatases localized mainly in the Triton X-100-soluble cell fraction; this tyrosine phosphatase activity was apparently initiated after the release of Ca2+ from intracellular stores.	Octoxynol	115-127	kininogen 1	Homo sapiens	0-10
9287200-4	1997	In the first, bradykinin augments the current activated by heat through a mechanism that involves activation of protein kinase C. In a second sensitization mechanism, prostaglandin E2 alters the voltage threshold of several ion channels, including a novel tetrodotoxin-insensitive Na+ channel, in such a way that initiation of action potentials is facilitated.	Dinoprostone	167-183	kininogen 1	Homo sapiens	14-24
9277488-7	1997	In DAHP-treated arteries, endothelium-dependent relaxations to bradykinin (10(-10)-10(-6) M) or calcium ionophore A23187 (10(-9)-10(-6) M) were significantly reduced, whereas endothelium-independent relaxations to a nitric oxide donor, 3-morpholinosydnonimine (10(-9)-10(-4) M), were not affected.	2,4-diaminohypoxanthine	3-7	kininogen 1	Homo sapiens	63-73
9341974-5	1997	As determined by anion exchange chromatography and HPLC analysis, HaCaT keratinocytes treated with 1 microM RA for up to 72 h showed a marked decrease in Ins(1,4,5)P3 release upon stimulation with 10 microM bradykinin or 10 microM ionomycin.	Tretinoin	108-110	kininogen 1	Homo sapiens	207-217
9341974-5	1997	As determined by anion exchange chromatography and HPLC analysis, HaCaT keratinocytes treated with 1 microM RA for up to 72 h showed a marked decrease in Ins(1,4,5)P3 release upon stimulation with 10 microM bradykinin or 10 microM ionomycin.	Inositol 1,4,5-Trisphosphate	154-166	kininogen 1	Homo sapiens	207-217
9242187-6	1997	Preincubation with 14,15-EET, 11,12-EET, 14,15-DHET, and 11,12-DHET augmented the magnitude and duration of bradykinin-induced relaxation, whereas endothelium-independent relaxations to aprikalim and sodium nitroprusside were not potentiated.	14,15-epoxy-5,8,11-eicosatrienoic acid	19-28	kininogen 1	Homo sapiens	108-118
9242187-6	1997	Preincubation with 14,15-EET, 11,12-EET, 14,15-DHET, and 11,12-DHET augmented the magnitude and duration of bradykinin-induced relaxation, whereas endothelium-independent relaxations to aprikalim and sodium nitroprusside were not potentiated.	11,12-epoxy-5,8,14-eicosatrienoic acid	30-39	kininogen 1	Homo sapiens	108-118
9242187-6	1997	Preincubation with 14,15-EET, 11,12-EET, 14,15-DHET, and 11,12-DHET augmented the magnitude and duration of bradykinin-induced relaxation, whereas endothelium-independent relaxations to aprikalim and sodium nitroprusside were not potentiated.	14,15-dihydroxyeicosatrienoic acid	41-51	kininogen 1	Homo sapiens	108-118
9242187-6	1997	Preincubation with 14,15-EET, 11,12-EET, 14,15-DHET, and 11,12-DHET augmented the magnitude and duration of bradykinin-induced relaxation, whereas endothelium-independent relaxations to aprikalim and sodium nitroprusside were not potentiated.	11,12-dihydroxy-5Z,8Z,14Z-eicosatrienoic acid	57-67	kininogen 1	Homo sapiens	108-118
9242187-6	1997	Preincubation with 14,15-EET, 11,12-EET, 14,15-DHET, and 11,12-DHET augmented the magnitude and duration of bradykinin-induced relaxation, whereas endothelium-independent relaxations to aprikalim and sodium nitroprusside were not potentiated.	Nitroprusside	200-220	kininogen 1	Homo sapiens	108-118
9242187-7	1997	Pretreatment with 2 mumol/L triacsin C (an inhibitor of acyl coenzyme A synthases) inhibited [3H]14,15-EET incorporation into endothelial phospholipids and blocked 11,12-EET- and 14,15-DHET-induced potentiation of relaxation to bradykinin.	triacsin C	28-38	kininogen 1	Homo sapiens	228-238
9242187-9	1997	We conclude that incorporation of EETs and DHETs into cell lipids results in potentiation of bradykinin-induced relaxation in porcine coronary arteries, providing the first evidence that incorporated EETs and DHETs are capable of modulating vascular function.	eets	34-38	kininogen 1	Homo sapiens	93-103
9242187-9	1997	We conclude that incorporation of EETs and DHETs into cell lipids results in potentiation of bradykinin-induced relaxation in porcine coronary arteries, providing the first evidence that incorporated EETs and DHETs are capable of modulating vascular function.	dhets	43-48	kininogen 1	Homo sapiens	93-103
9242187-9	1997	We conclude that incorporation of EETs and DHETs into cell lipids results in potentiation of bradykinin-induced relaxation in porcine coronary arteries, providing the first evidence that incorporated EETs and DHETs are capable of modulating vascular function.	eets	200-204	kininogen 1	Homo sapiens	93-103
9242187-9	1997	We conclude that incorporation of EETs and DHETs into cell lipids results in potentiation of bradykinin-induced relaxation in porcine coronary arteries, providing the first evidence that incorporated EETs and DHETs are capable of modulating vascular function.	dhets	209-214	kininogen 1	Homo sapiens	93-103
9287200-4	1997	In the first, bradykinin augments the current activated by heat through a mechanism that involves activation of protein kinase C. In a second sensitization mechanism, prostaglandin E2 alters the voltage threshold of several ion channels, including a novel tetrodotoxin-insensitive Na+ channel, in such a way that initiation of action potentials is facilitated.	Tetrodotoxin	256-268	kininogen 1	Homo sapiens	14-24
9286264-7	1997	RESULTS: Endothelium-dependent relaxations to bradykinin (maximal [max], 99% +/- 3%) were strongly inhibited by L-NAME (max, 39% +/- 4%, P &lt; 0.01) and partially by TEA (max, 62% +/- 3%, P &lt; 0.01) or glibenclamide (max, 77% +/- 4%, P &lt; 0.01).	NG-Nitroarginine Methyl Ester	112-118	kininogen 1	Homo sapiens	46-56
9286264-7	1997	RESULTS: Endothelium-dependent relaxations to bradykinin (maximal [max], 99% +/- 3%) were strongly inhibited by L-NAME (max, 39% +/- 4%, P &lt; 0.01) and partially by TEA (max, 62% +/- 3%, P &lt; 0.01) or glibenclamide (max, 77% +/- 4%, P &lt; 0.01).	Tetraethylammonium	167-170	kininogen 1	Homo sapiens	46-56
9286264-7	1997	RESULTS: Endothelium-dependent relaxations to bradykinin (maximal [max], 99% +/- 3%) were strongly inhibited by L-NAME (max, 39% +/- 4%, P &lt; 0.01) and partially by TEA (max, 62% +/- 3%, P &lt; 0.01) or glibenclamide (max, 77% +/- 4%, P &lt; 0.01).	p &lt	137-142	kininogen 1	Homo sapiens	46-56
9297575-0	1997	Histamine release from human bronchoalveolar lavage mast cells by neurokinin A and bradykinin.	Histamine	0-9	kininogen 1	Homo sapiens	83-93
9286264-7	1997	RESULTS: Endothelium-dependent relaxations to bradykinin (maximal [max], 99% +/- 3%) were strongly inhibited by L-NAME (max, 39% +/- 4%, P &lt; 0.01) and partially by TEA (max, 62% +/- 3%, P &lt; 0.01) or glibenclamide (max, 77% +/- 4%, P &lt; 0.01).	Glyburide	205-218	kininogen 1	Homo sapiens	46-56
9286264-8	1997	Administration of glibenclamide plus L-NAME further suppressed bradykinin-induced relaxation (max, 23% +/- 6%; P &lt; 0.01), whereas TEA and L-NAME (max, 6% +/- 2%; P &lt; 0.01) abolished the relaxation.	Glyburide	18-31	kininogen 1	Homo sapiens	63-73
9286264-8	1997	Administration of glibenclamide plus L-NAME further suppressed bradykinin-induced relaxation (max, 23% +/- 6%; P &lt; 0.01), whereas TEA and L-NAME (max, 6% +/- 2%; P &lt; 0.01) abolished the relaxation.	NG-Nitroarginine Methyl Ester	37-43	kininogen 1	Homo sapiens	63-73
9286264-12	1997	As only relaxations to bradykinin, but not those mediated by SNP, were inhibited by TEA, this implies that K(+)-channel blockers most likely affect the bradykinin-evoked NO production or release by the endothelium.	Tetraethylammonium	84-87	kininogen 1	Homo sapiens	23-33
9286264-12	1997	As only relaxations to bradykinin, but not those mediated by SNP, were inhibited by TEA, this implies that K(+)-channel blockers most likely affect the bradykinin-evoked NO production or release by the endothelium.	Tetraethylammonium	84-87	kininogen 1	Homo sapiens	152-162
9262428-11	1997	Bradykinin produced substantial airway wall thickening and slight potentiation of the MCh-induced airway constriction at low lung volume.	Methacholine Chloride	86-89	kininogen 1	Homo sapiens	0-10
9235967-0	1997	Modulation of bradykinin receptor ligand binding affinity and its coupled G-proteins by nitric oxide.	Nitric Oxide	88-100	kininogen 1	Homo sapiens	14-24
9235967-8	1997	However, GSNO decreased BK-stimulated Galphai2, Galphai3, and Galphaq/11 GTP binding activity by 93, 61, and 90%, respectively, whereas epinephrine-stimulated Galphas GTP binding activity was unaffected.	S-Nitrosoglutathione	9-13	kininogen 1	Homo sapiens	24-26
9235967-8	1997	However, GSNO decreased BK-stimulated Galphai2, Galphai3, and Galphaq/11 GTP binding activity by 93, 61, and 90%, respectively, whereas epinephrine-stimulated Galphas GTP binding activity was unaffected.	galphaq/11 gtp	62-76	kininogen 1	Homo sapiens	24-26
9266709-5	1997	The importance of the P2" residue for rK1 specificity was further demonstrated using a human-kininogen-derived substrate that included the N-terminal insertion site of bradykinin (Abz-LMKRP-EDDnp).	abz-lmkrp-eddnp	180-195	kininogen 1	Homo sapiens	168-178
9271333-0	1997	Bradykinin antagonists in human systems: correlation between receptor binding, calcium signalling in isolated cells, and functional activity in isolated ileum.	Calcium	79-86	kininogen 1	Homo sapiens	0-10
9246383-0	1997	5-Hydroxytryptamine, angiotensin and bradykinin transiently increase intracellular calcium concentrations and PKC-alpha activity, but do not induce mitogenesis in human vascular smooth muscle cells.	Calcium	83-90	kininogen 1	Homo sapiens	37-47
9246383-3	1997	Using binding of [3H]-phorbol dibutyrate (PDBu) to quantify membrane-associated protein kinase C (PKC) we also showed that 5-HT, A II and bradykinin induced a rapid but transient translocation of protein kinase C (PKC) to the plasma membrane.	3h]-phorbol dibutyrate	18-40	kininogen 1	Homo sapiens	138-148
9246383-3	1997	Using binding of [3H]-phorbol dibutyrate (PDBu) to quantify membrane-associated protein kinase C (PKC) we also showed that 5-HT, A II and bradykinin induced a rapid but transient translocation of protein kinase C (PKC) to the plasma membrane.	Phorbol 12,13-Dibutyrate	42-46	kininogen 1	Homo sapiens	138-148
9249510-7	1997	In conclusion, the pathways of flow- and bradykinin-mediated NO production in endothelial cells did not require actin filament turnover or intact actin or microtubule cytoskeletons, and cholesterol, possibly by stiffening the plasma membrane, attenuated the flow response.	Cholesterol	186-197	kininogen 1	Homo sapiens	41-51
9249580-0	1997	Vasodilator responses to acetylcholine, bradykinin, and substance P are mediated by a TEA-sensitive mechanism.	Tetraethylammonium	86-89	kininogen 1	Homo sapiens	40-50
9249580-5	1997	The results of the present investigation suggest that TEA attenuates vasodilator responses to acetylcholine, bradykinin, and substance P by inhibiting the release of endothelium-derived relaxing factor.	Tetraethylammonium	54-57	kininogen 1	Homo sapiens	109-119
9249580-6	1997	These data suggest that the acetylcholine-, bradykinin-, and substance P-stimulated release of endothelium-derived relaxing factor may involve the opening of a TEA-sensitive K+ channel in the endothelium in the hindlimb vascular bed of the cat, but that a TEA-sensitive mechanism is not involved in the maintenance of baseline tone in this vascular bed.	Tetraethylammonium	160-163	kininogen 1	Homo sapiens	44-54
9316493-2	1997	When administered in doses of 1 and 5 mg/kg i.v., L-NIO inhibited pulmonary vasodilator responses to acetylcholine, bradykinin, and substance P but did not alter vasodilator responses to adenosine, pinacidil, or adrenomedullin.	N(G)-iminoethylornithine	50-55	kininogen 1	Homo sapiens	116-126
9212711-5	1997	Spectra have been obtained from 50 fmol of total loading of bombesin, MS/MS has been performed on 5 pmol of des-Arg9-bradykinin, and the analyte ion signal is shown to last for over 2500 laser shots for 2 pmol of bombesin.	des-arg9	108-116	kininogen 1	Homo sapiens	117-127
9207629-0	1997	Bradykinin-induced vasodilation of human coronary arteries in vivo: role of nitric oxide and angiotensin-converting enzyme.	Nitric Oxide	76-88	kininogen 1	Homo sapiens	0-10
9207629-1	1997	OBJECTIVES: The present study aimed to determine the role of nitric oxide (NO) and angiotensin-converting enzyme (ACE) in bradykinin (BK)-induced dilation of human coronary arteries in vivo.	Nitric Oxide	61-73	kininogen 1	Homo sapiens	122-132
9207629-1	1997	OBJECTIVES: The present study aimed to determine the role of nitric oxide (NO) and angiotensin-converting enzyme (ACE) in bradykinin (BK)-induced dilation of human coronary arteries in vivo.	Nitric Oxide	61-73	kininogen 1	Homo sapiens	134-136
9207629-7	1997	The BK-induced increases in coronary artery diameter and CBF were significantly reduced (p &lt; 0.01) after pretreatment with NG-monomethyl-L-arginine (200 mumol) and were significantly increased (p &lt; 0.01) after pretreatment with enalaprilat (50 micrograms).	omega-N-Methylarginine	126-150	kininogen 1	Homo sapiens	4-6
9224807-4	1997	FR190997 markedly stimulated phosphatidylinositol hydrolysis in Chinese hamster ovary cells permanently expressing the human bradykinin B2 receptor.	Phosphatidylinositols	29-49	kininogen 1	Homo sapiens	125-135
9224807-5	1997	The response of phosphatidylinositol hydrolysis was antagonized by the B2 receptor selective antagonist Hoe 140 (D-Arg-[hydroxyproline3,beta-thienylalanine4,D-Tic7,++ +Oic8]bradykinin).	Phosphatidylinositols	16-36	kininogen 1	Homo sapiens	173-183
9224807-5	1997	The response of phosphatidylinositol hydrolysis was antagonized by the B2 receptor selective antagonist Hoe 140 (D-Arg-[hydroxyproline3,beta-thienylalanine4,D-Tic7,++ +Oic8]bradykinin).	4-hydroxy-2-octenal	104-107	kininogen 1	Homo sapiens	173-183
9224807-5	1997	The response of phosphatidylinositol hydrolysis was antagonized by the B2 receptor selective antagonist Hoe 140 (D-Arg-[hydroxyproline3,beta-thienylalanine4,D-Tic7,++ +Oic8]bradykinin).	d-arg-[hydroxyproline3	113-135	kininogen 1	Homo sapiens	173-183
9207629-7	1997	The BK-induced increases in coronary artery diameter and CBF were significantly reduced (p &lt; 0.01) after pretreatment with NG-monomethyl-L-arginine (200 mumol) and were significantly increased (p &lt; 0.01) after pretreatment with enalaprilat (50 micrograms).	Enalaprilat	234-245	kininogen 1	Homo sapiens	4-6
9208130-5	1997	The purpose of the present studies, therefore, was to determine the presence of and the pharmacological characteristics of bradykinin receptors on normal cultured primary and SV40 virus-transformed human corneal epithelial (CEPI) cells by use of the accumulation of [3H]-inositol phosphates ([3H]-IPs) as a bioassay.	3h]-inositol phosphates	267-290	kininogen 1	Homo sapiens	123-133
9208131-12	1997	The indomethacin plus L-NAME resistant component of BK relaxation was abolished in physiological solution (PSS) containing 40 mM KCl and vice versa.	Potassium Chloride	129-132	kininogen 1	Homo sapiens	52-54
9276139-6	1997	FR173657 inhibited [3H]BK binding to A431, W138, and IMR90 cell lines of human origin with IC50 values of 2.0 x 10(-9), 2.3 x 10(-9), and 1.7 x 10(-9) M, respectively.	Tritium	20-22	kininogen 1	Homo sapiens	23-25
9276139-9	1997	(iii) Oral administration of FR173657 dose-dependently inhibited BK (5 micrograms/kg) and dextran sulfate (activator of kinin-kallikrein cascade) induced bronchoconstriction with ED50 values of 0.075 and 0.057 mg/kg, respectively.	FR 173657	29-37	kininogen 1	Homo sapiens	65-67
9276139-10	1997	In conclusion, FR173657 is a selective potent, orally active B2 receptor antagonist that can be used to investigate the role of BK in allergic and inflammatory diseases.	FR 173657	15-23	kininogen 1	Homo sapiens	128-130
9276160-8	1997	Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-Ser-Ser-Arg-Gln-Eddnp++ + was hydrolyzed by the renal acidic proteinase and yielded the peptide Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg (Abz-bradykinin).	abz-arg	0-7	kininogen 1	Homo sapiens	181-191
9276160-8	1997	Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-Ser-Ser-Arg-Gln-Eddnp++ + was hydrolyzed by the renal acidic proteinase and yielded the peptide Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg (Abz-bradykinin).	prolyl-prolyl-glycine	8-19	kininogen 1	Homo sapiens	181-191
9276160-8	1997	Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-Ser-Ser-Arg-Gln-Eddnp++ + was hydrolyzed by the renal acidic proteinase and yielded the peptide Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg (Abz-bradykinin).	Phenylalanine	20-23	kininogen 1	Homo sapiens	181-191
9276160-8	1997	Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-Ser-Ser-Arg-Gln-Eddnp++ + was hydrolyzed by the renal acidic proteinase and yielded the peptide Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg (Abz-bradykinin).	Serine	24-27	kininogen 1	Homo sapiens	181-191
9276160-8	1997	Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-Ser-Ser-Arg-Gln-Eddnp++ + was hydrolyzed by the renal acidic proteinase and yielded the peptide Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg (Abz-bradykinin).	Serine	40-43	kininogen 1	Homo sapiens	181-191
9276160-8	1997	Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-Ser-Ser-Arg-Gln-Eddnp++ + was hydrolyzed by the renal acidic proteinase and yielded the peptide Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg (Abz-bradykinin).	Serine	40-43	kininogen 1	Homo sapiens	181-191
9276160-8	1997	Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-Ser-Ser-Arg-Gln-Eddnp++ + was hydrolyzed by the renal acidic proteinase and yielded the peptide Abz-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg (Abz-bradykinin).	Glutamine	52-55	kininogen 1	Homo sapiens	181-191
9289376-1	1997	ACE-inhibitors antagonize both angiotensin production and bradykinin breakdown, resulting in enhancement of vasodilating prostaglandin release.	Prostaglandins	121-134	kininogen 1	Homo sapiens	58-68
9208131-15	1997	The indomethacin plus L-NAME resistant component of the relaxation to BK was significantly attenuated by the K+ channel blocker tetrabutylammonium (TBA, 1 mM).	Indomethacin	4-16	kininogen 1	Homo sapiens	70-72
9208131-15	1997	The indomethacin plus L-NAME resistant component of the relaxation to BK was significantly attenuated by the K+ channel blocker tetrabutylammonium (TBA, 1 mM).	NG-Nitroarginine Methyl Ester	22-28	kininogen 1	Homo sapiens	70-72
9208131-15	1997	The indomethacin plus L-NAME resistant component of the relaxation to BK was significantly attenuated by the K+ channel blocker tetrabutylammonium (TBA, 1 mM).	tetrabutylammonium	128-146	kininogen 1	Homo sapiens	70-72
9208131-15	1997	The indomethacin plus L-NAME resistant component of the relaxation to BK was significantly attenuated by the K+ channel blocker tetrabutylammonium (TBA, 1 mM).	tetrabutylammonium	148-151	kininogen 1	Homo sapiens	70-72
9208131-18	1997	In the presence of indomethacin plus L-NAME, the relaxation produced by BK was not affected by the phospholipase A2 inhibitor, quinacrine (10 microM) or by the inhibitor of cytochrome P450, SKF 525a (10 microM).	Indomethacin	19-31	kininogen 1	Homo sapiens	72-74
9208131-18	1997	In the presence of indomethacin plus L-NAME, the relaxation produced by BK was not affected by the phospholipase A2 inhibitor, quinacrine (10 microM) or by the inhibitor of cytochrome P450, SKF 525a (10 microM).	NG-Nitroarginine Methyl Ester	37-43	kininogen 1	Homo sapiens	72-74
9208131-18	1997	In the presence of indomethacin plus L-NAME, the relaxation produced by BK was not affected by the phospholipase A2 inhibitor, quinacrine (10 microM) or by the inhibitor of cytochrome P450, SKF 525a (10 microM).	Proadifen	190-198	kininogen 1	Homo sapiens	72-74
9208131-19	1997	Another cytochrome P450 inhibitor, clotrimazole (10 microM) which also inhibits K+ channels, inhibited the relaxation to BK.	Clotrimazole	35-47	kininogen 1	Homo sapiens	121-123
9208131-21	1997	These results show that BK induces endothelium-dependent relaxation in human small omental arteries via multiple mechanisms involving nitric oxide, cyclo-oxygenase derived prostanoid(s) and another factor (probably an endothelium-derived hyperpolarizing factor).	Nitric Oxide	134-146	kininogen 1	Homo sapiens	24-26
9208131-21	1997	These results show that BK induces endothelium-dependent relaxation in human small omental arteries via multiple mechanisms involving nitric oxide, cyclo-oxygenase derived prostanoid(s) and another factor (probably an endothelium-derived hyperpolarizing factor).	Prostaglandins	172-182	kininogen 1	Homo sapiens	24-26
9228537-7	1997	Competitive binding studies showed displacement of [3H]-bradykinin by HOE 140, but not by the ligands for the bradykinin B1-receptor, des-Arg10-kallidin and [Leu8]-des-Arg9-bradykinin.	Tritium	52-54	kininogen 1	Homo sapiens	56-66
9246571-6	1997	Pre-treatment of the HUVEC with the bradykinin receptor antagonist, Na-adamantaneacetyl-bradykinin (NA-BK) (1 microM), prior to addition of AT, reduced the AT permeability coefficient to 2.69 x 10(-6) cm/sec.	na-bk	100-105	kininogen 1	Homo sapiens	36-46
9246571-6	1997	Pre-treatment of the HUVEC with the bradykinin receptor antagonist, Na-adamantaneacetyl-bradykinin (NA-BK) (1 microM), prior to addition of AT, reduced the AT permeability coefficient to 2.69 x 10(-6) cm/sec.	na-bk	100-105	kininogen 1	Homo sapiens	88-98
9246571-8	1997	AT (1 microM) increased HUVEC intracellular calcium mobilization, as monitored by FURA-2, to 245 nM from control (70 nM), however, pre-treatment with either BK or the bradykinin receptor antagonist decreased the AT induced intracellular calcium mobilization compared to AT alone.	Fura-2	82-88	kininogen 1	Homo sapiens	167-177
9246571-8	1997	AT (1 microM) increased HUVEC intracellular calcium mobilization, as monitored by FURA-2, to 245 nM from control (70 nM), however, pre-treatment with either BK or the bradykinin receptor antagonist decreased the AT induced intracellular calcium mobilization compared to AT alone.	Calcium	237-244	kininogen 1	Homo sapiens	157-159
9246571-8	1997	AT (1 microM) increased HUVEC intracellular calcium mobilization, as monitored by FURA-2, to 245 nM from control (70 nM), however, pre-treatment with either BK or the bradykinin receptor antagonist decreased the AT induced intracellular calcium mobilization compared to AT alone.	Calcium	237-244	kininogen 1	Homo sapiens	167-177
9161752-6	1997	RESULTS: Enflurane added to the perfusate either upstream or downstream in relation to BAEC attenuated the relaxation induced by Bk at low concentrations.	Enflurane	9-18	kininogen 1	Homo sapiens	129-131
9219222-9	1997	Inhibition of venular EDNO with NG-monomethyl-L-arginine (L-NMMA; 10(-5) mol/L; 1 hour) completely abolished the arteriolar dilation observed in response to acetylcholine or bradykinin during venule to arteriole perfusion.	edno	22-26	kininogen 1	Homo sapiens	174-184
9219222-9	1997	Inhibition of venular EDNO with NG-monomethyl-L-arginine (L-NMMA; 10(-5) mol/L; 1 hour) completely abolished the arteriolar dilation observed in response to acetylcholine or bradykinin during venule to arteriole perfusion.	omega-N-Methylarginine	32-56	kininogen 1	Homo sapiens	174-184
9219222-9	1997	Inhibition of venular EDNO with NG-monomethyl-L-arginine (L-NMMA; 10(-5) mol/L; 1 hour) completely abolished the arteriolar dilation observed in response to acetylcholine or bradykinin during venule to arteriole perfusion.	omega-N-Methylarginine	58-64	kininogen 1	Homo sapiens	174-184
9180216-3	1997	L-NAME prevented in a concentration-related manner the algesic action of bradykinin, but had no effect on pain evoked by heat, cold, or stretch.	NG-Nitroarginine Methyl Ester	0-6	kininogen 1	Homo sapiens	73-83
9139696-3	1997	The known mammalian kinin receptors are classified as two subtypes, i.e. the B1 receptor triggered by [des-Arg9]bradykinin and inhibited by [des-Arg9,Leu8]bradykinin, and the B2 receptor stimulated by bradykinin and antagonized by HOE140.	des-arg9	103-111	kininogen 1	Homo sapiens	112-122
9161752-6	1997	RESULTS: Enflurane added to the perfusate either upstream or downstream in relation to BAEC attenuated the relaxation induced by Bk at low concentrations.	baec	87-91	kininogen 1	Homo sapiens	129-131
9161752-7	1997	On the other hand, isoflurane, added either upstream or down-stream to BAEC, potentiated the relaxation induced by the basal release of EDRF but attenuated the relaxation induced by the Bk stimulated release of EDRF.	Isoflurane	19-29	kininogen 1	Homo sapiens	186-188
9161752-9	1997	CONCLUSION: Enflurane decreases the stability of EDRF/NO released after Bk stimulation while isoflurane can have opposite effects depending on whether the relaxation results from basal or Bk-stimulated release of endothelial derived relaxing factor(s).	Enflurane	12-21	kininogen 1	Homo sapiens	72-74
9161752-9	1997	CONCLUSION: Enflurane decreases the stability of EDRF/NO released after Bk stimulation while isoflurane can have opposite effects depending on whether the relaxation results from basal or Bk-stimulated release of endothelial derived relaxing factor(s).	Enflurane	12-21	kininogen 1	Homo sapiens	188-190
9161752-9	1997	CONCLUSION: Enflurane decreases the stability of EDRF/NO released after Bk stimulation while isoflurane can have opposite effects depending on whether the relaxation results from basal or Bk-stimulated release of endothelial derived relaxing factor(s).	Isoflurane	93-103	kininogen 1	Homo sapiens	188-190
9174646-0	1997	Bradykinin regulates the histamine-induced Ca2+ mobilization via protein kinase C activation in human gingival fibroblasts.	Histamine	25-34	kininogen 1	Homo sapiens	0-10
9174646-1	1997	We previously demonstrated that histamine and bradykinin evoke an increase in intracellular Ca2+ ([Ca2+]i) in human gingival fibroblasts by using a fluorescent Ca2+ indicator Fura-2.	Fura-2	175-181	kininogen 1	Homo sapiens	46-56
9174646-2	1997	In this paper, we further demonstrate the regulation of the histamine-induced Ca2+ mobilization by bradykinin.	Histamine	60-69	kininogen 1	Homo sapiens	99-109
9174646-3	1997	In fibroblasts stimulated with bradykinin (1 microM), subsequent stimulation with histamine (100 microM) failed to mobilize Ca2+, whereas bradykinin induced an increase in [Ca2+]i in the cells pre-stimulated with histamine.	Histamine	213-222	kininogen 1	Homo sapiens	138-148
9174646-4	1997	The attenuation of the histamine response was dependent on the concentration of bradykinin for the first stimulation.	Histamine	23-32	kininogen 1	Homo sapiens	80-90
9174646-6	1997	In fibroblasts pretreated with bradykinin (1 microM) for 3 min and then washed with fresh medium, the effect of histamine on [Ca2+]i quickly returned to the control level.	Histamine	112-121	kininogen 1	Homo sapiens	31-41
9174646-10	1997	These results suggest that the histamine response is regulated by bradykinin receptor activation via the activation of protein kinase C in human gingival fibroblasts.	Histamine	31-40	kininogen 1	Homo sapiens	66-76
27520751-5	1997	Notable among the latter is bradykinin, which induces a transient, specific increase in permeability that is more pronounced in tumour than in normal brain.The nonapeptide RMP-7 [H-Arg-Pro-Hyp-Gly-Thi-Ser-Pro-Tyr(Me)-psi(CH2NH)-Arg-OH] was developed as a bradykinin analogue.	h-arg-pro-hyp-gly-thi-ser-pro-tyr	179-212	kininogen 1	Homo sapiens	28-38
9208130-5	1997	The purpose of the present studies, therefore, was to determine the presence of and the pharmacological characteristics of bradykinin receptors on normal cultured primary and SV40 virus-transformed human corneal epithelial (CEPI) cells by use of the accumulation of [3H]-inositol phosphates ([3H]-IPs) as a bioassay.	3h]-ips	293-300	kininogen 1	Homo sapiens	123-133
9208130-7	1997	Bradykinin (BK) induced a maximal 1.95 +/- 0.24 fold (n = 17) and 2.51 +/- 0.29 fold (n = 26) stimulation of [3H]-IPs accumulation in normal, primary (P-CEPI) and SV40-immortalized (CEPI-17-CL4) cells, respectively.	Tritium	110-112	kininogen 1	Homo sapiens	0-10
9208130-7	1997	Bradykinin (BK) induced a maximal 1.95 +/- 0.24 fold (n = 17) and 2.51 +/- 0.29 fold (n = 26) stimulation of [3H]-IPs accumulation in normal, primary (P-CEPI) and SV40-immortalized (CEPI-17-CL4) cells, respectively.	Tritium	110-112	kininogen 1	Homo sapiens	12-14
9208130-7	1997	Bradykinin (BK) induced a maximal 1.95 +/- 0.24 fold (n = 17) and 2.51 +/- 0.29 fold (n = 26) stimulation of [3H]-IPs accumulation in normal, primary (P-CEPI) and SV40-immortalized (CEPI-17-CL4) cells, respectively.	p-cepi	151-157	kininogen 1	Homo sapiens	0-10
9208130-7	1997	Bradykinin (BK) induced a maximal 1.95 +/- 0.24 fold (n = 17) and 2.51 +/- 0.29 fold (n = 26) stimulation of [3H]-IPs accumulation in normal, primary (P-CEPI) and SV40-immortalized (CEPI-17-CL4) cells, respectively.	p-cepi	151-157	kininogen 1	Homo sapiens	12-14
9208130-10	1997	The molar potencies of BK and some of its analogues in the CEPI-17-CL4 cells were as follows: BK (EC50 = 3.26 +/- 0.61 nM, n = 18), Lys-BK (EC50 = 0.95 +/- 0.16 nM, n = 5), Met-Lys-BK (EC50 = 2.3 +/- 0.42 nM, n = 5), Ile-Ser-BK (EC50 = 5.19 +/- 1.23 nM, n = 6), Ala3-Lys-BK (EC50 = 12.7 +/- 2.08 nM, n = 3), Tyr8-BK (EC50 = 19.3 +/- 0.77 nM, n = 3), Tyr5-BK (EC50 = 467 +/- 53 nM, n = 4) and des-Arg9-BK (EC50 = 14.1 +/- 2.7 microM, n = 4).	cepi-17-cl4	59-70	kininogen 1	Homo sapiens	23-25
9208130-13	1997	The bradykinin-induced responses were competitively antagonized by the B2-receptor selective BK antagonists, Hoe-140 (D-Arg-[Hyp3, Thi5, D-Tic7, Oic8]BK; Icatibant; molar antagonist potency = 2.9 nM; pA2 = 8.54 +/- 0.06, n = 4; and slope = 1.04 +/- 0.08) and D-Arg0[Hyp3,Thi5,8, DPhe7]-BK (KB = 371 nM; pKB = 6.43 +/- 0.08, n = 4) in CEPI-17-CL4 cells.	cepi	334-338	kininogen 1	Homo sapiens	4-14
9208130-13	1997	The bradykinin-induced responses were competitively antagonized by the B2-receptor selective BK antagonists, Hoe-140 (D-Arg-[Hyp3, Thi5, D-Tic7, Oic8]BK; Icatibant; molar antagonist potency = 2.9 nM; pA2 = 8.54 +/- 0.06, n = 4; and slope = 1.04 +/- 0.08) and D-Arg0[Hyp3,Thi5,8, DPhe7]-BK (KB = 371 nM; pKB = 6.43 +/- 0.08, n = 4) in CEPI-17-CL4 cells.	cepi	334-338	kininogen 1	Homo sapiens	150-152
9208130-13	1997	The bradykinin-induced responses were competitively antagonized by the B2-receptor selective BK antagonists, Hoe-140 (D-Arg-[Hyp3, Thi5, D-Tic7, Oic8]BK; Icatibant; molar antagonist potency = 2.9 nM; pA2 = 8.54 +/- 0.06, n = 4; and slope = 1.04 +/- 0.08) and D-Arg0[Hyp3,Thi5,8, DPhe7]-BK (KB = 371 nM; pKB = 6.43 +/- 0.08, n = 4) in CEPI-17-CL4 cells.	cepi	334-338	kininogen 1	Homo sapiens	150-152
9208130-13	1997	The bradykinin-induced responses were competitively antagonized by the B2-receptor selective BK antagonists, Hoe-140 (D-Arg-[Hyp3, Thi5, D-Tic7, Oic8]BK; Icatibant; molar antagonist potency = 2.9 nM; pA2 = 8.54 +/- 0.06, n = 4; and slope = 1.04 +/- 0.08) and D-Arg0[Hyp3,Thi5,8, DPhe7]-BK (KB = 371 nM; pKB = 6.43 +/- 0.08, n = 4) in CEPI-17-CL4 cells.	17-cl4	339-345	kininogen 1	Homo sapiens	4-14
9208130-13	1997	The bradykinin-induced responses were competitively antagonized by the B2-receptor selective BK antagonists, Hoe-140 (D-Arg-[Hyp3, Thi5, D-Tic7, Oic8]BK; Icatibant; molar antagonist potency = 2.9 nM; pA2 = 8.54 +/- 0.06, n = 4; and slope = 1.04 +/- 0.08) and D-Arg0[Hyp3,Thi5,8, DPhe7]-BK (KB = 371 nM; pKB = 6.43 +/- 0.08, n = 4) in CEPI-17-CL4 cells.	17-cl4	339-345	kininogen 1	Homo sapiens	150-152
9208130-13	1997	The bradykinin-induced responses were competitively antagonized by the B2-receptor selective BK antagonists, Hoe-140 (D-Arg-[Hyp3, Thi5, D-Tic7, Oic8]BK; Icatibant; molar antagonist potency = 2.9 nM; pA2 = 8.54 +/- 0.06, n = 4; and slope = 1.04 +/- 0.08) and D-Arg0[Hyp3,Thi5,8, DPhe7]-BK (KB = 371 nM; pKB = 6.43 +/- 0.08, n = 4) in CEPI-17-CL4 cells.	17-cl4	339-345	kininogen 1	Homo sapiens	150-152
9208130-16	1997	This rank order of potency of agonist BK-related peptides, coupled with the antagonism of the BK-induced [3H]-IPs by the specific B2-receptor antagonists, strongly suggests that a B2-receptor subtype is involved in mediating functional phosphoinositide (PI) responses in the CEPI-17-CL4 and P-CEPI cells.	Phosphatidylinositols	236-252	kininogen 1	Homo sapiens	38-40
9208130-16	1997	This rank order of potency of agonist BK-related peptides, coupled with the antagonism of the BK-induced [3H]-IPs by the specific B2-receptor antagonists, strongly suggests that a B2-receptor subtype is involved in mediating functional phosphoinositide (PI) responses in the CEPI-17-CL4 and P-CEPI cells.	cepi-17-cl4	275-286	kininogen 1	Homo sapiens	38-40
9208130-16	1997	This rank order of potency of agonist BK-related peptides, coupled with the antagonism of the BK-induced [3H]-IPs by the specific B2-receptor antagonists, strongly suggests that a B2-receptor subtype is involved in mediating functional phosphoinositide (PI) responses in the CEPI-17-CL4 and P-CEPI cells.	p-cepi	291-297	kininogen 1	Homo sapiens	38-40
9208131-12	1997	The indomethacin plus L-NAME resistant component of BK relaxation was abolished in physiological solution (PSS) containing 40 mM KCl and vice versa.	Indomethacin	4-16	kininogen 1	Homo sapiens	52-54
9208131-12	1997	The indomethacin plus L-NAME resistant component of BK relaxation was abolished in physiological solution (PSS) containing 40 mM KCl and vice versa.	NG-Nitroarginine Methyl Ester	22-28	kininogen 1	Homo sapiens	52-54
9208131-12	1997	The indomethacin plus L-NAME resistant component of BK relaxation was abolished in physiological solution (PSS) containing 40 mM KCl and vice versa.	pss	107-110	kininogen 1	Homo sapiens	52-54
9141588-2	1997	Bradykinin can also contribute to this process, increasing the release of eicosanoids from decidua cells.	Eicosanoids	74-85	kininogen 1	Homo sapiens	0-10
9107182-1	1997	BACKGROUND: KII ACE, the enzyme that converts angiotensin I and inactivates bradykinin, is highly concentrated in the lungs; its blockade reduces exposure to angiotensin II and enhances exposure to prostaglandins generated by local kinin hyperconcentration.	Prostaglandins	198-212	kininogen 1	Homo sapiens	76-86
9129633-9	1997	In both types of arteries cryopreservation also attenuated significantly the endothelium-dependent relaxant responses to bradykinin during U46619 (10 nmol/L)-induced tone.	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	139-145	kininogen 1	Homo sapiens	121-131
9129633-10	1997	In HMA the maximal bradykinin-induced relaxation (85% +/- 4%) was significantly diminished to 29% +/- 7% and 38% +/- 9% after cryopreservation without and with FCS (mean +/- SEM, n = 6).	5-(N,N-hexamethylene)amiloride	3-6	kininogen 1	Homo sapiens	19-29
9150326-0	1997	Activity of inhaled lysine acetylsalicylate (L-ASA) on bradykinin-induced bronchoconstriction in asthmatics: evidence of contribution of prostaglandins.	acetylsalicylic acid lysinate	20-43	kininogen 1	Homo sapiens	55-65
9150326-0	1997	Activity of inhaled lysine acetylsalicylate (L-ASA) on bradykinin-induced bronchoconstriction in asthmatics: evidence of contribution of prostaglandins.	acetylsalicylic acid lysinate	45-50	kininogen 1	Homo sapiens	55-65
9150326-3	1997	The aim of the present study was to investigate the effect of the potent cyclo-oxygenase inhibitor, lysine acetylsalicylate (L-ASA), administered by inhalation, on bradykinin-induced bronchoconstriction in a group of 12 asthmatic subjects.	acetylsalicylic acid lysinate	100-123	kininogen 1	Homo sapiens	164-174
9150326-3	1997	The aim of the present study was to investigate the effect of the potent cyclo-oxygenase inhibitor, lysine acetylsalicylate (L-ASA), administered by inhalation, on bradykinin-induced bronchoconstriction in a group of 12 asthmatic subjects.	acetylsalicylic acid lysinate	125-130	kininogen 1	Homo sapiens	164-174
9150326-7	1997	When compared to placebo, inhaled L-ASA reduced the airway responsiveness to bradykinin in 11 of the 12 subjects studied, the geometric mean (range) values for PC20 bradykinin increasing significantly (p&lt;0.001) by 1.7 doubling dose from 0.55 (0.11-5.05) to 1.72 (0.26-6.05) mg x mL(-1) after placebo and L-ASA, respectively.	acetylsalicylic acid lysinate	34-39	kininogen 1	Homo sapiens	77-87
9150326-7	1997	When compared to placebo, inhaled L-ASA reduced the airway responsiveness to bradykinin in 11 of the 12 subjects studied, the geometric mean (range) values for PC20 bradykinin increasing significantly (p&lt;0.001) by 1.7 doubling dose from 0.55 (0.11-5.05) to 1.72 (0.26-6.05) mg x mL(-1) after placebo and L-ASA, respectively.	acetylsalicylic acid lysinate	34-39	kininogen 1	Homo sapiens	165-175
9150326-9	1997	It is concluded that administration of lysine acetylsalicylate by inhalation protects the asthmatic airways against bradykinin-induced bronchoconstriction, thus suggesting that endogenous prostaglandins may play a contributory role in the bronchoconstriction to kinins in human asthma.	acetylsalicylic acid lysinate	39-62	kininogen 1	Homo sapiens	116-126
10495785-9	1997	G alpha 13 increased bradykinin-stimulated Ca influx by a mechanism that depends on NO and cGMP.	Cyclic GMP	91-95	kininogen 1	Homo sapiens	21-31
9120622-1	1997	The bradykinin analog, RMP-7, was investigated for its ability to increase selectively the transport of 68Ga ethylenediamine tetraacetic acid (EDTA) into recurrent malignant gliomas in nine patients.	68ga ethylenediamine tetraacetic acid	104-141	kininogen 1	Homo sapiens	4-14
9120622-1	1997	The bradykinin analog, RMP-7, was investigated for its ability to increase selectively the transport of 68Ga ethylenediamine tetraacetic acid (EDTA) into recurrent malignant gliomas in nine patients.	Edetic Acid	143-147	kininogen 1	Homo sapiens	4-14
27520751-5	1997	Notable among the latter is bradykinin, which induces a transient, specific increase in permeability that is more pronounced in tumour than in normal brain.The nonapeptide RMP-7 [H-Arg-Pro-Hyp-Gly-Thi-Ser-Pro-Tyr(Me)-psi(CH2NH)-Arg-OH] was developed as a bradykinin analogue.	ch2nh)	221-227	kininogen 1	Homo sapiens	28-38
27520751-5	1997	Notable among the latter is bradykinin, which induces a transient, specific increase in permeability that is more pronounced in tumour than in normal brain.The nonapeptide RMP-7 [H-Arg-Pro-Hyp-Gly-Thi-Ser-Pro-Tyr(Me)-psi(CH2NH)-Arg-OH] was developed as a bradykinin analogue.	arg-oh	228-234	kininogen 1	Homo sapiens	28-38
9056177-0	1997	Identification of endogenous Des-Arg9-[Hyp3]-bradykinin in human plasma with post-source-decay matrix-assisted laser desorption/ionization mass spectrometry.	des-arg9	29-37	kininogen 1	Homo sapiens	45-55
9056177-5	1997	A comparison with a data base suggested that the sequence is very similar to des-arg9bradykinin (arg-pro-pro-gly-phe-ser-pro-phe).	Arginine	81-84	kininogen 1	Homo sapiens	85-95
9056177-5	1997	A comparison with a data base suggested that the sequence is very similar to des-arg9bradykinin (arg-pro-pro-gly-phe-ser-pro-phe).	prolyl-proline	101-108	kininogen 1	Homo sapiens	85-95
9098527-1	1997	Bradykinin induces receptor-mediated calcium-dependent release of glutamate from cultured astrocytes through a mechanism that is neither due to cell-swelling mechanism nor due to the reversal of the glutamate transporter.	Calcium	37-44	kininogen 1	Homo sapiens	0-10
9098527-1	1997	Bradykinin induces receptor-mediated calcium-dependent release of glutamate from cultured astrocytes through a mechanism that is neither due to cell-swelling mechanism nor due to the reversal of the glutamate transporter.	Glutamic Acid	66-75	kininogen 1	Homo sapiens	0-10
9138678-0	1997	Evidence that mechanisms dependent and independent of nitric oxide mediate endothelium-dependent relaxation to bradykinin in human small resistance-like coronary arteries.	Nitric Oxide	54-66	kininogen 1	Homo sapiens	111-121
9119014-0	1997	An NMR study of the interaction of 15N-labelled bradykinin with an antibody mimic of the bradykinin B2 receptor.	15n	35-38	kininogen 1	Homo sapiens	48-58
9119014-0	1997	An NMR study of the interaction of 15N-labelled bradykinin with an antibody mimic of the bradykinin B2 receptor.	15n	35-38	kininogen 1	Homo sapiens	89-99
9119014-5	1997	Bradykinin was obtained in a uniformly 15N-labelled form using recombinant expression of a fusion protein consisting of the glutathione-binding domain of glutathione S-transferase fused to residues 354-375 of the high-molecular-mass kininogen from which bradykinin was released by proteolytic digestion with its natural protease plasma kallikrein.	15n	39-42	kininogen 1	Homo sapiens	0-10
9119014-5	1997	Bradykinin was obtained in a uniformly 15N-labelled form using recombinant expression of a fusion protein consisting of the glutathione-binding domain of glutathione S-transferase fused to residues 354-375 of the high-molecular-mass kininogen from which bradykinin was released by proteolytic digestion with its natural protease plasma kallikrein.	Glutathione	124-135	kininogen 1	Homo sapiens	0-10
9119014-7	1997	The 15N and 1H resonances of the tightly bound residues of bradykinin show appreciable changes in chemical shift with respect to the free form, while the 15N and 1H linewidths indicate that the hydrodynamic behaviour of bound bradykinin is dominated by the high-molecular-mass Fab fragment.	15n	4-7	kininogen 1	Homo sapiens	59-69
9119014-7	1997	The 15N and 1H resonances of the tightly bound residues of bradykinin show appreciable changes in chemical shift with respect to the free form, while the 15N and 1H linewidths indicate that the hydrodynamic behaviour of bound bradykinin is dominated by the high-molecular-mass Fab fragment.	Hydrogen	12-14	kininogen 1	Homo sapiens	59-69
9119014-10	1997	indicate that bradykinin binds to MBK3 only in the all-trans conformation at all three Xaa-Pro amide bonds.	xanthenone-4-acetic acid	87-90	kininogen 1	Homo sapiens	14-24
9119014-10	1997	indicate that bradykinin binds to MBK3 only in the all-trans conformation at all three Xaa-Pro amide bonds.	pro amide	91-100	kininogen 1	Homo sapiens	14-24
9218207-4	1997	In addition, they improve endothelium-dependent vasodilation by increasing the expression of endothelial inositol by a bradykinin-related mechanism.	Inositol	105-113	kininogen 1	Homo sapiens	119-129
9106812-12	1997	For the afferents that were responsive to injection of Tyrode, the effects were always considerably smaller and with shorter duration than those evoked by BK injections.	tyrode	55-61	kininogen 1	Homo sapiens	155-157
9066005-4	1997	Bradykinin was infused in seventeen hypertensive patients randomized to treatment with the ACEIs captopril and quinapril or with placebo.	aceis	91-96	kininogen 1	Homo sapiens	0-10
9066005-4	1997	Bradykinin was infused in seventeen hypertensive patients randomized to treatment with the ACEIs captopril and quinapril or with placebo.	Captopril	97-106	kininogen 1	Homo sapiens	0-10
9066005-4	1997	Bradykinin was infused in seventeen hypertensive patients randomized to treatment with the ACEIs captopril and quinapril or with placebo.	Quinapril	111-120	kininogen 1	Homo sapiens	0-10
9066005-7	1997	Although baseline t-PA antigen levels were similar in the ACEI-treated (6.85 +/- 0.85 ng/ml) and placebo-treated (7.85 +/- 0.68 ng/ml) subjects, bradykinin caused a significant (p &lt; 0.01) increase in t-PA antigen levels (to 19.3 +/- 8.2) only in the ACEI-treated patients.	acei	253-257	kininogen 1	Homo sapiens	145-155
9083783-4	1997	The maximal response to des-Arg9-bradykinin, expressed as percentage of the maximum elicited by serotonin, was: 10 +/- 2 at 15 min, 55 +/- 5 at 120 min and 80 +/- 3 at 300 min.	Serotonin	96-105	kininogen 1	Homo sapiens	33-43
9083783-8	1997	On the other hand, continuous exposure to the anti-inflammatory steroid dexamethasone (100 microM) or to the protein synthesis inhibitor cycloheximide (70 microM) largely prevented the sensitization to des-Arg9-bradykinin in incubated human umbilical vein rings.	Steroids	64-71	kininogen 1	Homo sapiens	211-221
9083783-8	1997	On the other hand, continuous exposure to the anti-inflammatory steroid dexamethasone (100 microM) or to the protein synthesis inhibitor cycloheximide (70 microM) largely prevented the sensitization to des-Arg9-bradykinin in incubated human umbilical vein rings.	Dexamethasone	72-85	kininogen 1	Homo sapiens	211-221
9083783-8	1997	On the other hand, continuous exposure to the anti-inflammatory steroid dexamethasone (100 microM) or to the protein synthesis inhibitor cycloheximide (70 microM) largely prevented the sensitization to des-Arg9-bradykinin in incubated human umbilical vein rings.	Cycloheximide	137-150	kininogen 1	Homo sapiens	211-221
9012741-10	1997	The association of losartan (10 mumol/L) with the bradykinin B2 receptor antagonist HOE 140 (1 mumol/L) totally prevented the relaxation due to the ACEI.	Losartan	19-27	kininogen 1	Homo sapiens	50-60
9012741-10	1997	The association of losartan (10 mumol/L) with the bradykinin B2 receptor antagonist HOE 140 (1 mumol/L) totally prevented the relaxation due to the ACEI.	4-hydroxy-2-octenal	84-87	kininogen 1	Homo sapiens	50-60
9023330-2	1997	In this study, the B2 kinin receptor agonist bradykinin increased cGMP in rat microvascular coronary endothelial cells (RMCECs) and human umbilical vein endothelial cells (HUVECs), which could be prevented with the specific B2 kinin receptor antagonist icatibant but not with the B1 kinin receptor antagonist des-Arg9-[Leu8]bradykinin or with the nonpeptide kinin receptor antagonist WIN 64338.	Cyclic GMP	66-70	kininogen 1	Homo sapiens	45-55
9023330-2	1997	In this study, the B2 kinin receptor agonist bradykinin increased cGMP in rat microvascular coronary endothelial cells (RMCECs) and human umbilical vein endothelial cells (HUVECs), which could be prevented with the specific B2 kinin receptor antagonist icatibant but not with the B1 kinin receptor antagonist des-Arg9-[Leu8]bradykinin or with the nonpeptide kinin receptor antagonist WIN 64338.	WIN 64338	384-393	kininogen 1	Homo sapiens	45-55
9023330-4	1997	The B1 kinin receptor agonist des-Arg9-bradykinin increased cGMP in RMCECs but not in HUVECs.	Cyclic GMP	60-64	kininogen 1	Homo sapiens	39-49
9023330-6	1997	In BAECs, the B1 kinin receptor-mediated cGMP synthesis could be prevented by icatibant and desensitized by preincubation with des-Arg9-bradykinin as well as bradykinin.	Cyclic GMP	41-45	kininogen 1	Homo sapiens	136-146
9023330-6	1997	In BAECs, the B1 kinin receptor-mediated cGMP synthesis could be prevented by icatibant and desensitized by preincubation with des-Arg9-bradykinin as well as bradykinin.	Cyclic GMP	41-45	kininogen 1	Homo sapiens	158-168
9098527-5	1997	Furthermore, we demonstrate that botulinus toxin type B and tetanus toxin cause a decrease in synaptobrevin II immunoreactivity and abolish bradykinin-induced release of glutamate from cultured astrocytes.	Glutamic Acid	170-179	kininogen 1	Homo sapiens	140-150
9138678-9	1997	HbO (20 microM) and a combination of HbO (20 microM) and L-NOARG (100 microM) reduced Rmax to bradykinin by 58% (P &lt; 0.05) and 54% (P &lt; 0.05), respectively.	2,4-dihydroxy-7-methoxy-1,4-benzoxazin-3-one	0-3	kininogen 1	Homo sapiens	94-104
9138678-9	1997	HbO (20 microM) and a combination of HbO (20 microM) and L-NOARG (100 microM) reduced Rmax to bradykinin by 58% (P &lt; 0.05) and 54% (P &lt; 0.05), respectively.	2,4-dihydroxy-7-methoxy-1,4-benzoxazin-3-one	37-40	kininogen 1	Homo sapiens	94-104
9138678-9	1997	HbO (20 microM) and a combination of HbO (20 microM) and L-NOARG (100 microM) reduced Rmax to bradykinin by 58% (P &lt; 0.05) and 54% (P &lt; 0.05), respectively.	Nitroarginine	57-64	kininogen 1	Homo sapiens	94-104
9138678-10	1997	HbO (20 microM) and L-NOARG (100 microM, combined but not HbO (20 microM) alone, caused a significant 11 fold (P &lt; 0.05) decrease in sensitivity to bradykinin.	2,4-dihydroxy-7-methoxy-1,4-benzoxazin-3-one	0-3	kininogen 1	Homo sapiens	151-161
9138678-10	1997	HbO (20 microM) and L-NOARG (100 microM, combined but not HbO (20 microM) alone, caused a significant 11 fold (P &lt; 0.05) decrease in sensitivity to bradykinin.	Nitroarginine	20-27	kininogen 1	Homo sapiens	151-161
9138678-14	1997	A combination of HbO, L-NOARG and high K+ (30 mM) abolished the response to bradykinin.	2,4-dihydroxy-7-methoxy-1,4-benzoxazin-3-one	17-20	kininogen 1	Homo sapiens	76-86
9138678-14	1997	A combination of HbO, L-NOARG and high K+ (30 mM) abolished the response to bradykinin.	Nitroarginine	22-29	kininogen 1	Homo sapiens	76-86
9138678-19	1997	The non-NO -dependent relaxation to bradykinin in the human isolated small coronary arteries appeared to be mediated by a K(+)-sensitive vasodilator mechanism, possibly endothelium-derived hyperpolarizing factor (EDHF).	-derived hyperpolarizing factor	180-211	kininogen 1	Homo sapiens	36-46
9138678-19	1997	The non-NO -dependent relaxation to bradykinin in the human isolated small coronary arteries appeared to be mediated by a K(+)-sensitive vasodilator mechanism, possibly endothelium-derived hyperpolarizing factor (EDHF).	edhf	213-217	kininogen 1	Homo sapiens	36-46
9088736-0	1997	Amlodipine and benazeprilat differently affect the responses to endothelin-1 and bradykinin in porcine ciliary arteries: effects of a low and high dose combination.	Amlodipine	0-10	kininogen 1	Homo sapiens	81-91
9088736-0	1997	Amlodipine and benazeprilat differently affect the responses to endothelin-1 and bradykinin in porcine ciliary arteries: effects of a low and high dose combination.	benazeprilat	15-27	kininogen 1	Homo sapiens	81-91
9088736-8	1997	On the other hand, benazeprilat enhanced the sensitivity (concentration shift 73-fold; p &lt; 0.05) and maximal relaxation to bradykinin (by 27%; p &lt; 0.01), whereas amlodipine or the low or high dose combination were ineffective.	benazeprilat	19-31	kininogen 1	Homo sapiens	126-136
9088736-11	1997	In contrast, endothelium-dependent relaxations to bradykinin were enhanced by benazeprilat alone, but not when combined with amlodipine.	benazeprilat	78-90	kininogen 1	Homo sapiens	50-60
9151155-0	1997	Changes in bradykinin and prostaglandins plasma levels during dextran-sulfate low-density-lipoprotein apheresis.	Dextran Sulfate	62-77	kininogen 1	Homo sapiens	11-21
9151155-1	1997	The negative charges of dextran-sulfate (DS) used for low-density-lipoprotein (LDL) apheresis initiate the intrinsic coagulation pathway in which plasma kallikrein acts on the high-molecular-weight kininogen to produce large amounts of bradykinin.	Dextran Sulfate	24-39	kininogen 1	Homo sapiens	236-246
9151155-1	1997	The negative charges of dextran-sulfate (DS) used for low-density-lipoprotein (LDL) apheresis initiate the intrinsic coagulation pathway in which plasma kallikrein acts on the high-molecular-weight kininogen to produce large amounts of bradykinin.	Dextran Sulfate	41-43	kininogen 1	Homo sapiens	236-246
9151155-6	1997	During apheresis using heparin, the plasma levels of prostaglandin E2 (PGE2) increased significantly (5.6 +/- 1.2 (mean +/- SE, n = 4) pg/ml before apheresis and 33.4 +/- 13.2 after apheresis, p &lt; 0.05) in association with an increase in bradykinin levels (17.9 +/- 2.6 pg/ml before apheresis and 470 +/- 135 after apheresis, p &lt; 0.01).	Heparin	23-30	kininogen 1	Homo sapiens	241-251
9151155-6	1997	During apheresis using heparin, the plasma levels of prostaglandin E2 (PGE2) increased significantly (5.6 +/- 1.2 (mean +/- SE, n = 4) pg/ml before apheresis and 33.4 +/- 13.2 after apheresis, p &lt; 0.05) in association with an increase in bradykinin levels (17.9 +/- 2.6 pg/ml before apheresis and 470 +/- 135 after apheresis, p &lt; 0.01).	Dinoprostone	53-69	kininogen 1	Homo sapiens	241-251
9151155-6	1997	During apheresis using heparin, the plasma levels of prostaglandin E2 (PGE2) increased significantly (5.6 +/- 1.2 (mean +/- SE, n = 4) pg/ml before apheresis and 33.4 +/- 13.2 after apheresis, p &lt; 0.05) in association with an increase in bradykinin levels (17.9 +/- 2.6 pg/ml before apheresis and 470 +/- 135 after apheresis, p &lt; 0.01).	Dinoprostone	71-75	kininogen 1	Homo sapiens	241-251
9151155-9	1997	This finding suggests that bradykinin generated during apheresis has some pathophysiological effects via activation of the prostaglandin system.	Prostaglandins	123-136	kininogen 1	Homo sapiens	27-37
9020273-0	1997	Treatment of severe systemic inflammatory response syndrome and sepsis with a novel bradykinin antagonist, deltibant (CP-0127).	deltibant	118-125	kininogen 1	Homo sapiens	84-94
9020273-3	1997	OBJECTIVE: To test the effect of a novel bradykinin antagonist, deltibant (CP-0127), on survival, organ dysfunction, and other outcomes in patients with the systemic inflammatory response syndrome (SIRS) and presumed sepsis.	deltibant	64-73	kininogen 1	Homo sapiens	41-51
9020273-3	1997	OBJECTIVE: To test the effect of a novel bradykinin antagonist, deltibant (CP-0127), on survival, organ dysfunction, and other outcomes in patients with the systemic inflammatory response syndrome (SIRS) and presumed sepsis.	deltibant	75-82	kininogen 1	Homo sapiens	41-51
9124496-4	1997	Two agents that elicit EDNO production, bradykinin (BK) and carbamylcholine (Cch), increased J(H) when added to the peritubular capillary perfusate.	Nitric Oxide	23-27	kininogen 1	Homo sapiens	40-50
9124496-4	1997	Two agents that elicit EDNO production, bradykinin (BK) and carbamylcholine (Cch), increased J(H) when added to the peritubular capillary perfusate.	Nitric Oxide	23-27	kininogen 1	Homo sapiens	52-54
9124496-7	1997	Bradykinin increased cGMP content of isolated proximal convoluted tubules, but only if they were coincubated with endothelial cells.	Cyclic GMP	21-25	kininogen 1	Homo sapiens	0-10
9124496-8	1997	This effect of BK was blocked by L-NAME.	NG-Nitroarginine Methyl Ester	33-39	kininogen 1	Homo sapiens	15-17
9051315-11	1997	Bradykinin evoked endothelium-dependent relaxation that was inhibited by L-NAME (44 microM) but not glibenclamide 0.44 microM).	NG-Nitroarginine Methyl Ester	73-79	kininogen 1	Homo sapiens	0-10
9051332-1	1997	Long-acting somatostatin analogue (SMS 201-995) inhibits serotonin, bradykinin, prostaglandins, substance P, and vasoactive intestinal peptide, which may be involved in migraine.	Octreotide	35-46	kininogen 1	Homo sapiens	68-78
9056177-5	1997	A comparison with a data base suggested that the sequence is very similar to des-arg9bradykinin (arg-pro-pro-gly-phe-ser-pro-phe).	Glycine	109-112	kininogen 1	Homo sapiens	85-95
9056177-5	1997	A comparison with a data base suggested that the sequence is very similar to des-arg9bradykinin (arg-pro-pro-gly-phe-ser-pro-phe).	Phenylalanine	113-116	kininogen 1	Homo sapiens	85-95
9056177-5	1997	A comparison with a data base suggested that the sequence is very similar to des-arg9bradykinin (arg-pro-pro-gly-phe-ser-pro-phe).	Serine	117-120	kininogen 1	Homo sapiens	85-95
9056177-5	1997	A comparison with a data base suggested that the sequence is very similar to des-arg9bradykinin (arg-pro-pro-gly-phe-ser-pro-phe).	Phenylalanine	125-128	kininogen 1	Homo sapiens	85-95
9056177-6	1997	But many fragment masses, including the mass of the parent ion of the unknown peptide, are 16 Da larger than the corresponding fragment masses of des-arg9-bradykinin.	des-arg9	146-154	kininogen 1	Homo sapiens	155-165
9056177-10	1997	In conclusion, the existence of des-arg9[hyp3]-bradykinin (arg-pro-hyp-gly-phe-ser-pro-phe) in human plasma is described.	des-arg9	32-40	kininogen 1	Homo sapiens	47-57
9056177-10	1997	In conclusion, the existence of des-arg9[hyp3]-bradykinin (arg-pro-hyp-gly-phe-ser-pro-phe) in human plasma is described.	Arginine	36-39	kininogen 1	Homo sapiens	47-57
9056177-10	1997	In conclusion, the existence of des-arg9[hyp3]-bradykinin (arg-pro-hyp-gly-phe-ser-pro-phe) in human plasma is described.	Serine	79-82	kininogen 1	Homo sapiens	47-57
9056177-10	1997	In conclusion, the existence of des-arg9[hyp3]-bradykinin (arg-pro-hyp-gly-phe-ser-pro-phe) in human plasma is described.	Phenylalanine	75-78	kininogen 1	Homo sapiens	47-57
9038949-1	1997	We have recently reported that halothane (Hal) anesthesia attenuates the pulmonary vasodilator responses to both bradykinin (BK) and sodium nitroprusside (SNP) compared with responses measured in the conscious state.	Halothane	31-40	kininogen 1	Homo sapiens	113-123
9203620-0	1997	Novel subtype-selective nonpeptide bradykinin receptor antagonists FR167344 and FR173657.	FR 167344	67-75	kininogen 1	Homo sapiens	35-45
9203620-0	1997	Novel subtype-selective nonpeptide bradykinin receptor antagonists FR167344 and FR173657.	FR 173657	80-88	kininogen 1	Homo sapiens	35-45
9203620-3	1997	FR167344 and FR173657 inhibited the B2 receptor-mediated phosphatidylinositol (PI) hydrolysis and produced a concentration-dependent rightward shift in the dose-response curve to bradykinin.	FR 167344	0-8	kininogen 1	Homo sapiens	179-189
9203620-3	1997	FR167344 and FR173657 inhibited the B2 receptor-mediated phosphatidylinositol (PI) hydrolysis and produced a concentration-dependent rightward shift in the dose-response curve to bradykinin.	FR 173657	13-21	kininogen 1	Homo sapiens	179-189
9203620-7	1997	Therefore, FR167344 and FR173657 are potent, highly selective, and insurmountable antagonists for the human bradykinin B2 receptor.	FR 167344	11-19	kininogen 1	Homo sapiens	108-118
9203620-7	1997	Therefore, FR167344 and FR173657 are potent, highly selective, and insurmountable antagonists for the human bradykinin B2 receptor.	FR 173657	24-32	kininogen 1	Homo sapiens	108-118
9203625-0	1997	Antisense oligonucleotides targeting human protein kinase C-alpha inhibit phorbol ester-induced reduction of bradykinin-evoked calcium mobilization in A549 cells.	Oligonucleotides	10-26	kininogen 1	Homo sapiens	109-119
9203625-0	1997	Antisense oligonucleotides targeting human protein kinase C-alpha inhibit phorbol ester-induced reduction of bradykinin-evoked calcium mobilization in A549 cells.	Phorbol Esters	74-87	kininogen 1	Homo sapiens	109-119
9203625-0	1997	Antisense oligonucleotides targeting human protein kinase C-alpha inhibit phorbol ester-induced reduction of bradykinin-evoked calcium mobilization in A549 cells.	Calcium	127-134	kininogen 1	Homo sapiens	109-119
9203625-2	1997	Bradykinin, a potent and selective kinin B2 receptor agonist, induces calcium mobilization in a concentration-dependent fashion in this cell line.	Calcium	70-77	kininogen 1	Homo sapiens	0-10
9060089-7	1997	Furthermore, it was shown that indomethacin in combination with an ACE inhibitor or bradykinin converted a suppressive response into proliferation indicating an immunostimulatory activity by indomethacin.	Indomethacin	191-203	kininogen 1	Homo sapiens	84-94
9016332-1	1997	The conformation of the natural peptide [Thr6]-bradykinin, Arg1-Pro2-Pro3-Gly4-Phe5-Thr6-Pro7-Phe8-Arg9, is investigated by NMR spectroscopy and computer simulations in an aqueous solution of sodium dodecyl sulfate micelles.	glycyl-glycyl-glycyl-glycine	74-78	kininogen 1	Homo sapiens	47-57
9016332-1	1997	The conformation of the natural peptide [Thr6]-bradykinin, Arg1-Pro2-Pro3-Gly4-Phe5-Thr6-Pro7-Phe8-Arg9, is investigated by NMR spectroscopy and computer simulations in an aqueous solution of sodium dodecyl sulfate micelles.	Sodium Dodecyl Sulfate	192-214	kininogen 1	Homo sapiens	47-57
9016333-1	1997	The natural peptide [Thr6]-bradykinin, Arg1-Pro2-Pro3-Gly4-Phe5-Thr6-Pro7-Phe8-Arg9, has been conformationally examined by molecular dynamics simulations using a two-phase box consisting of H2O and CCl4 to mimic the micellar environment utilized in the 1H-NMR studies.	Water	190-193	kininogen 1	Homo sapiens	27-37
9016333-1	1997	The natural peptide [Thr6]-bradykinin, Arg1-Pro2-Pro3-Gly4-Phe5-Thr6-Pro7-Phe8-Arg9, has been conformationally examined by molecular dynamics simulations using a two-phase box consisting of H2O and CCl4 to mimic the micellar environment utilized in the 1H-NMR studies.	Carbon Tetrachloride	198-202	kininogen 1	Homo sapiens	27-37
9016333-1	1997	The natural peptide [Thr6]-bradykinin, Arg1-Pro2-Pro3-Gly4-Phe5-Thr6-Pro7-Phe8-Arg9, has been conformationally examined by molecular dynamics simulations using a two-phase box consisting of H2O and CCl4 to mimic the micellar environment utilized in the 1H-NMR studies.	Hydrogen	253-255	kininogen 1	Homo sapiens	27-37
9016333-6	1997	The structures of membrane-bound [Thr6]-bradykinin developed here provide experimental support for the interaction of residues 7 and 8 with the core of the membrane-bound receptor and the N-terminus and C-terminal arginine interacting with the extracellular portion of the receptor.	Arginine	214-222	kininogen 1	Homo sapiens	40-50
9038949-1	1997	We have recently reported that halothane (Hal) anesthesia attenuates the pulmonary vasodilator responses to both bradykinin (BK) and sodium nitroprusside (SNP) compared with responses measured in the conscious state.	Halothane	31-40	kininogen 1	Homo sapiens	125-127
9038949-1	1997	We have recently reported that halothane (Hal) anesthesia attenuates the pulmonary vasodilator responses to both bradykinin (BK) and sodium nitroprusside (SNP) compared with responses measured in the conscious state.	Halothane	42-45	kininogen 1	Homo sapiens	113-123
9038949-1	1997	We have recently reported that halothane (Hal) anesthesia attenuates the pulmonary vasodilator responses to both bradykinin (BK) and sodium nitroprusside (SNP) compared with responses measured in the conscious state.	Halothane	42-45	kininogen 1	Homo sapiens	125-127
9038949-10	1997	Thus Iso and Hal selectively attenuate the endothelium-dependent pulmonary vasodilator response to BK.	Halothane	13-16	kininogen 1	Homo sapiens	99-101
8988040-3	1997	Colony formation stimulated by multiple neuropeptides, including vasopressin and bradykinin, was also blocked by [D-Arg1,D-Trp5,7,9,Leu11]SP.	d-trp5	121-127	kininogen 1	Homo sapiens	81-91
8988040-3	1997	Colony formation stimulated by multiple neuropeptides, including vasopressin and bradykinin, was also blocked by [D-Arg1,D-Trp5,7,9,Leu11]SP.	sp	138-140	kininogen 1	Homo sapiens	81-91
8988040-4	1997	This new SP analogue inhibited vasopressin- or bradykinin-induced Ca2+ mobilization and mitogen-activated protein kinase activation.	sp	9-11	kininogen 1	Homo sapiens	47-57
9056076-1	1997	In cultured endothelial cells, the temperature dependence of bradykinin-initiated Ca2+ signaling was studied using Fura-2 technique.	Fura-2	115-121	kininogen 1	Homo sapiens	61-71
9110121-2	1997	In many models, adenosine plays a role by triggering the activation of protein kinase C. It may work in conjunction with other agents, such as bradykinin, but the putative role of noradrenaline is uncertain.	Adenosine	16-25	kininogen 1	Homo sapiens	143-153
9397288-10	1997	Beyond inhibiting the renin-angiotensin system, angiotensin-converting enzyme inhibitors diminish the inactivation of bradykinin, thus leading to an augmentation of nitric oxide release.	Nitric Oxide	165-177	kininogen 1	Homo sapiens	118-128
9203625-8	1997	This reduction in PKC-alpha was sufficient to inhibit the reduction of bradykinin-induced calcium mobilization by TPA.	Calcium	90-97	kininogen 1	Homo sapiens	71-81
9203625-8	1997	This reduction in PKC-alpha was sufficient to inhibit the reduction of bradykinin-induced calcium mobilization by TPA.	Tetradecanoylphorbol Acetate	114-117	kininogen 1	Homo sapiens	71-81
9056076-7	1997	In contrast to the temperature dependence of bradykinin-stimulated Ca2+/Mn2+ entry, the temperature dependence of Mn2+ entry on addition of agonist did not correlate with Fick"s law of diffusion, but followed the same exponential function obtained for Ca2+ release, sequestration and extrusion.	Manganese(2+)	72-76	kininogen 1	Homo sapiens	45-55
9429844-6	1997	Bradykinin is a very potent vasodilator that exerts its vasodilatory actions by causing endothelial release of nitric oxide, prostacyclin and/or a hyperpolarising factor [endothelium-derived hyperpolarising factor (EDHF)].	Nitric Oxide	111-123	kininogen 1	Homo sapiens	0-10
26582443-0	1997	Antamanide Prevents Bradykinin-lnduced Filamin Translocation by Inhibiting Extracellular Calcium Influx.	antamanide	0-10	kininogen 1	Homo sapiens	20-30
26582443-0	1997	Antamanide Prevents Bradykinin-lnduced Filamin Translocation by Inhibiting Extracellular Calcium Influx.	Calcium	89-96	kininogen 1	Homo sapiens	20-30
26582443-9	1997	Moreover, incubation of ECs in high-K(+) saline inhibits bradykinin-induced extracellular Ca(2+) influx as well as filamin translocation.	Sodium Chloride	41-47	kininogen 1	Homo sapiens	57-67
26582443-10	1997	To examine the efficacy of antamanide as an anti-inflammatory drug that affects filamin translocation, bradykinin-induced paracellular gap formation is quantified and compared in the presence or absence of antamanide pretreatment.	antamanide	27-37	kininogen 1	Homo sapiens	103-113
26582443-12	1997	This suggests that extracellular Ca(2+) influx is required for bradykinin-induced filamin translocation, which in part regulates microvascular EC barrier function, and that antamanide may be a useful anti-inflammatory agent.	antamanide	173-183	kininogen 1	Homo sapiens	63-73
9588823-10	1997	Treatments of bradykinin and TNF that translocated PKC also showed cytoskeletal rearrangement of rhodamine-phalloidin stained actin, causing it to become more prevalent near cell membranes and concentrated at focal points between cells.	Rhodamines	97-106	kininogen 1	Homo sapiens	14-24
9588823-10	1997	Treatments of bradykinin and TNF that translocated PKC also showed cytoskeletal rearrangement of rhodamine-phalloidin stained actin, causing it to become more prevalent near cell membranes and concentrated at focal points between cells.	Phalloidine	107-117	kininogen 1	Homo sapiens	14-24
9429844-6	1997	Bradykinin is a very potent vasodilator that exerts its vasodilatory actions by causing endothelial release of nitric oxide, prostacyclin and/or a hyperpolarising factor [endothelium-derived hyperpolarising factor (EDHF)].	Epoprostenol	125-137	kininogen 1	Homo sapiens	0-10
9429844-6	1997	Bradykinin is a very potent vasodilator that exerts its vasodilatory actions by causing endothelial release of nitric oxide, prostacyclin and/or a hyperpolarising factor [endothelium-derived hyperpolarising factor (EDHF)].	edhf	215-219	kininogen 1	Homo sapiens	0-10
9263768-5	1997	Addition of acetylcholine (1 nM-10 microM) or bradykinin (1 nM-10 microM) to precontracted preparations elicited concentration-dependent relaxation responses that were dependent on the presence of the endothelium and were partially inhibited by the NO-synthase inhibitor nitro-L-arginine (0.1 mM).	Nitroarginine	271-287	kininogen 1	Homo sapiens	46-56
9606729-0	1997	NMR investigations of recombinant 15N/13C/2H-labeled bradykinin bound to a Fab mimic of the B2 receptor.	15n	34-37	kininogen 1	Homo sapiens	53-63
9049653-5	1997	Bradykinin induced the production of 6-keto-PGF1 alpha by BAEC.	6-Ketoprostaglandin F1 alpha	37-54	kininogen 1	Homo sapiens	0-10
9049653-5	1997	Bradykinin induced the production of 6-keto-PGF1 alpha by BAEC.	baec	58-62	kininogen 1	Homo sapiens	0-10
9060017-3	1997	To test this hypothesis, the effect of the specific guanylate cyclase inhibitor methylene blue was studied on bradykinin-evoked, i.e. NO-mediated pain and, for control, on mechanically-evoked pain, which is probably not mediated by NO.	Methylene Blue	80-94	kininogen 1	Homo sapiens	110-120
9060017-5	1997	Pretreatment of the vein segments with methylene blue inhibited bradykinin-evoked pain in a concentration-dependent manner and abolished pain at a concentration of 1 x 10(-3) M. Methylene blue had no effect on mechanically evoked pain.	Methylene Blue	39-53	kininogen 1	Homo sapiens	64-74
9392837-3	1997	Responses to T-kinin and bradykinin were inhibited by the kinin B2 receptor antagonist Hoe-140, but were not altered by the B1 receptor antagonist des-Arg9-[Leu8]-BK, the histamine H1 antagonist pyrilamine, the histamine H2 receptor antagonist cimetidine, or the H3 receptor antagonist thioperamide.	Pyrilamine	195-205	kininogen 1	Homo sapiens	25-35
9392837-3	1997	Responses to T-kinin and bradykinin were inhibited by the kinin B2 receptor antagonist Hoe-140, but were not altered by the B1 receptor antagonist des-Arg9-[Leu8]-BK, the histamine H1 antagonist pyrilamine, the histamine H2 receptor antagonist cimetidine, or the H3 receptor antagonist thioperamide.	Cimetidine	244-254	kininogen 1	Homo sapiens	25-35
9392837-3	1997	Responses to T-kinin and bradykinin were inhibited by the kinin B2 receptor antagonist Hoe-140, but were not altered by the B1 receptor antagonist des-Arg9-[Leu8]-BK, the histamine H1 antagonist pyrilamine, the histamine H2 receptor antagonist cimetidine, or the H3 receptor antagonist thioperamide.	thioperamide	286-298	kininogen 1	Homo sapiens	25-35
9392837-4	1997	Vasodilator responses to T-kinin and bradykinin were attenuated by the nitric oxide synthase inhibitor, N omega Nitro-L-arginine methyl ester (L-NAME), but were not altered by the cyclooxygenase inhibitor, sodium meclofenamate, or the K+ ATP channel antagonist, U37883A.	nitric	71-77	kininogen 1	Homo sapiens	37-47
9392837-4	1997	Vasodilator responses to T-kinin and bradykinin were attenuated by the nitric oxide synthase inhibitor, N omega Nitro-L-arginine methyl ester (L-NAME), but were not altered by the cyclooxygenase inhibitor, sodium meclofenamate, or the K+ ATP channel antagonist, U37883A.	NG-Nitroarginine Methyl Ester	104-141	kininogen 1	Homo sapiens	37-47
9392837-4	1997	Vasodilator responses to T-kinin and bradykinin were attenuated by the nitric oxide synthase inhibitor, N omega Nitro-L-arginine methyl ester (L-NAME), but were not altered by the cyclooxygenase inhibitor, sodium meclofenamate, or the K+ ATP channel antagonist, U37883A.	NG-Nitroarginine Methyl Ester	143-149	kininogen 1	Homo sapiens	37-47
9392837-4	1997	Vasodilator responses to T-kinin and bradykinin were attenuated by the nitric oxide synthase inhibitor, N omega Nitro-L-arginine methyl ester (L-NAME), but were not altered by the cyclooxygenase inhibitor, sodium meclofenamate, or the K+ ATP channel antagonist, U37883A.	Meclofenamic Acid	206-226	kininogen 1	Homo sapiens	37-47
9392837-4	1997	Vasodilator responses to T-kinin and bradykinin were attenuated by the nitric oxide synthase inhibitor, N omega Nitro-L-arginine methyl ester (L-NAME), but were not altered by the cyclooxygenase inhibitor, sodium meclofenamate, or the K+ ATP channel antagonist, U37883A.	U 37883A	262-269	kininogen 1	Homo sapiens	37-47
9392837-5	1997	These data suggest that vasodilator responses to T-kinin and bradykinin are mediated by kinin B2 receptor stimulated release of nitric oxide from the endothelium, but that the activation of kinin B1 receptors, the release of vasodilator prostaglandins, or the opening of K+ ATP channels are not involved in the response to T-kinin in the mesenteric vascular bed of the cat.	Nitric Oxide	128-140	kininogen 1	Homo sapiens	61-71
9392837-5	1997	These data suggest that vasodilator responses to T-kinin and bradykinin are mediated by kinin B2 receptor stimulated release of nitric oxide from the endothelium, but that the activation of kinin B1 receptors, the release of vasodilator prostaglandins, or the opening of K+ ATP channels are not involved in the response to T-kinin in the mesenteric vascular bed of the cat.	Prostaglandins	237-251	kininogen 1	Homo sapiens	61-71
9606729-1	1997	NMR spectroscopy has been used to obtain structural information on the bioactive conformation of the nonapeptide hormone bradykinin (Arg-Pro-Pro-Gly-Ser-Pro-Phe-Arg, BK) bound to the Fab-fragment of an antibody that mimics the hormone binding site of the natural bradykinin B2-receptor.	Arginine	133-136	kininogen 1	Homo sapiens	263-273
9606729-1	1997	NMR spectroscopy has been used to obtain structural information on the bioactive conformation of the nonapeptide hormone bradykinin (Arg-Pro-Pro-Gly-Ser-Pro-Phe-Arg, BK) bound to the Fab-fragment of an antibody that mimics the hormone binding site of the natural bradykinin B2-receptor.	Proline	137-140	kininogen 1	Homo sapiens	121-131
9606729-1	1997	NMR spectroscopy has been used to obtain structural information on the bioactive conformation of the nonapeptide hormone bradykinin (Arg-Pro-Pro-Gly-Ser-Pro-Phe-Arg, BK) bound to the Fab-fragment of an antibody that mimics the hormone binding site of the natural bradykinin B2-receptor.	Proline	137-140	kininogen 1	Homo sapiens	263-273
9606729-1	1997	NMR spectroscopy has been used to obtain structural information on the bioactive conformation of the nonapeptide hormone bradykinin (Arg-Pro-Pro-Gly-Ser-Pro-Phe-Arg, BK) bound to the Fab-fragment of an antibody that mimics the hormone binding site of the natural bradykinin B2-receptor.	Proline	141-144	kininogen 1	Homo sapiens	121-131
9606729-1	1997	NMR spectroscopy has been used to obtain structural information on the bioactive conformation of the nonapeptide hormone bradykinin (Arg-Pro-Pro-Gly-Ser-Pro-Phe-Arg, BK) bound to the Fab-fragment of an antibody that mimics the hormone binding site of the natural bradykinin B2-receptor.	Proline	141-144	kininogen 1	Homo sapiens	263-273
9606729-1	1997	NMR spectroscopy has been used to obtain structural information on the bioactive conformation of the nonapeptide hormone bradykinin (Arg-Pro-Pro-Gly-Ser-Pro-Phe-Arg, BK) bound to the Fab-fragment of an antibody that mimics the hormone binding site of the natural bradykinin B2-receptor.	Glycine	145-148	kininogen 1	Homo sapiens	121-131
9606729-1	1997	NMR spectroscopy has been used to obtain structural information on the bioactive conformation of the nonapeptide hormone bradykinin (Arg-Pro-Pro-Gly-Ser-Pro-Phe-Arg, BK) bound to the Fab-fragment of an antibody that mimics the hormone binding site of the natural bradykinin B2-receptor.	Serine	149-152	kininogen 1	Homo sapiens	121-131
9606729-1	1997	NMR spectroscopy has been used to obtain structural information on the bioactive conformation of the nonapeptide hormone bradykinin (Arg-Pro-Pro-Gly-Ser-Pro-Phe-Arg, BK) bound to the Fab-fragment of an antibody that mimics the hormone binding site of the natural bradykinin B2-receptor.	Serine	149-152	kininogen 1	Homo sapiens	263-273
9606729-1	1997	NMR spectroscopy has been used to obtain structural information on the bioactive conformation of the nonapeptide hormone bradykinin (Arg-Pro-Pro-Gly-Ser-Pro-Phe-Arg, BK) bound to the Fab-fragment of an antibody that mimics the hormone binding site of the natural bradykinin B2-receptor.	phenylalanylarginine	157-164	kininogen 1	Homo sapiens	121-131
9606729-2	1997	Using 15N or 15N,13C, 60% 2H isotope labelled bradykinin, complete 1H, 13C and 15N assignments for bradykinin bound to the Fab-fragment have been obtained.	15n	6-9	kininogen 1	Homo sapiens	99-109
9606729-2	1997	Using 15N or 15N,13C, 60% 2H isotope labelled bradykinin, complete 1H, 13C and 15N assignments for bradykinin bound to the Fab-fragment have been obtained.	15n	13-16	kininogen 1	Homo sapiens	99-109
9606729-2	1997	Using 15N or 15N,13C, 60% 2H isotope labelled bradykinin, complete 1H, 13C and 15N assignments for bradykinin bound to the Fab-fragment have been obtained.	Hydrogen	67-69	kininogen 1	Homo sapiens	99-109
9606729-2	1997	Using 15N or 15N,13C, 60% 2H isotope labelled bradykinin, complete 1H, 13C and 15N assignments for bradykinin bound to the Fab-fragment have been obtained.	15n	13-16	kininogen 1	Homo sapiens	99-109
9606729-3	1997	Preliminary interpretation of 15N edited NOE spectra indicates that the conformation of bradykinin bound to the model receptor differs substantially from previous computer models of the bioactive conformation of bradykinin.	15n	30-33	kininogen 1	Homo sapiens	88-98
9606729-3	1997	Preliminary interpretation of 15N edited NOE spectra indicates that the conformation of bradykinin bound to the model receptor differs substantially from previous computer models of the bioactive conformation of bradykinin.	noe	41-44	kininogen 1	Homo sapiens	88-98
8940106-0	1996	Tyrosine phosphorylation of GSalpha and inhibition of bradykinin-induced activation of the cyclic AMP pathway in A431 cells by epidermal growth factor receptor.	Cyclic AMP	91-101	kininogen 1	Homo sapiens	54-64
8940106-2	1996	In a previous study, we demonstrated that bradykinin (BK) increases the intracellular accumulation of cAMP in the human epidermoid carcinoma cell line A431 by stimulating adenylate cyclase activity via a stimulatory G protein (Gsalpha) (Liebmann, C., Graness, A., Ludwig, B., Adomeit, A., Boehmer, A., Boehmer, F.-D., Nurnberg, B., and Wetzker, R. (1996) Biochem.	Cyclic AMP	102-106	kininogen 1	Homo sapiens	42-52
8940106-2	1996	In a previous study, we demonstrated that bradykinin (BK) increases the intracellular accumulation of cAMP in the human epidermoid carcinoma cell line A431 by stimulating adenylate cyclase activity via a stimulatory G protein (Gsalpha) (Liebmann, C., Graness, A., Ludwig, B., Adomeit, A., Boehmer, A., Boehmer, F.-D., Nurnberg, B., and Wetzker, R. (1996) Biochem.	Cyclic AMP	102-106	kininogen 1	Homo sapiens	54-56
8940106-5	1996	Here, we present several lines of evidence indicating the ability of epidermal growth factor (EGF) to suppress BK-induced activation of the cAMP pathway in A431 cells via tyrosine phosphorylation of Gsalpha.	Cyclic AMP	140-144	kininogen 1	Homo sapiens	111-113
8940106-5	1996	Here, we present several lines of evidence indicating the ability of epidermal growth factor (EGF) to suppress BK-induced activation of the cAMP pathway in A431 cells via tyrosine phosphorylation of Gsalpha.	Tyrosine	171-179	kininogen 1	Homo sapiens	111-113
8940106-10	1996	Treatment of A431 cells with EGF decreased BK-induced cAMP accumulation in intact cells as well as the stimulation of adenylate cyclase by BK, NaF, and guanyl nucleotides, but not by forskolin.	Cyclic AMP	54-58	kininogen 1	Homo sapiens	43-45
8987958-6	1996	Indomethacin had a small but significant inhibitory effect on bradykinin-induced relaxation, but this component of relaxation was no different among groups.	Indomethacin	0-12	kininogen 1	Homo sapiens	62-72
8987958-8	1996	CONCLUSION: This study provides evidence for an increase in bradykinin-mediated nitric oxide synthesis from the vascular endothelium of small arteries from the peripheral circulation of normotensive pregnant women and a relative reduction in women with preeclampsia.	Nitric Oxide	80-92	kininogen 1	Homo sapiens	60-70
8971427-2	1996	Angiotensin converting enzyme inhibitors have been suggested to act in part by potentiating the stimulatory effect of bradykinin on endothelial prostacyclin and/or nitric oxide (NO) formation.	Epoprostenol	144-156	kininogen 1	Homo sapiens	118-128
8971427-2	1996	Angiotensin converting enzyme inhibitors have been suggested to act in part by potentiating the stimulatory effect of bradykinin on endothelial prostacyclin and/or nitric oxide (NO) formation.	Nitric Oxide	164-176	kininogen 1	Homo sapiens	118-128
8971090-4	1997	Endothelium-dependent relaxation by nitric oxide pathways stimulated after receptor activation (bradykinin and thrombin) was not different in vein rings from diabetic (n = 12) and nondiabetic patients (n = 12).	Nitric Oxide	36-48	kininogen 1	Homo sapiens	96-106
9106985-6	1997	The activity of adenosine-sensitized afferent nerves may become enhanced by additional stimuli such as potassium, protons, substance P and bradykinin.	Adenosine	16-25	kininogen 1	Homo sapiens	139-149
9003555-15	1996	Moreover, induction of P450 activity by beta-naphthoflavone (3 mumol l-1, 48 h), significantly increased the bradykinin-induced release of EDHF.	beta-Naphthoflavone	40-59	kininogen 1	Homo sapiens	109-119
9003555-15	1996	Moreover, induction of P450 activity by beta-naphthoflavone (3 mumol l-1, 48 h), significantly increased the bradykinin-induced release of EDHF.	Deferiprone	69-72	kininogen 1	Homo sapiens	109-119
8940106-11	1996	Also, EGF treatment abolished both the BK- and isoprenaline-induced stimulation of guanosine 5"-O-(3-[35S]thiotriphosphate) binding to Gsalpha.	guanosine 5"-o-(3-[35s]thiotriphosphate	83-122	kininogen 1	Homo sapiens	39-41
8940106-12	1996	In contrast, the BK-evoked, Gq-mediated stimulation of inositol phosphate formation in A431 cells was not affected by EGF pretreatment.	glycylglutamine	28-30	kininogen 1	Homo sapiens	17-19
8940106-12	1996	In contrast, the BK-evoked, Gq-mediated stimulation of inositol phosphate formation in A431 cells was not affected by EGF pretreatment.	Inositol Phosphates	55-73	kininogen 1	Homo sapiens	17-19
9034614-5	1996	The bradykinin-induced contraction results from a contractile component due to stimulation of the TP receptor, and of a relaxant component due to relaxant prostanoids.	Prostaglandins	155-166	kininogen 1	Homo sapiens	4-14
9606729-0	1997	NMR investigations of recombinant 15N/13C/2H-labeled bradykinin bound to a Fab mimic of the B2 receptor.	13c	38-41	kininogen 1	Homo sapiens	53-63
9606729-0	1997	NMR investigations of recombinant 15N/13C/2H-labeled bradykinin bound to a Fab mimic of the B2 receptor.	Deuterium	42-44	kininogen 1	Homo sapiens	53-63
9606729-1	1997	NMR spectroscopy has been used to obtain structural information on the bioactive conformation of the nonapeptide hormone bradykinin (Arg-Pro-Pro-Gly-Ser-Pro-Phe-Arg, BK) bound to the Fab-fragment of an antibody that mimics the hormone binding site of the natural bradykinin B2-receptor.	Arginine	133-136	kininogen 1	Homo sapiens	121-131
9068370-0	1996	Pharmacological characterization of bradykinin receptors coupled to phosphoinositide turnover in SV40-immortalized human trabecular meshwork cells.	Phosphatidylinositols	68-84	kininogen 1	Homo sapiens	36-46
9068370-2	1996	Phosphoinositide (PI) turnover studies were conducted using [3H]myo-inositol-labeled HTM3 cells and anion exchange chromatography to quantify [3H]inositol phosphates generated in response to bradykinin (BK) and various BK analogs.	Phosphatidylinositols	0-16	kininogen 1	Homo sapiens	191-201
9068370-2	1996	Phosphoinositide (PI) turnover studies were conducted using [3H]myo-inositol-labeled HTM3 cells and anion exchange chromatography to quantify [3H]inositol phosphates generated in response to bradykinin (BK) and various BK analogs.	3h]inositol phosphates	143-165	kininogen 1	Homo sapiens	191-201
9068370-6	1996	The molar potencies (EC50) of BK, TK and close analogs were: BK = 4.5 +/- 0.5 nM (n = 6), Lys-BK = 6.5 +/- 0.7 nM (n = 3), TK = 38.8 +/- 6.6 nM (n = 8), Met-Lys-BK = 41.5 +/- 13.4 nM (n = 4), Des-Arg9-BK = 2093 +/- 626 nM (n = 4).	Lysine	90-93	kininogen 1	Homo sapiens	30-32
8939910-1	1996	Chemical cross-linking combined with site-directed mutagenesis was used to evaluate the role of extracellular cysteines and their positions relative to the binding site for the agonist bradykinin (BK) in the human BK B2 receptor.	Cysteine	110-119	kininogen 1	Homo sapiens	185-195
8939910-3	1996	The Ser20 and Ser277 single mutants and the Ser20/Ser277 double mutant bound [3H]BK and the antagonist [3H]NPC17731 with pharmacological profiles identical to the wild-type B2 receptor.	Tritium	78-80	kininogen 1	Homo sapiens	81-83
8939910-9	1996	Here, we show that m-maleimidobenzoyl-N-hydroxysuccinimide ester and 1,5-difluoro-2, 4-dinitrobenzene cross-linked BK to the wild-type human B2 receptor and the Ser20 and Ser277 single mutant receptors, whereas these reagents were unable to cross-link BK to the Ser20/Ser277 double mutant.	3-maleimidobenzoyl N-hydroxysuccinimide	19-64	kininogen 1	Homo sapiens	115-117
8939910-9	1996	Here, we show that m-maleimidobenzoyl-N-hydroxysuccinimide ester and 1,5-difluoro-2, 4-dinitrobenzene cross-linked BK to the wild-type human B2 receptor and the Ser20 and Ser277 single mutant receptors, whereas these reagents were unable to cross-link BK to the Ser20/Ser277 double mutant.	3-maleimidobenzoyl N-hydroxysuccinimide	19-64	kininogen 1	Homo sapiens	252-254
8939910-9	1996	Here, we show that m-maleimidobenzoyl-N-hydroxysuccinimide ester and 1,5-difluoro-2, 4-dinitrobenzene cross-linked BK to the wild-type human B2 receptor and the Ser20 and Ser277 single mutant receptors, whereas these reagents were unable to cross-link BK to the Ser20/Ser277 double mutant.	1,5-difluoro-2,4-dinitrobenzene	69-101	kininogen 1	Homo sapiens	115-117
8939910-9	1996	Here, we show that m-maleimidobenzoyl-N-hydroxysuccinimide ester and 1,5-difluoro-2, 4-dinitrobenzene cross-linked BK to the wild-type human B2 receptor and the Ser20 and Ser277 single mutant receptors, whereas these reagents were unable to cross-link BK to the Ser20/Ser277 double mutant.	1,5-difluoro-2,4-dinitrobenzene	69-101	kininogen 1	Homo sapiens	252-254
9068370-6	1996	The molar potencies (EC50) of BK, TK and close analogs were: BK = 4.5 +/- 0.5 nM (n = 6), Lys-BK = 6.5 +/- 0.7 nM (n = 3), TK = 38.8 +/- 6.6 nM (n = 8), Met-Lys-BK = 41.5 +/- 13.4 nM (n = 4), Des-Arg9-BK = 2093 +/- 626 nM (n = 4).	des-arg9	192-200	kininogen 1	Homo sapiens	30-32
9068370-8	1996	The actions of BK and TK were potently and competitively antagonized by Hoe-140 (molar potency = 0.6-1 nM; pA2 = 8.97-9.21. n = 3-4) and by D-Arg0[Hyp3,-Thi5.8,-DPhe7]-BK (molar potency = 251 nM; -log potency, pKb = 6.6), two selective B2-type BK antagonists.	d-arg0	140-146	kininogen 1	Homo sapiens	15-17
9068370-8	1996	The actions of BK and TK were potently and competitively antagonized by Hoe-140 (molar potency = 0.6-1 nM; pA2 = 8.97-9.21. n = 3-4) and by D-Arg0[Hyp3,-Thi5.8,-DPhe7]-BK (molar potency = 251 nM; -log potency, pKb = 6.6), two selective B2-type BK antagonists.	thi5	153-157	kininogen 1	Homo sapiens	15-17
11667793-7	1996	The method is applied to predict the relative configuration of two stereocenters in the side chains of two natural products, sambutoxin and the bradykinin inhibitor L-755,897.	l-755	165-170	kininogen 1	Homo sapiens	144-154
8910447-1	1996	The B2 bradykinin receptor, a seven-helix transmembrane receptor, binds the inflammatory mediator bradykinin (BK) and the structurally related peptide antagonist HOE-140.	4-hydroxy-2-octenal	162-165	kininogen 1	Homo sapiens	7-17
8944650-6	1996	HASM cells plated on high-density collagen were stiffer than cells plated on low-density collagen (126 +/- 16 vs. 43 +/- 3 dyn/cm2) and developed more pronounced increases in stiffness in response to bradykinin as well as more pronounced decreases in stiffness in response to isoproterenol.	Isoproterenol	276-289	kininogen 1	Homo sapiens	200-210
8922733-10	1996	This is the first characterization of [3H]-des-Arg10-KD binding to include both kinetic and equilibrium data, and demonstrates that [3H]-des-Arg10-KD has a high affinity for human B1 bradykinin receptors and is sufficiently selective to be used as a radioligand for B1 receptors in human cells or tissues expressing an excess of B2 BK receptors.	Tritium	39-41	kininogen 1	Homo sapiens	183-193
8922733-10	1996	This is the first characterization of [3H]-des-Arg10-KD binding to include both kinetic and equilibrium data, and demonstrates that [3H]-des-Arg10-KD has a high affinity for human B1 bradykinin receptors and is sufficiently selective to be used as a radioligand for B1 receptors in human cells or tissues expressing an excess of B2 BK receptors.	Tritium	133-135	kininogen 1	Homo sapiens	183-193
8922758-15	1996	The bradykinin antagonist, Hoe 140, 10 to 200 micrograms, given by intranasal aerosol, produced a dose-related inhibition of the reduction in minimal nasal cross-sectional area (Amin) induced by bradykinin in normal subjects and by house dust mite antigen in subjects with allergic rhinitis to house dust mite.	4-hydroxy-2-octenal	27-30	kininogen 1	Homo sapiens	4-14
8922758-15	1996	The bradykinin antagonist, Hoe 140, 10 to 200 micrograms, given by intranasal aerosol, produced a dose-related inhibition of the reduction in minimal nasal cross-sectional area (Amin) induced by bradykinin in normal subjects and by house dust mite antigen in subjects with allergic rhinitis to house dust mite.	4-hydroxy-2-octenal	27-30	kininogen 1	Homo sapiens	195-205
8922758-18	1996	[1-Adamantane acetyl-D-Arg0, Hyp3, Thi5,8, D-Phe7]-bradykinin, 30 to 200 micrograms, caused a dose-related inhibition of the reduction in Amin and the release of albumin into the nasal cavity induced by bradykinin.	[1-adamantane acetyl-d-arg0	0-27	kininogen 1	Homo sapiens	51-61
8922758-18	1996	[1-Adamantane acetyl-D-Arg0, Hyp3, Thi5,8, D-Phe7]-bradykinin, 30 to 200 micrograms, caused a dose-related inhibition of the reduction in Amin and the release of albumin into the nasal cavity induced by bradykinin.	[1-adamantane acetyl-d-arg0	0-27	kininogen 1	Homo sapiens	203-213
8922758-18	1996	[1-Adamantane acetyl-D-Arg0, Hyp3, Thi5,8, D-Phe7]-bradykinin, 30 to 200 micrograms, caused a dose-related inhibition of the reduction in Amin and the release of albumin into the nasal cavity induced by bradykinin.	thi5	35-39	kininogen 1	Homo sapiens	51-61
8922758-18	1996	[1-Adamantane acetyl-D-Arg0, Hyp3, Thi5,8, D-Phe7]-bradykinin, 30 to 200 micrograms, caused a dose-related inhibition of the reduction in Amin and the release of albumin into the nasal cavity induced by bradykinin.	thi5	35-39	kininogen 1	Homo sapiens	203-213
9115953-6	1996	Bradykinin is a direct stimulant of nitric oxide release from the intact endothelial cell.	Nitric Oxide	36-48	kininogen 1	Homo sapiens	0-10
8939189-3	1996	Nedocromil sodium is highly effective against bronchoconstriction induced by bradykinin, the tachykinins substance P and neurokinin A, and sulfur dioxide and metabisulfite.	Nedocromil	0-17	kininogen 1	Homo sapiens	77-87
8910316-1	1996	To obtain data of the bradykinin B2 receptor"s agonist binding site, we used a combined approach of affinity labeling and "immunoidentification" of receptor fragments generated by cyanogen bromide cleavage.	Cyanogen Bromide	180-196	kininogen 1	Homo sapiens	22-32
8910316-2	1996	Domain-specific antibodies to the various extracellular receptor domains were applied to detect receptor fragments with covalently attached [125I-Tyr8]bradykinin.	125i-tyr8	141-150	kininogen 1	Homo sapiens	151-161
8903323-5	1996	Whereas cycloheximide and actinomycin D both inhibited BK-induced IL-1beta synthesis, results from Northern blot and nuclear run-on assays suggested that BK acted primarily at the transcription level which led to the accumulation of IL-1beta message in stimulated cells.	Cycloheximide	8-21	kininogen 1	Homo sapiens	55-57
8903323-5	1996	Whereas cycloheximide and actinomycin D both inhibited BK-induced IL-1beta synthesis, results from Northern blot and nuclear run-on assays suggested that BK acted primarily at the transcription level which led to the accumulation of IL-1beta message in stimulated cells.	Dactinomycin	26-39	kininogen 1	Homo sapiens	55-57
8875961-4	1996	The receptor agonist bradykinin, which increases intracellular Ca2+ (Ca(i)) level, shows no effect on the distribution of HSP27 isoforms.	carboxyamido-triazole	69-74	kininogen 1	Homo sapiens	21-31
8930174-0	1996	Differential effects of angiotensin converting enzyme inhibitors on the vasodepressor and prostacyclin responses to bradykinin.	Epoprostenol	90-102	kininogen 1	Homo sapiens	116-126
8930174-1	1996	Angiotensin converting enzyme (ACE) inhibitors block degradation of bradykinin and bradykinin stimulates prostacyclin production.	Epoprostenol	105-117	kininogen 1	Homo sapiens	83-93
8930174-5	1996	bradykinin in 21 salt-replete normal-to-high renin hypertensive patients.	Salts	17-21	kininogen 1	Homo sapiens	0-10
8930174-8	1996	Both ACE inhibitors dramatically, equally potentiated the vasodepressor response to bradykinin; the bradykinin dose required to decrease mean arterial pressure 15 mm Hg or increase pulse 20 bpm was 50-fold lower in ACEI-treated than in placebo-treated subjects (10 +/- 0 and 12.1 +/- 2.1 ng/kg/min in captopril and quinapril groups vs. 567 +/- 109 ng/kg/min in the placebo group; P &lt; .005).	acei	215-219	kininogen 1	Homo sapiens	84-94
8930174-8	1996	Both ACE inhibitors dramatically, equally potentiated the vasodepressor response to bradykinin; the bradykinin dose required to decrease mean arterial pressure 15 mm Hg or increase pulse 20 bpm was 50-fold lower in ACEI-treated than in placebo-treated subjects (10 +/- 0 and 12.1 +/- 2.1 ng/kg/min in captopril and quinapril groups vs. 567 +/- 109 ng/kg/min in the placebo group; P &lt; .005).	acei	215-219	kininogen 1	Homo sapiens	100-110
8930174-8	1996	Both ACE inhibitors dramatically, equally potentiated the vasodepressor response to bradykinin; the bradykinin dose required to decrease mean arterial pressure 15 mm Hg or increase pulse 20 bpm was 50-fold lower in ACEI-treated than in placebo-treated subjects (10 +/- 0 and 12.1 +/- 2.1 ng/kg/min in captopril and quinapril groups vs. 567 +/- 109 ng/kg/min in the placebo group; P &lt; .005).	Captopril	301-310	kininogen 1	Homo sapiens	100-110
8930174-8	1996	Both ACE inhibitors dramatically, equally potentiated the vasodepressor response to bradykinin; the bradykinin dose required to decrease mean arterial pressure 15 mm Hg or increase pulse 20 bpm was 50-fold lower in ACEI-treated than in placebo-treated subjects (10 +/- 0 and 12.1 +/- 2.1 ng/kg/min in captopril and quinapril groups vs. 567 +/- 109 ng/kg/min in the placebo group; P &lt; .005).	Quinapril	315-324	kininogen 1	Homo sapiens	100-110
8930174-9	1996	ACE inhibition significantly attenuated the prostacyclin response to bradykinin at any given level of hypotensive response.	Epoprostenol	44-56	kininogen 1	Homo sapiens	69-79
8930174-10	1996	Indomethacin abolished the prostacyclin response to bradykinin but did not alter the vasodepressor response.	Indomethacin	0-12	kininogen 1	Homo sapiens	52-62
8930174-10	1996	Indomethacin abolished the prostacyclin response to bradykinin but did not alter the vasodepressor response.	Epoprostenol	27-39	kininogen 1	Homo sapiens	52-62
8930174-11	1996	These data demonstrate that ACE inhibitors potentiate bradykinin-mediated vasodepression through a prostaglandin-independent mechanism.	Prostaglandins	99-112	kininogen 1	Homo sapiens	54-64
8930174-12	1996	They suggest that although ACE inhibitors increase prostaglandins by increasing bradykinin, ACE inhibitors may attenuate prostaglandin production through a second bradykinin-independent mechanism.	Prostaglandins	51-64	kininogen 1	Homo sapiens	80-90
21594530-2	1996	Bradykinin stimulated an increase in [Ca2+](i), (monitored by the fura-2 fluorescence) in fibroblasts obtained from both the skin of a normal donor and the mesenter of a familial adenomatous polyposis (FAP) patient.	Fura-2	66-72	kininogen 1	Homo sapiens	0-10
8917448-2	1996	Therefore, we analyzed bradykinin-activated Ca2+ influx into human foreskin fibroblast cells, HF-15, by fura-2 and 45Ca labeling to discriminate between Ca2+ influx into the fura-sensitive compartment and Ca uptake into fura-insensitive Ca stores.	Fura-2	104-110	kininogen 1	Homo sapiens	23-33
8947490-12	1996	ATP and UTP, even when eliciting responses of comparable size in the neuronal cell line, affect the desensitization of the bradykinin receptor differently.	Adenosine Triphosphate	0-3	kininogen 1	Homo sapiens	123-133
8947490-12	1996	ATP and UTP, even when eliciting responses of comparable size in the neuronal cell line, affect the desensitization of the bradykinin receptor differently.	Uridine Triphosphate	8-11	kininogen 1	Homo sapiens	123-133
8897926-0	1996	Serum interspecies differences in metabolic pathways of bradykinin and [des-Arg9]BK: influence of enalaprilat.	Enalaprilat	98-109	kininogen 1	Homo sapiens	56-66
8897926-6	1996	Enalaprilat significantly prevented the rapid BK and [des-Arg9]BK degradation in all species except that of [des-Arg9]BK in rat serum.	Enalaprilat	0-11	kininogen 1	Homo sapiens	46-48
8897926-6	1996	Enalaprilat significantly prevented the rapid BK and [des-Arg9]BK degradation in all species except that of [des-Arg9]BK in rat serum.	Enalaprilat	0-11	kininogen 1	Homo sapiens	63-65
8897926-6	1996	Enalaprilat significantly prevented the rapid BK and [des-Arg9]BK degradation in all species except that of [des-Arg9]BK in rat serum.	Enalaprilat	0-11	kininogen 1	Homo sapiens	63-65
8894164-12	1996	Stimulation of endothelial cells with bradykinin enhanced cell injury provoked by the exogenous superoxide generating system, but not by the exogenous hydroxyl radical generating system.	Superoxides	96-106	kininogen 1	Homo sapiens	38-48
8894164-13	1996	The enhancement by bradykinin was inhibited by NG-monomethyl-L-arginine and bradykinin B2-receptor antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7] bradykinin, suggesting that an interaction of NO with superoxide is involved in the enhanced cytotoxicity.	omega-N-Methylarginine	47-71	kininogen 1	Homo sapiens	19-29
8894164-13	1996	The enhancement by bradykinin was inhibited by NG-monomethyl-L-arginine and bradykinin B2-receptor antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7] bradykinin, suggesting that an interaction of NO with superoxide is involved in the enhanced cytotoxicity.	Superoxides	194-204	kininogen 1	Homo sapiens	19-29
8894164-13	1996	The enhancement by bradykinin was inhibited by NG-monomethyl-L-arginine and bradykinin B2-receptor antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7] bradykinin, suggesting that an interaction of NO with superoxide is involved in the enhanced cytotoxicity.	Superoxides	194-204	kininogen 1	Homo sapiens	76-86
8894164-13	1996	The enhancement by bradykinin was inhibited by NG-monomethyl-L-arginine and bradykinin B2-receptor antagonist, D-Arg-[Hyp3, Thi5,8, D-Phe7] bradykinin, suggesting that an interaction of NO with superoxide is involved in the enhanced cytotoxicity.	Superoxides	194-204	kininogen 1	Homo sapiens	76-86
8840871-10	1996	Suppression of ET-1 results from both removal of endogenous angiotensin II and accumulation of endogenous bradykinin/nitric oxide.	Nitric Oxide	117-129	kininogen 1	Homo sapiens	106-116
8826976-1	1996	Pretreatment of porcine aortic endothelial cells with high D-glucose results in enhanced endothelium-derived relaxing factor (EDRF) formation (39%) due to increased endothelial Ca2+ release (57%) and Ca2+ entry (97%) to bradykinin.	Glucose	59-68	kininogen 1	Homo sapiens	220-230
8826976-4	1996	Pretreatment of cells with the nonmetabolizing D-glucose analog, 3-O-methylglucopyranose (3-OMG), mimicked the effect of high D-glucose on Ca2+ release (41%) and Ca2+ entry (114%) to bradykinin, associated with elevated EDRF formation (26%).	Glucose	47-56	kininogen 1	Homo sapiens	183-193
8826976-4	1996	Pretreatment of cells with the nonmetabolizing D-glucose analog, 3-O-methylglucopyranose (3-OMG), mimicked the effect of high D-glucose on Ca2+ release (41%) and Ca2+ entry (114%) to bradykinin, associated with elevated EDRF formation (26%).	3-O-Methyl-D-glucopyranose	65-88	kininogen 1	Homo sapiens	183-193
8826976-4	1996	Pretreatment of cells with the nonmetabolizing D-glucose analog, 3-O-methylglucopyranose (3-OMG), mimicked the effect of high D-glucose on Ca2+ release (41%) and Ca2+ entry (114%) to bradykinin, associated with elevated EDRF formation (26%).	3'-O-methylguanosine	90-95	kininogen 1	Homo sapiens	183-193
8826976-4	1996	Pretreatment of cells with the nonmetabolizing D-glucose analog, 3-O-methylglucopyranose (3-OMG), mimicked the effect of high D-glucose on Ca2+ release (41%) and Ca2+ entry (114%) to bradykinin, associated with elevated EDRF formation (26%).	Glucose	126-135	kininogen 1	Homo sapiens	183-193
8826976-8	1996	Like high D-glucose, pretreatment with the O2(-)-generating system, xanthine oxidase/hypoxanthine, elevated bradykinin-stimulated Ca2+ release (+10%), Ca2+ entry (+75%), and EDRF (+73%).	Glucose	10-19	kininogen 1	Homo sapiens	108-118
8826976-8	1996	Like high D-glucose, pretreatment with the O2(-)-generating system, xanthine oxidase/hypoxanthine, elevated bradykinin-stimulated Ca2+ release (+10%), Ca2+ entry (+75%), and EDRF (+73%).	Superoxides	43-45	kininogen 1	Homo sapiens	108-118
9048263-6	1996	In the hypercholesterolaemic patients compared with control subjects maximal forearm blood flow was significantly impaired after stimulation of endogenous nitric oxide synthesis by acetylcholine and bradykinin and during infusion of the nitric oxide donor sodium nitroprusside (acetylcholine: -19%, bradykinin: -29%, sodium nitroprusside: -24% versus control individuals; P &lt; 0.05).	Nitric Oxide	155-167	kininogen 1	Homo sapiens	199-209
9048263-6	1996	In the hypercholesterolaemic patients compared with control subjects maximal forearm blood flow was significantly impaired after stimulation of endogenous nitric oxide synthesis by acetylcholine and bradykinin and during infusion of the nitric oxide donor sodium nitroprusside (acetylcholine: -19%, bradykinin: -29%, sodium nitroprusside: -24% versus control individuals; P &lt; 0.05).	Nitric Oxide	237-249	kininogen 1	Homo sapiens	299-309
9048263-6	1996	In the hypercholesterolaemic patients compared with control subjects maximal forearm blood flow was significantly impaired after stimulation of endogenous nitric oxide synthesis by acetylcholine and bradykinin and during infusion of the nitric oxide donor sodium nitroprusside (acetylcholine: -19%, bradykinin: -29%, sodium nitroprusside: -24% versus control individuals; P &lt; 0.05).	Nitroprusside	256-276	kininogen 1	Homo sapiens	299-309
9238639-0	1996	Rationally designed non-peptides: variously substituted piperazine libraries for the discovery of bradykinin antagonists and other G-protein-coupled receptor ligands.	Piperazine	56-66	kininogen 1	Homo sapiens	98-108
9238639-1	1996	Molecular modeling studies of potent decapeptide bradykinin antagonists suggested the de novo design of peptide mimetics based on a 1,2,3,4-tetrasubstituted 1,4-piperazin-6-one scaffold.	1,2,3,4-tetrasubstituted	132-156	kininogen 1	Homo sapiens	49-59
9238639-1	1996	Molecular modeling studies of potent decapeptide bradykinin antagonists suggested the de novo design of peptide mimetics based on a 1,2,3,4-tetrasubstituted 1,4-piperazin-6-one scaffold.	1,4-piperazin-6-one	157-176	kininogen 1	Homo sapiens	49-59
9238639-7	1996	Notably, a bradykinin antagonist lead, CP-2458, with good receptor selectivity and antagonist activity in human-cell assays was identified and is undergoing optimization by traditional and combinatorial methods.	cp-2458	39-46	kininogen 1	Homo sapiens	11-21
8849775-2	1996	5"-phosphorothioate-modified RNA (GMPS-RNA) sequences were selected from a randomized pool of oligoribonucleotides for their ability to accelerate a halide substitution reaction with N-bromoacetyl-bradykinin (BrBK).	5"-phosphorothioate	0-19	kininogen 1	Homo sapiens	197-207
8849775-2	1996	5"-phosphorothioate-modified RNA (GMPS-RNA) sequences were selected from a randomized pool of oligoribonucleotides for their ability to accelerate a halide substitution reaction with N-bromoacetyl-bradykinin (BrBK).	halide	149-155	kininogen 1	Homo sapiens	197-207
8876745-4	1996	This dilation could be abolished by the selective bradykinin B2-receptor antagonist Hoe 140 (2 mg kg-1 min-1, i.a.	4-hydroxy-2-octenal	84-87	kininogen 1	Homo sapiens	50-60
8938754-10	1996	Blocking the bradykinin binding at the B1 receptor with (Des-Arg10)-Lys-bradykinin and at the B2 receptor with D-Arg(Hyp3-Thi5.8-D-Phe7)-bradykinin, respectively, revealed that in 0.75-day-old cultures no or only a very small amount of B1 receptors are present.	D-Arginine	111-116	kininogen 1	Homo sapiens	13-23
8938754-10	1996	Blocking the bradykinin binding at the B1 receptor with (Des-Arg10)-Lys-bradykinin and at the B2 receptor with D-Arg(Hyp3-Thi5.8-D-Phe7)-bradykinin, respectively, revealed that in 0.75-day-old cultures no or only a very small amount of B1 receptors are present.	thi5	122-126	kininogen 1	Homo sapiens	13-23
8917448-2	1996	Therefore, we analyzed bradykinin-activated Ca2+ influx into human foreskin fibroblast cells, HF-15, by fura-2 and 45Ca labeling to discriminate between Ca2+ influx into the fura-sensitive compartment and Ca uptake into fura-insensitive Ca stores.	fura	104-108	kininogen 1	Homo sapiens	23-33
8917448-3	1996	Bradykinin-activated Ca2+ influx into the fura-sensitive compartment was blocked by inhibitors of NO synthases.	fura	42-46	kininogen 1	Homo sapiens	0-10
8917448-4	1996	These inhibitors also suppressed bradykinin-activated increases in cGMP, indicating that the NO-dependent increase in cGMP is involved in the activation of the Ca2+ influx into the fura-sensitive compartment.	Cyclic GMP	67-71	kininogen 1	Homo sapiens	33-43
8917448-4	1996	These inhibitors also suppressed bradykinin-activated increases in cGMP, indicating that the NO-dependent increase in cGMP is involved in the activation of the Ca2+ influx into the fura-sensitive compartment.	Cyclic GMP	118-122	kininogen 1	Homo sapiens	33-43
8917448-4	1996	These inhibitors also suppressed bradykinin-activated increases in cGMP, indicating that the NO-dependent increase in cGMP is involved in the activation of the Ca2+ influx into the fura-sensitive compartment.	fura	181-185	kininogen 1	Homo sapiens	33-43
8917448-5	1996	The cGMP-dependent kinase inhibitors KT5823 and Rp-8-(parachlorophenylthio)-cGMP (Rp-8-pCPT-cGMPS) blocked bradykinin-activated Ca2+ influx into the fura-sensitive compartment, suggesting that a cGMP-dependent kinase step participates in the activation of this Ca2+ influx pathway.	Cyclic GMP	4-8	kininogen 1	Homo sapiens	107-117
8917448-5	1996	The cGMP-dependent kinase inhibitors KT5823 and Rp-8-(parachlorophenylthio)-cGMP (Rp-8-pCPT-cGMPS) blocked bradykinin-activated Ca2+ influx into the fura-sensitive compartment, suggesting that a cGMP-dependent kinase step participates in the activation of this Ca2+ influx pathway.	KT 5823	37-43	kininogen 1	Homo sapiens	107-117
8917448-5	1996	The cGMP-dependent kinase inhibitors KT5823 and Rp-8-(parachlorophenylthio)-cGMP (Rp-8-pCPT-cGMPS) blocked bradykinin-activated Ca2+ influx into the fura-sensitive compartment, suggesting that a cGMP-dependent kinase step participates in the activation of this Ca2+ influx pathway.	rp-8-(parachlorophenylthio)-cgmp	48-80	kininogen 1	Homo sapiens	107-117
8917448-5	1996	The cGMP-dependent kinase inhibitors KT5823 and Rp-8-(parachlorophenylthio)-cGMP (Rp-8-pCPT-cGMPS) blocked bradykinin-activated Ca2+ influx into the fura-sensitive compartment, suggesting that a cGMP-dependent kinase step participates in the activation of this Ca2+ influx pathway.	8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphorothioate	82-97	kininogen 1	Homo sapiens	107-117
8917448-5	1996	The cGMP-dependent kinase inhibitors KT5823 and Rp-8-(parachlorophenylthio)-cGMP (Rp-8-pCPT-cGMPS) blocked bradykinin-activated Ca2+ influx into the fura-sensitive compartment, suggesting that a cGMP-dependent kinase step participates in the activation of this Ca2+ influx pathway.	fura	149-153	kininogen 1	Homo sapiens	107-117
8917448-5	1996	The cGMP-dependent kinase inhibitors KT5823 and Rp-8-(parachlorophenylthio)-cGMP (Rp-8-pCPT-cGMPS) blocked bradykinin-activated Ca2+ influx into the fura-sensitive compartment, suggesting that a cGMP-dependent kinase step participates in the activation of this Ca2+ influx pathway.	Cyclic GMP	76-80	kininogen 1	Homo sapiens	107-117
8917448-6	1996	In addition to the NO/cGMP-mediated Ca2+ influx into the fura-sensitive compartment, bradykinin enhanced 45Ca uptake into Ca stores that were not accessible to fura-2.	Fura-2	160-166	kininogen 1	Homo sapiens	85-95
8917448-9	1996	Hence, bradykinin stimulates two distinct Ca2+ influx pathways in HF-15 cells, (a) Ca2+ influx into the fura-sensitive compartment which is NO/cGMP-dependent and (b) Ca uptake into Ca stores which bypasses the cytoplasm, which is NO insensitive and which is linked to cell proliferation.	fura	104-108	kininogen 1	Homo sapiens	7-17
8917448-9	1996	Hence, bradykinin stimulates two distinct Ca2+ influx pathways in HF-15 cells, (a) Ca2+ influx into the fura-sensitive compartment which is NO/cGMP-dependent and (b) Ca uptake into Ca stores which bypasses the cytoplasm, which is NO insensitive and which is linked to cell proliferation.	Cyclic GMP	143-147	kininogen 1	Homo sapiens	7-17
8886417-4	1996	The integrity of the endothelium was assessed by the bradykinin-induced relaxation of prostaglandin F2 alpha (PGF2 alpha, 3 microM)-precontracted vessels.	Dinoprost	86-108	kininogen 1	Homo sapiens	53-63
8886417-4	1996	The integrity of the endothelium was assessed by the bradykinin-induced relaxation of prostaglandin F2 alpha (PGF2 alpha, 3 microM)-precontracted vessels.	Dinoprost	110-120	kininogen 1	Homo sapiens	53-63
8891757-4	1996	Addition of PGE2 or increasing the endogenous formation of PGE2 by treating the cells with arachidonic acid, bradykinin, Lys-bradykinin or des-Arg9-bradykinin, did not affect osteocalcin and type I collagen formation in unstimulated or 1,25(OH)2-vitamin D3-stimulated osteoblasts.	Dinoprostone	12-16	kininogen 1	Homo sapiens	109-119
8886862-0	1996	The contribution of histamine to the action of bradykinin in the human nasal airway.	Histamine	20-29	kininogen 1	Homo sapiens	47-57
8886862-3	1996	Pretreatment with cetirizine (10 mg orally) reduced the fall in Amin induced by bradykinin, 300 micrograms, but not by bradykinin, 100 micrograms.	Cetirizine	18-28	kininogen 1	Homo sapiens	80-90
8891757-4	1996	Addition of PGE2 or increasing the endogenous formation of PGE2 by treating the cells with arachidonic acid, bradykinin, Lys-bradykinin or des-Arg9-bradykinin, did not affect osteocalcin and type I collagen formation in unstimulated or 1,25(OH)2-vitamin D3-stimulated osteoblasts.	Dinoprostone	59-63	kininogen 1	Homo sapiens	109-119
8886862-4	1996	Pre-treatment of the subjects with the H1 histamine receptor antgonist cetirizine (10 mg, orally) or terfenadine (60 mg, orally) 3 h before bradykinin administration caused significant reduction of the bradykinin-induced increase in nasal airway resistance in the upper range of bradykinin doses (300-1000 micrograms) but not in the lower range (10-100 micrograms).	Cetirizine	71-81	kininogen 1	Homo sapiens	140-150
8886862-4	1996	Pre-treatment of the subjects with the H1 histamine receptor antgonist cetirizine (10 mg, orally) or terfenadine (60 mg, orally) 3 h before bradykinin administration caused significant reduction of the bradykinin-induced increase in nasal airway resistance in the upper range of bradykinin doses (300-1000 micrograms) but not in the lower range (10-100 micrograms).	Cetirizine	71-81	kininogen 1	Homo sapiens	202-212
8891757-4	1996	Addition of PGE2 or increasing the endogenous formation of PGE2 by treating the cells with arachidonic acid, bradykinin, Lys-bradykinin or des-Arg9-bradykinin, did not affect osteocalcin and type I collagen formation in unstimulated or 1,25(OH)2-vitamin D3-stimulated osteoblasts.	Dinoprostone	59-63	kininogen 1	Homo sapiens	125-135
8886862-4	1996	Pre-treatment of the subjects with the H1 histamine receptor antgonist cetirizine (10 mg, orally) or terfenadine (60 mg, orally) 3 h before bradykinin administration caused significant reduction of the bradykinin-induced increase in nasal airway resistance in the upper range of bradykinin doses (300-1000 micrograms) but not in the lower range (10-100 micrograms).	Cetirizine	71-81	kininogen 1	Homo sapiens	202-212
8886862-4	1996	Pre-treatment of the subjects with the H1 histamine receptor antgonist cetirizine (10 mg, orally) or terfenadine (60 mg, orally) 3 h before bradykinin administration caused significant reduction of the bradykinin-induced increase in nasal airway resistance in the upper range of bradykinin doses (300-1000 micrograms) but not in the lower range (10-100 micrograms).	Terfenadine	101-112	kininogen 1	Homo sapiens	140-150
8891757-4	1996	Addition of PGE2 or increasing the endogenous formation of PGE2 by treating the cells with arachidonic acid, bradykinin, Lys-bradykinin or des-Arg9-bradykinin, did not affect osteocalcin and type I collagen formation in unstimulated or 1,25(OH)2-vitamin D3-stimulated osteoblasts.	Dinoprostone	59-63	kininogen 1	Homo sapiens	125-135
8886862-4	1996	Pre-treatment of the subjects with the H1 histamine receptor antgonist cetirizine (10 mg, orally) or terfenadine (60 mg, orally) 3 h before bradykinin administration caused significant reduction of the bradykinin-induced increase in nasal airway resistance in the upper range of bradykinin doses (300-1000 micrograms) but not in the lower range (10-100 micrograms).	Terfenadine	101-112	kininogen 1	Homo sapiens	202-212
8886862-4	1996	Pre-treatment of the subjects with the H1 histamine receptor antgonist cetirizine (10 mg, orally) or terfenadine (60 mg, orally) 3 h before bradykinin administration caused significant reduction of the bradykinin-induced increase in nasal airway resistance in the upper range of bradykinin doses (300-1000 micrograms) but not in the lower range (10-100 micrograms).	Terfenadine	101-112	kininogen 1	Homo sapiens	202-212
8951657-6	1996	The results indicate that albumin flux significantly increased in the peritoneum, pancreas, stomach, PSI, DSI, colon, kidneys, liver, lungs, and brain, TBC significantly increased in the kidneys, liver, lungs, and heart, as well as in the intestine, and an increased ALI, assaying endothelial permeability considering local hemodynamic alterations was noted in the pancreas, kidneys, liver, lungs, PSI, and DSI in the group with BK alone.	tbc	152-155	kininogen 1	Homo sapiens	429-431
8886862-5	1996	Cetirizine reduced the albumin release into the nasal airway and the symptoms induced by bradykinin, 1000 micrograms.	Cetirizine	0-10	kininogen 1	Homo sapiens	89-99
8886862-7	1996	Isolated human nasal cells released histamine in response to bradykinin, 33 and 100 microM, anti-IgE and calcium ionophore, A23187.	Histamine	36-45	kininogen 1	Homo sapiens	61-71
8886862-8	1996	We conclude that the actions of bradykinin in the human nasal airway are, in part, accounted for by the release of histamine.	Histamine	115-124	kininogen 1	Homo sapiens	32-42
8816908-6	1996	A23187 was a less potent vasodilator of resistance arteries studied in vitro, compared to epicardial conduit arteries (EC50 = 1.6 microM, resistance artery vs. EC50 = 0.03 microM, conduit artery); however, bradykinin was more potent in resistance arteries (EC50 = 0.3 nM, resistance artery vs. EC50 = 2 nM, conduit artery).	Calcimycin	0-6	kininogen 1	Homo sapiens	206-216
8874148-4	1996	Responses to angiotensin I and angiotensin I-(3-10) were decreased by the angiotensin converting enzyme inhibitor enalaprilat in a dose of the angiotensin converting enzyme inhibitor that had no effect on responses to angiotensin II and IV and that enhanced vasodilator responses to bradykinin.	Enalaprilat	114-125	kininogen 1	Homo sapiens	283-293
8877579-3	1996	Bradykinin (BK: Gi-2 protein-independent), serotonin (5-HT: Gi-2 protein-dependent), or direct activation of the G(i-2)-protein by mastoparan increased the release of endothelium-derived nitric oxide (EDNO) from porcine arterial endothelial cells (EC).	Nitric Oxide	187-199	kininogen 1	Homo sapiens	0-10
8877579-3	1996	Bradykinin (BK: Gi-2 protein-independent), serotonin (5-HT: Gi-2 protein-dependent), or direct activation of the G(i-2)-protein by mastoparan increased the release of endothelium-derived nitric oxide (EDNO) from porcine arterial endothelial cells (EC).	Nitric Oxide	201-205	kininogen 1	Homo sapiens	0-10
8753774-7	1996	C6-ceramide or SMase treatment did not affect the action of BK on PLD either in young or in old cells, whereas sphingosine further increased PLD activity stimulated by BK in young but not in old cells.	Sphingosine	111-122	kininogen 1	Homo sapiens	168-170
8709736-0	1996	Randomised double-blind placebo-controlled study of the effect of inhibition of nitric oxide synthesis in bradykinin-induced asthma.	Nitric Oxide	80-92	kininogen 1	Homo sapiens	106-116
8709736-1	1996	BACKGROUND: Bronchoconstriction induced by bradykinin is reduced by the release of nitric oxide (NO) in the airways of guinea pigs.	Nitric Oxide	83-95	kininogen 1	Homo sapiens	43-53
8709736-10	1996	FINDINGS: The geometric mean of the provocative dose producing a 20% fall in FEV1 to bradykinin was 138.0 nmol (range 48.2-475.2 nmol) after placebo and 11.2 nmol (range 0.9-51.3 nmol) after L-NMMA (p &lt; 0.01).	omega-N-Methylarginine	191-197	kininogen 1	Homo sapiens	85-95
8753774-6	1996	The modulatory role of sphingoid molecules on the action of bradykinin (BK) in PLD activation was then evaluated in young and old fibroblasts.	Sphingosine	23-32	kininogen 1	Homo sapiens	60-70
8853439-2	1996	[3H]BK bound specifically in a manner consistent with a single high-affinity site.	Tritium	1-3	kininogen 1	Homo sapiens	4-6
8853439-5	1996	BK stimulated intracellular calcium ion concentration ([Ca2+]i) release in a dose-dependent manner with a threshold at 1 nM.	Calcium	28-35	kininogen 1	Homo sapiens	0-2
8853439-6	1996	Hoe-140, in contrast with [des-Arg9]BK, abolished this effect.	des-arg9	27-35	kininogen 1	Homo sapiens	36-38
8853439-9	1996	These results associated with the stimulatory effect of BK on inositol phosphate production indicated that [Ca2+]i stimulation was produced both by [Ca2+] mobilization from its intracellular stores and by [Ca2+] entry into the cells.	Inositol Phosphates	62-80	kininogen 1	Homo sapiens	56-58
8753774-6	1996	The modulatory role of sphingoid molecules on the action of bradykinin (BK) in PLD activation was then evaluated in young and old fibroblasts.	Sphingosine	23-32	kininogen 1	Homo sapiens	72-74
8753774-9	1996	These results suggest that a specific alteration of BK segnalatory pathway occurs in old fibroblasts, likely involving sphingosine formation which may account for the potentiated PLD activity induced by the peptide in these cells.	Sphingosine	119-130	kininogen 1	Homo sapiens	52-54
8770120-4	1996	After incubation with 20 or 50 mM K+ for 1 h, the indomethacin- and NG-nitro-L-arginine+ (L-NNA)-resistant relaxation induced by A23187 or bradykinin, which could be further inhibited by tetraethylammonium but not glibenclamide, was significantly reduced.	Indomethacin	50-62	kininogen 1	Homo sapiens	139-149
8759638-0	1996	Synthesis and characterization of pseudopeptide bradykinin B2 receptor antagonists containing the 1,3,8-triazaspiro[4.5]decan-4-one ring system.	1,3,8-Triazaspiro[4.5]decan-4-one	98-131	kininogen 1	Homo sapiens	48-58
8770120-4	1996	After incubation with 20 or 50 mM K+ for 1 h, the indomethacin- and NG-nitro-L-arginine+ (L-NNA)-resistant relaxation induced by A23187 or bradykinin, which could be further inhibited by tetraethylammonium but not glibenclamide, was significantly reduced.	Nitroarginine	68-87	kininogen 1	Homo sapiens	139-149
8770120-4	1996	After incubation with 20 or 50 mM K+ for 1 h, the indomethacin- and NG-nitro-L-arginine+ (L-NNA)-resistant relaxation induced by A23187 or bradykinin, which could be further inhibited by tetraethylammonium but not glibenclamide, was significantly reduced.	Nitroarginine	90-95	kininogen 1	Homo sapiens	139-149
8770120-4	1996	After incubation with 20 or 50 mM K+ for 1 h, the indomethacin- and NG-nitro-L-arginine+ (L-NNA)-resistant relaxation induced by A23187 or bradykinin, which could be further inhibited by tetraethylammonium but not glibenclamide, was significantly reduced.	Tetraethylammonium	187-205	kininogen 1	Homo sapiens	139-149
8770120-4	1996	After incubation with 20 or 50 mM K+ for 1 h, the indomethacin- and NG-nitro-L-arginine+ (L-NNA)-resistant relaxation induced by A23187 or bradykinin, which could be further inhibited by tetraethylammonium but not glibenclamide, was significantly reduced.	Glyburide	214-227	kininogen 1	Homo sapiens	139-149
8795298-7	1996	The bradykinin effect was blocked by 5 mumol/L U-73122 (an inhibitor of inositol trisphosphate production); the ionomycin effect was inhibited by increasing intracellular pH (pHi) or treatment with 100 mumol/L ryanodine while the monensin effect was enhanced by increasing pHi, but was not inhibited by ryanodine.	Ryanodine	303-312	kininogen 1	Homo sapiens	4-14
8886495-12	1996	Although it has been suggested that these endings are activated by bradykinin, recent evidence indicates that they are activated by adenosine released from the ischaemic myocardium.	Adenosine	132-141	kininogen 1	Homo sapiens	67-77
8757204-5	1996	OBJECTIVE: To test this hypothesis, we measured the wheal response to intradermal injection of bradykinin in salt-replete hypertensive and normotensive African Americans and Caucasians.	Salts	109-113	kininogen 1	Homo sapiens	95-105
8795298-7	1996	The bradykinin effect was blocked by 5 mumol/L U-73122 (an inhibitor of inositol trisphosphate production); the ionomycin effect was inhibited by increasing intracellular pH (pHi) or treatment with 100 mumol/L ryanodine while the monensin effect was enhanced by increasing pHi, but was not inhibited by ryanodine.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	47-54	kininogen 1	Homo sapiens	4-14
8795298-7	1996	The bradykinin effect was blocked by 5 mumol/L U-73122 (an inhibitor of inositol trisphosphate production); the ionomycin effect was inhibited by increasing intracellular pH (pHi) or treatment with 100 mumol/L ryanodine while the monensin effect was enhanced by increasing pHi, but was not inhibited by ryanodine.	inositol 1,2,3-trisphosphate	72-94	kininogen 1	Homo sapiens	4-14
8795298-7	1996	The bradykinin effect was blocked by 5 mumol/L U-73122 (an inhibitor of inositol trisphosphate production); the ionomycin effect was inhibited by increasing intracellular pH (pHi) or treatment with 100 mumol/L ryanodine while the monensin effect was enhanced by increasing pHi, but was not inhibited by ryanodine.	Ryanodine	210-219	kininogen 1	Homo sapiens	4-14
8683731-4	1996	RESULTS: Substance P and BK potentiated responses to the purinergic component of the neurogenic stimulation (that part of the contractile response that remains after treatment with atropine) and potentiated responses to exogenously applied adenosine triphosphate (ATP).	Atropine	181-189	kininogen 1	Homo sapiens	25-27
8683731-4	1996	RESULTS: Substance P and BK potentiated responses to the purinergic component of the neurogenic stimulation (that part of the contractile response that remains after treatment with atropine) and potentiated responses to exogenously applied adenosine triphosphate (ATP).	Adenosine Triphosphate	240-262	kininogen 1	Homo sapiens	25-27
8683731-4	1996	RESULTS: Substance P and BK potentiated responses to the purinergic component of the neurogenic stimulation (that part of the contractile response that remains after treatment with atropine) and potentiated responses to exogenously applied adenosine triphosphate (ATP).	Adenosine Triphosphate	264-267	kininogen 1	Homo sapiens	25-27
8914860-11	1996	Stimulation of phosphatidylinositol turnover and calcium mobilization were also induced by 10 nM bradykinin; these effects were influenced neither by the previous administration of the NK1 receptor agonist nor by the three antagonists tested.	Phosphatidylinositols	15-35	kininogen 1	Homo sapiens	97-107
8914860-11	1996	Stimulation of phosphatidylinositol turnover and calcium mobilization were also induced by 10 nM bradykinin; these effects were influenced neither by the previous administration of the NK1 receptor agonist nor by the three antagonists tested.	Calcium	49-56	kininogen 1	Homo sapiens	97-107
8706894-6	1996	The M(r) of high-molecular-weight kininogen was determined to be 83,500 by sedimentation equilibrium measurements, in agreement with the value calculated from amino acid sequence and carbohydrate analysis.	Carbohydrates	183-195	kininogen 1	Homo sapiens	12-43
8759097-9	1996	CONCLUSIONS: These results indicate that bradykinin and its metabolites are selective antithrombins by preventing alpha-thrombin cleavage of the cloned thrombin receptor between arginine-41 and serine-42.	Arginine	178-186	kininogen 1	Homo sapiens	41-51
8759097-9	1996	CONCLUSIONS: These results indicate that bradykinin and its metabolites are selective antithrombins by preventing alpha-thrombin cleavage of the cloned thrombin receptor between arginine-41 and serine-42.	Serine	194-200	kininogen 1	Homo sapiens	41-51
8883499-6	1996	Bradykinin-induced nitric oxide production is reduced by angiotensin-converting enzyme.	Nitric Oxide	19-31	kininogen 1	Homo sapiens	0-10
8707379-7	1996	We conclude that bradykinin relaxes these human resistance arteries in an endothelium-dependent but predominantly nitric oxide- and prostanoid-independent manner; relaxation likely depends on the action of an endothelium-derived hyperpolarizing vasodilator.	Nitric Oxide	114-126	kininogen 1	Homo sapiens	17-27
8707379-7	1996	We conclude that bradykinin relaxes these human resistance arteries in an endothelium-dependent but predominantly nitric oxide- and prostanoid-independent manner; relaxation likely depends on the action of an endothelium-derived hyperpolarizing vasodilator.	Prostaglandins	132-142	kininogen 1	Homo sapiens	17-27
8795298-11	1996	The bradykinin-induced increase in inositol trisphosphates in thermotolerant cells was also reduced, which perhaps accounts for the attenuation in Ca2+ mobilization.	inositol trisphosphates	35-58	kininogen 1	Homo sapiens	4-14
8764214-2	1996	Bradykinin induced a significant increase in [3H]glycoconjugate secretion in a dose-dependent manner from isolated glands, which was significantly inhibited by D-Arg-(Hyp3, Thi5,8, D-Phe7)-bradykinin (the B2-receptor antagonist), whereas Des-Arg9-(Leu8)-bradykinin (B1-receptor antagonist) or indomethacin did not significantly alter it.	Tritium	46-48	kininogen 1	Homo sapiens	0-10
16525512-0	1996	Blackbody infrared radiative dissociation of bradykinin and its analogues: energetics, dynamics, and evidence for salt-bridge structures in the gas phase.	Salts	114-118	kininogen 1	Homo sapiens	45-55
16525512-5	1996	For bradykinin and its analogues differing by modification of the residues between the two arginine groups on either end of the molecule, the singly and doubly protonated ions have average activation energies of 1.2 and 0.8 eV, respectively, and average A values of 10(8) and 10(12) s(-1), respectively, i.e., the presence of a second charge reduces the activation energy by 0.4 eV and decreases the A value by a factor of 10(4).	Arginine	91-99	kininogen 1	Homo sapiens	4-14
16525512-7	1996	The doubly protonated methyl ester of bradykinin has an E(a) of 0.82 eV, comparable to the value of 0.84 eV for bradykinin itself.	methyl ester	22-34	kininogen 1	Homo sapiens	38-48
16525512-7	1996	The doubly protonated methyl ester of bradykinin has an E(a) of 0.82 eV, comparable to the value of 0.84 eV for bradykinin itself.	methyl ester	22-34	kininogen 1	Homo sapiens	112-122
16525512-8	1996	However, this value is 0.21 +/- 0.08 eV greater than that of singly protonated methyl ester of bradykinin, indicating that the Coulomb repulsion is not the most significant factor in the activation energy of this ion.	methyl ester	79-91	kininogen 1	Homo sapiens	95-105
16525512-12	1996	Similar results are observed for [Ala(6)]-bradykinin and its methyl ester.	ala(6)	34-40	kininogen 1	Homo sapiens	42-52
8760168-5	1996	Under these in vivo conditions, the NO donor agent S-nitroso-N-acetylpenicillamine (SNAP) reversibly attenuated responses to the endothelium-dependent vasodilators, acetylcholine and bradykinin.	S-Nitroso-N-Acetylpenicillamine	51-82	kininogen 1	Homo sapiens	183-193
8760168-5	1996	Under these in vivo conditions, the NO donor agent S-nitroso-N-acetylpenicillamine (SNAP) reversibly attenuated responses to the endothelium-dependent vasodilators, acetylcholine and bradykinin.	S-Nitroso-N-Acetylpenicillamine	84-88	kininogen 1	Homo sapiens	183-193
8964116-4	1996	Microvessels were incubated in the presence of agonists for nitric oxide production (acetylcholine and bradykinin), which caused dose-dependent increases in nitrite, a response that was blocked by NG-nitro-L-arginine methyl ester and receptor-specific antagonists (atropine and HOE 140, respectively).	Nitric Oxide	60-72	kininogen 1	Homo sapiens	103-113
8964116-4	1996	Microvessels were incubated in the presence of agonists for nitric oxide production (acetylcholine and bradykinin), which caused dose-dependent increases in nitrite, a response that was blocked by NG-nitro-L-arginine methyl ester and receptor-specific antagonists (atropine and HOE 140, respectively).	Nitrites	157-164	kininogen 1	Homo sapiens	103-113
8964116-4	1996	Microvessels were incubated in the presence of agonists for nitric oxide production (acetylcholine and bradykinin), which caused dose-dependent increases in nitrite, a response that was blocked by NG-nitro-L-arginine methyl ester and receptor-specific antagonists (atropine and HOE 140, respectively).	NG-Nitroarginine Methyl Ester	197-229	kininogen 1	Homo sapiens	103-113
8964116-4	1996	Microvessels were incubated in the presence of agonists for nitric oxide production (acetylcholine and bradykinin), which caused dose-dependent increases in nitrite, a response that was blocked by NG-nitro-L-arginine methyl ester and receptor-specific antagonists (atropine and HOE 140, respectively).	Atropine	265-273	kininogen 1	Homo sapiens	103-113
8964116-4	1996	Microvessels were incubated in the presence of agonists for nitric oxide production (acetylcholine and bradykinin), which caused dose-dependent increases in nitrite, a response that was blocked by NG-nitro-L-arginine methyl ester and receptor-specific antagonists (atropine and HOE 140, respectively).	4-hydroxy-2-octenal	278-281	kininogen 1	Homo sapiens	103-113
8832629-4	1996	We also show that low doses of bradykinin elicit intracellular calcium release almost exclusively in AD cell lines in an all or none fashion that provide a clear measurement of enhanced IP3-mediated function in AD vs. controls.	Calcium	63-70	kininogen 1	Homo sapiens	31-41
8832629-4	1996	We also show that low doses of bradykinin elicit intracellular calcium release almost exclusively in AD cell lines in an all or none fashion that provide a clear measurement of enhanced IP3-mediated function in AD vs. controls.	Inositol 1,4,5-Trisphosphate	186-189	kininogen 1	Homo sapiens	31-41
8672553-2	1996	In the presence of external calcium, bradykinin (BK) increased cytosolic free calcium ([Ca2+]i) about 3-fold and then [Ca2+]i rapidly declined.	Calcium	28-35	kininogen 1	Homo sapiens	37-47
8672553-2	1996	In the presence of external calcium, bradykinin (BK) increased cytosolic free calcium ([Ca2+]i) about 3-fold and then [Ca2+]i rapidly declined.	Calcium	28-35	kininogen 1	Homo sapiens	49-51
8672553-2	1996	In the presence of external calcium, bradykinin (BK) increased cytosolic free calcium ([Ca2+]i) about 3-fold and then [Ca2+]i rapidly declined.	Calcium	78-85	kininogen 1	Homo sapiens	37-47
8672553-2	1996	In the presence of external calcium, bradykinin (BK) increased cytosolic free calcium ([Ca2+]i) about 3-fold and then [Ca2+]i rapidly declined.	Calcium	78-85	kininogen 1	Homo sapiens	49-51
8818341-2	1996	The effects of inhibitors of nitric oxide synthase and local anaesthetics were studied on changes in human nasal airway patency and albumin extravasation in response to bradykinin and histamine, in vivo.	Nitric Oxide	29-41	kininogen 1	Homo sapiens	169-179
8818341-5	1996	L-NAME, 0.1 to 10 mumol, produced a dose-related inhibition of the reduction in A min caused by bradykinin, 300 micrograms.	NG-Nitroarginine Methyl Ester	0-6	kininogen 1	Homo sapiens	96-106
8818341-6	1996	NG-monomethyl-L-arginine (L-NMMA), 1 mumol, similarly reduced the effect of bradykinin, 300 micrograms, on A min, but NG-nitro-D-arginine methyl ester (D-NAME), had no effect.	omega-N-Methylarginine	0-24	kininogen 1	Homo sapiens	76-86
8818341-6	1996	NG-monomethyl-L-arginine (L-NMMA), 1 mumol, similarly reduced the effect of bradykinin, 300 micrograms, on A min, but NG-nitro-D-arginine methyl ester (D-NAME), had no effect.	omega-N-Methylarginine	26-32	kininogen 1	Homo sapiens	76-86
8818341-9	1996	The inhibition by L-NAME, 1 mumol of the action of bradykinin, 300 micrograms on A min was maximal between 15 and 30 min after pretreatment with L-NAME.	NG-Nitroarginine Methyl Ester	18-24	kininogen 1	Homo sapiens	51-61
8818341-9	1996	The inhibition by L-NAME, 1 mumol of the action of bradykinin, 300 micrograms on A min was maximal between 15 and 30 min after pretreatment with L-NAME.	NG-Nitroarginine Methyl Ester	145-151	kininogen 1	Homo sapiens	51-61
8818341-11	1996	L-NAME, 1 and 10 mumol, inhibited the extravasation of albumin into the nasal cavity induced by bradykinin, 300 micrograms, and also by histamine, 300 micrograms.	NG-Nitroarginine Methyl Ester	0-6	kininogen 1	Homo sapiens	96-106
8818341-14	1996	L-Arginine, 30 mumol, reversed the effect of L-NAME, 1 mumol, on the bradykinin- and histamine-induced albumin extravasation into the nasal airway.	Arginine	0-10	kininogen 1	Homo sapiens	69-79
8818341-14	1996	L-Arginine, 30 mumol, reversed the effect of L-NAME, 1 mumol, on the bradykinin- and histamine-induced albumin extravasation into the nasal airway.	NG-Nitroarginine Methyl Ester	45-51	kininogen 1	Homo sapiens	69-79
8818341-18	1996	We conclude that the extravasation of plasma albumin caused by bradykinin and by histamine involves the generation of nitric oxide.	Nitric Oxide	118-130	kininogen 1	Homo sapiens	63-73
8818341-19	1996	The nasal blockage induced by bradykinin involves nitric oxide generation but the nasal blockage induced by histamine does not.	Nitric Oxide	50-62	kininogen 1	Homo sapiens	30-40
8764214-2	1996	Bradykinin induced a significant increase in [3H]glycoconjugate secretion in a dose-dependent manner from isolated glands, which was significantly inhibited by D-Arg-(Hyp3, Thi5,8, D-Phe7)-bradykinin (the B2-receptor antagonist), whereas Des-Arg9-(Leu8)-bradykinin (B1-receptor antagonist) or indomethacin did not significantly alter it.	Tritium	46-48	kininogen 1	Homo sapiens	189-199
8764214-2	1996	Bradykinin induced a significant increase in [3H]glycoconjugate secretion in a dose-dependent manner from isolated glands, which was significantly inhibited by D-Arg-(Hyp3, Thi5,8, D-Phe7)-bradykinin (the B2-receptor antagonist), whereas Des-Arg9-(Leu8)-bradykinin (B1-receptor antagonist) or indomethacin did not significantly alter it.	Arginine	162-165	kininogen 1	Homo sapiens	0-10
8764214-2	1996	Bradykinin induced a significant increase in [3H]glycoconjugate secretion in a dose-dependent manner from isolated glands, which was significantly inhibited by D-Arg-(Hyp3, Thi5,8, D-Phe7)-bradykinin (the B2-receptor antagonist), whereas Des-Arg9-(Leu8)-bradykinin (B1-receptor antagonist) or indomethacin did not significantly alter it.	Arginine	162-165	kininogen 1	Homo sapiens	189-199
8764214-2	1996	Bradykinin induced a significant increase in [3H]glycoconjugate secretion in a dose-dependent manner from isolated glands, which was significantly inhibited by D-Arg-(Hyp3, Thi5,8, D-Phe7)-bradykinin (the B2-receptor antagonist), whereas Des-Arg9-(Leu8)-bradykinin (B1-receptor antagonist) or indomethacin did not significantly alter it.	thi5,8, d-phe7	173-187	kininogen 1	Homo sapiens	0-10
8764214-2	1996	Bradykinin induced a significant increase in [3H]glycoconjugate secretion in a dose-dependent manner from isolated glands, which was significantly inhibited by D-Arg-(Hyp3, Thi5,8, D-Phe7)-bradykinin (the B2-receptor antagonist), whereas Des-Arg9-(Leu8)-bradykinin (B1-receptor antagonist) or indomethacin did not significantly alter it.	thi5,8, d-phe7	173-187	kininogen 1	Homo sapiens	189-199
8764214-2	1996	Bradykinin induced a significant increase in [3H]glycoconjugate secretion in a dose-dependent manner from isolated glands, which was significantly inhibited by D-Arg-(Hyp3, Thi5,8, D-Phe7)-bradykinin (the B2-receptor antagonist), whereas Des-Arg9-(Leu8)-bradykinin (B1-receptor antagonist) or indomethacin did not significantly alter it.	Indomethacin	293-305	kininogen 1	Homo sapiens	0-10
8764214-3	1996	Nitric oxide synthase inhibitor (nitro-L-arginine methyl ester) caused a significant inhibition of bradykinin-induced glycoconjugate secretion, which was reversed by the addition of L-arginine.	Nitric Oxide	0-12	kininogen 1	Homo sapiens	99-109
8764214-3	1996	Nitric oxide synthase inhibitor (nitro-L-arginine methyl ester) caused a significant inhibition of bradykinin-induced glycoconjugate secretion, which was reversed by the addition of L-arginine.	nitro-l-arginine methyl ester	33-62	kininogen 1	Homo sapiens	99-109
8764214-3	1996	Nitric oxide synthase inhibitor (nitro-L-arginine methyl ester) caused a significant inhibition of bradykinin-induced glycoconjugate secretion, which was reversed by the addition of L-arginine.	Arginine	39-49	kininogen 1	Homo sapiens	99-109
8764214-5	1996	Bradykinin induced an immediate increase in intracellular calcium concentration ([Ca2+]i) of the acinar cells followed by a prolonged plateau, and Ca2+ removal resulted in an initial increase alone.	Calcium	58-65	kininogen 1	Homo sapiens	0-10
8790952-7	1996	However, during the nipradilol phase, bradykinin did not change significantly at rest and at peak exercise.	nipradilol	20-30	kininogen 1	Homo sapiens	38-48
8767925-6	1996	It is released under basal conditions and in response to mechanical stimuli such as shear stress and in response to receptor-operated agonists such as bradykinin, serotonin, ADP/ATP, thrombin, histamine and substance P. NO is the mediator of endothelium-dependent relaxation in the circulation and exerts its effects by activating soluble guanylyl cyclase in vascular smooth muscle, which in turn leads to the formation of cyclic guanosine monophosphate (cyclic GMP) and to relaxation.	Cyclic GMP	423-453	kininogen 1	Homo sapiens	151-161
8665034-3	1996	Inhaled FK224 protected against bradykinin-induced bronchoconstriction and cough in asthmatics.	FK 224	8-13	kininogen 1	Homo sapiens	32-42
8856114-1	1996	Bradykinin causes vasodilatation by stimulating the production of vasodilator prostanoids and nitric oxide (NO).	Prostaglandins	78-89	kininogen 1	Homo sapiens	0-10
8856114-1	1996	Bradykinin causes vasodilatation by stimulating the production of vasodilator prostanoids and nitric oxide (NO).	Nitric Oxide	94-106	kininogen 1	Homo sapiens	0-10
8856114-3	1996	The non-selective inhibitor of arachidonic acid metabolism eicosatetraynoic acid inhibits the EDHF-mediated component of the relaxation to bradykinin.	Arachidonic Acid	31-47	kininogen 1	Homo sapiens	139-149
8856114-3	1996	The non-selective inhibitor of arachidonic acid metabolism eicosatetraynoic acid inhibits the EDHF-mediated component of the relaxation to bradykinin.	ETYA	59-80	kininogen 1	Homo sapiens	139-149
8856114-3	1996	The non-selective inhibitor of arachidonic acid metabolism eicosatetraynoic acid inhibits the EDHF-mediated component of the relaxation to bradykinin.	edhf	94-98	kininogen 1	Homo sapiens	139-149
8856129-2	1996	Dose/concentration response curves to BK were performed +/-2.79 microM indomethacin.	Indomethacin	71-83	kininogen 1	Homo sapiens	38-40
8856129-5	1996	In tissues from NP donors indomethacin significantly enhanced the BK effect at higher doses and the inhibitory component of the response was reduced.	Indomethacin	26-38	kininogen 1	Homo sapiens	66-68
8856131-0	1996	A preliminary study of prostaglandin release by bradykinin (BK) on isolated human myometrium.	Prostaglandins	23-36	kininogen 1	Homo sapiens	48-58
8856131-0	1996	A preliminary study of prostaglandin release by bradykinin (BK) on isolated human myometrium.	Prostaglandins	23-36	kininogen 1	Homo sapiens	60-62
8856131-1	1996	The aim of this study was to investigate whether the response to BK on isolated human myometrium from non-pregnant (NP) and pregnant (P) donors involves the release of prostaglandin I2 (PGI2) and/or of PGE2.	Epoprostenol	168-184	kininogen 1	Homo sapiens	65-67
8856131-1	1996	The aim of this study was to investigate whether the response to BK on isolated human myometrium from non-pregnant (NP) and pregnant (P) donors involves the release of prostaglandin I2 (PGI2) and/or of PGE2.	Epoprostenol	186-190	kininogen 1	Homo sapiens	65-67
8856131-1	1996	The aim of this study was to investigate whether the response to BK on isolated human myometrium from non-pregnant (NP) and pregnant (P) donors involves the release of prostaglandin I2 (PGI2) and/or of PGE2.	Dinoprostone	202-206	kininogen 1	Homo sapiens	65-67
8856131-6	1996	BK evoked PGE2 release which was greater during the contractile response than in the inhibitory response.	Dinoprostone	10-14	kininogen 1	Homo sapiens	0-2
8856131-7	1996	Following the same dose of BK, PGI2 release was found to be greater in the inhibitory response than in the contractile phase.	Epoprostenol	31-35	kininogen 1	Homo sapiens	27-29
8856131-8	1996	The findings indicate that in isolated human myometrium the response to BK does involve the release of PGE2 and PGI2 and in both NP and P tissue PGE2 release is greater in the contractile response phase whilst PGI2 predominates the inhibitory phase.	Dinoprostone	103-107	kininogen 1	Homo sapiens	72-74
8856131-8	1996	The findings indicate that in isolated human myometrium the response to BK does involve the release of PGE2 and PGI2 and in both NP and P tissue PGE2 release is greater in the contractile response phase whilst PGI2 predominates the inhibitory phase.	Epoprostenol	112-116	kininogen 1	Homo sapiens	72-74
8856131-8	1996	The findings indicate that in isolated human myometrium the response to BK does involve the release of PGE2 and PGI2 and in both NP and P tissue PGE2 release is greater in the contractile response phase whilst PGI2 predominates the inhibitory phase.	Epoprostenol	210-214	kininogen 1	Homo sapiens	72-74
8856140-0	1996	The B2 receptor on cultured human decidua cells: release of arachidonic acid by bradykinin.	Arachidonic Acid	60-76	kininogen 1	Homo sapiens	80-90
8856140-4	1996	Cells that had been incubated for 24 h with 14C-AA showed a bradykinin (BK)-induced release of radioactivity into the culture medium.	Carbon-14	44-47	kininogen 1	Homo sapiens	60-70
8856140-4	1996	Cells that had been incubated for 24 h with 14C-AA showed a bradykinin (BK)-induced release of radioactivity into the culture medium.	Carbon-14	44-47	kininogen 1	Homo sapiens	72-74
8856140-8	1996	We conclude that BK can play a role in the case of bacterial infection of the fetal membranes AND may stimulate labour by an augmented production of prostaglandins.	Prostaglandins	149-163	kininogen 1	Homo sapiens	17-19
8856164-0	1996	Biosynthesis of endothelium-derived nitric oxide by bradykinin as endogenous precursor.	Nitric Oxide	36-48	kininogen 1	Homo sapiens	52-62
8648021-10	1996	CONCLUSION: The induction of sneezing and of atropine-inhibitable contralateral glandular secretion demonstrates that allergic inflammation causes nasal hyperreactivity to bradykinin, at least in part, by enhancing neuronal responsiveness.	Atropine	45-53	kininogen 1	Homo sapiens	172-182
8655610-14	1996	These data also show, for the first time, that histamine and alpha-thrombin increased permeability by calcium-dependent intracellular pathways, but bradykinin operates through a calcium-independent mechanism.	Calcium	178-185	kininogen 1	Homo sapiens	148-158
8650249-6	1996	The administration of HOE-140, a bradykinin B2 receptor blocker, prior to PU-15, completely abolishes the anti-ANP action of PU-15.	4-hydroxy-2-octenal	22-25	kininogen 1	Homo sapiens	33-43
8650249-6	1996	The administration of HOE-140, a bradykinin B2 receptor blocker, prior to PU-15, completely abolishes the anti-ANP action of PU-15.	pu-15	125-130	kininogen 1	Homo sapiens	33-43
8813369-3	1996	Three factors were found to increase the probability (up to 70%) and the amplitude of the response to etorphine: (a) synchronization of the cultures; (b) differentiation of the cells; and (c) synergism with other stimulatory agents (carbachol in SK-N-SH and bradykinin in NG108-15 cells).	Etorphine	102-111	kininogen 1	Homo sapiens	258-268
8651483-6	1996	Measurements of two-photon-excited fluorescence of fluorescamine-labeled bradykinin and analysis of multiphoton-excited background reveal the potential of this method to detect fewer than 1000 neurotransmitter molecules.	Fluorescamine	51-64	kininogen 1	Homo sapiens	73-83
8642569-2	1996	Variations of the two first residues of the pentapeptide (Thi-Ser-D-Tic-Oic-Arg) were shown to modulate the biological activities of the analogs on bradykinin-induced smooth muscle contractions in rabbit jugular vein (RJV), a tissue preparation specific of the B2 bradykinin receptor.	Thi-Ser-D-Tic-Oic-Arg	58-79	kininogen 1	Homo sapiens	148-158
8630058-3	1996	Indirect inhibition of prenylation with the HMG CoA reductase inhibitors fluvastatin or compactin decreased bradykinin-stimulated inositol 1,4,5-triphosphate generation.	Fluvastatin	73-84	kininogen 1	Homo sapiens	108-118
8630058-3	1996	Indirect inhibition of prenylation with the HMG CoA reductase inhibitors fluvastatin or compactin decreased bradykinin-stimulated inositol 1,4,5-triphosphate generation.	Inositol 1,4,5-Trisphosphate	130-157	kininogen 1	Homo sapiens	108-118
8631922-5	1996	In bradykinin-stimulated cells the tyrosine phosphorylation of the same cytoskeletal proteins (most notably 85- and 100-kDa proteins) was transient when cells were stimulated in the presence of extracellular Ca2+, was maintained under Ca2+-free conditions, and was reversed following readdition of extracellular Ca2+.	Tyrosine	35-43	kininogen 1	Homo sapiens	3-13
8967444-0	1996	Tyrosine phosphorylation and activation of pp60c-src and pp125FAK in bradykinin-stimulated fibroblasts.	Tyrosine	0-8	kininogen 1	Homo sapiens	69-79
8856143-0	1996	A new class of bradykinin antagonists containing indanylglycine.	indanylglycine	49-63	kininogen 1	Homo sapiens	15-25
8856149-0	1996	An NMR, CD, molecular dynamics and fluorometric study of the conformation of bradykinin antagonists B9340, B9430, B9436 and B9452 in water and in aqueous micellar solutions.	Cadmium	8-10	kininogen 1	Homo sapiens	77-87
8856149-0	1996	An NMR, CD, molecular dynamics and fluorometric study of the conformation of bradykinin antagonists B9340, B9430, B9436 and B9452 in water and in aqueous micellar solutions.	Water	133-138	kininogen 1	Homo sapiens	77-87
8735629-13	1996	The B1 receptor antagonist, Lys[Leu8]desArg9BK (pA2 7.99), inhibits the response of the human vein to B1 receptor agonists (LysdesArg9BK or desArg9BK), but do not alter the effect of BK.	lys[leu8	28-36	kininogen 1	Homo sapiens	44-46
8723904-6	1996	Experiments with thapsigargin (TG), BK, and PDGF indicated that BK and PDGF share intracellular Ca2+ pools that are sensitive to TG.	Thapsigargin	17-29	kininogen 1	Homo sapiens	64-66
8796271-0	1996	Met-Lys-bradykinin-Ser, the kinin released from human kininogen by human pepsin.	Lysine	4-7	kininogen 1	Homo sapiens	8-18
8796271-0	1996	Met-Lys-bradykinin-Ser, the kinin released from human kininogen by human pepsin.	Serine	19-22	kininogen 1	Homo sapiens	8-18
8796271-5	1996	The results suggest that Met-Lys-Bradykinin-Ser, should be the peptide released from human kininogen by a purified human pepsin component.	Serine	44-47	kininogen 1	Homo sapiens	33-43
8660316-0	1996	Bradykinin increases ceramide and sphingosine content in human fibroblasts: possible involvement of glycosphingolipids.	Ceramides	21-29	kininogen 1	Homo sapiens	0-10
8660316-0	1996	Bradykinin increases ceramide and sphingosine content in human fibroblasts: possible involvement of glycosphingolipids.	Sphingosine	34-45	kininogen 1	Homo sapiens	0-10
8660316-0	1996	Bradykinin increases ceramide and sphingosine content in human fibroblasts: possible involvement of glycosphingolipids.	Glycosphingolipids	100-118	kininogen 1	Homo sapiens	0-10
8660316-2	1996	In the present study it is shown that also bradykinin (BK), a pro-inflammatory peptide acting through G-protein-coupled receptors, is able to activate sphingolipid metabolism.	Sphingolipids	151-163	kininogen 1	Homo sapiens	43-53
8660316-2	1996	In the present study it is shown that also bradykinin (BK), a pro-inflammatory peptide acting through G-protein-coupled receptors, is able to activate sphingolipid metabolism.	Sphingolipids	151-163	kininogen 1	Homo sapiens	55-57
8660316-5	1996	The observation that the labeled glycosphingolipid pool is decreased upon BK stimulation would rather suggest that the peptide increases ceramide cellular content by rapidly mobilizing neutral glycolipids.	Glycosphingolipids	33-50	kininogen 1	Homo sapiens	74-76
8660316-5	1996	The observation that the labeled glycosphingolipid pool is decreased upon BK stimulation would rather suggest that the peptide increases ceramide cellular content by rapidly mobilizing neutral glycolipids.	Ceramides	137-145	kininogen 1	Homo sapiens	74-76
8660316-6	1996	Even though the physiological relevance of ceramide and sphingosine increase induced by BK is not known, it is noteworthy that glycosphingolipids may participate in this lipid signalling pathway.	Ceramides	43-51	kininogen 1	Homo sapiens	88-90
8660316-6	1996	Even though the physiological relevance of ceramide and sphingosine increase induced by BK is not known, it is noteworthy that glycosphingolipids may participate in this lipid signalling pathway.	Sphingosine	56-67	kininogen 1	Homo sapiens	88-90
8665918-0	1996	Bradykinin induces tyrosine phosphorylation in human foreskin fibroblasts and 293 cells transfected with rat B2 kinin receptor.	Tyrosine	19-27	kininogen 1	Homo sapiens	0-10
8665918-3	1996	We studied whether in human foreskin fibroblasts bradykinin treatment induces tyrosine phosphorylation of cellular proteins.	Tyrosine	78-86	kininogen 1	Homo sapiens	49-59
8665918-4	1996	Using phosphotyrosine antibodies we detected a bradykinin-dependent phosphorylation of a group of proteins of about 130 kDa and an additional signal around 70kDa after starvation of cells.	Phosphotyrosine	6-21	kininogen 1	Homo sapiens	47-57
8665918-5	1996	The effect evoked by 10 nM bradykinin was rapid (2 min) and it was partially reduced by the B2-kinin-receptor antagonist Hoe 140 which was shown to be a weak inducer of tyrosine phosphorylation.	4-hydroxy-2-octenal	121-124	kininogen 1	Homo sapiens	27-37
8665918-5	1996	The effect evoked by 10 nM bradykinin was rapid (2 min) and it was partially reduced by the B2-kinin-receptor antagonist Hoe 140 which was shown to be a weak inducer of tyrosine phosphorylation.	Tyrosine	169-177	kininogen 1	Homo sapiens	27-37
8665918-6	1996	The bradykinin-mediated tyrosine phosphorylation events were reproduced in human embryonal kidney 293 fibroblasts which were transiently transfected with the rat B2 kinin receptor, but they were not observed in untransfected 293 control cells.	Tyrosine	24-32	kininogen 1	Homo sapiens	4-14
8665918-10	1996	While IGF-I, insulin and EGF were almost ineffective, PDGF stimulated the tyrosine phosphorylation of 130-kDa bands with a similar pattern to that produced by bradykinin.	Tyrosine	74-82	kininogen 1	Homo sapiens	159-169
8621428-3	1996	The order of potency of the agonists in terms of the peak Ca2+i in ECs was bradykinin (100 nM) &gt; ATP (10 microM) &gt; ionomycin (50 nM) &gt; thapsigargin (1 microM).	ca2+i	58-63	kininogen 1	Homo sapiens	75-85
8608168-4	1996	Treatment of cells with bradykinin or serum caused up-regulation of inositol phosphate levels; by contrast, TGF-beta 1, -beta 2 and -beta 3 failed to modulate inositol phosphates.	Inositol Phosphates	68-86	kininogen 1	Homo sapiens	24-34
8608646-0	1996	Effects of leukotriene C4 and D4, histamine and bradykinin on cytosolic calcium concentrations and adhesiveness of endothelial cells and neutrophils.	Calcium	72-79	kininogen 1	Homo sapiens	48-58
8672553-6	1996	BK depleted internal calcium pools such that subsequent stimulation with BK, FCCP or bombesin did not increase [Ca2+]i.	Calcium	21-28	kininogen 1	Homo sapiens	0-2
8672553-6	1996	BK depleted internal calcium pools such that subsequent stimulation with BK, FCCP or bombesin did not increase [Ca2+]i.	Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone	77-81	kininogen 1	Homo sapiens	0-2
8672553-9	1996	Either Tg or FCCP reduced the calcium stores that could be released by BK or A23187.	Thapsigargin	7-9	kininogen 1	Homo sapiens	71-73
8672553-9	1996	Either Tg or FCCP reduced the calcium stores that could be released by BK or A23187.	Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone	13-17	kininogen 1	Homo sapiens	71-73
8672553-9	1996	Either Tg or FCCP reduced the calcium stores that could be released by BK or A23187.	Calcium	30-37	kininogen 1	Homo sapiens	71-73
8672553-10	1996	Thus, cellular calcium compartments that respond to BK and A23187 partially overlap.	Calcium	15-22	kininogen 1	Homo sapiens	52-54
8638919-4	1996	Examination of RNA synthesis demonstrated that BK inhibits uridine incorporation in a dose-dependent manner.	Uridine	59-66	kininogen 1	Homo sapiens	47-49
8638919-6	1996	The latter result suggested that prostaglandins mediate the biological actions of BK.	Prostaglandins	33-47	kininogen 1	Homo sapiens	82-84
8638919-8	1996	PGE2 caused a decrease in RNA synthesis, thus mimicking the effect of BK, while PGI2 did not.	Dinoprostone	0-4	kininogen 1	Homo sapiens	70-72
8638919-9	1996	Therefore, the inhibition of RNA synthesis in A10 vascular smooth muscle cells by BK requires both B1 and B2 receptor subtypes and this action of BK is apparently mediated by de novo synthesis of prostaglandins.	Prostaglandins	196-210	kininogen 1	Homo sapiens	146-148
8737987-8	1996	It is also noteworthy that bacterial cell wall components themselves, i.e. endotoxin (or lipopolysaccharide) of gram negative bacteria and teichoic/lipoteichoic acid of gram positive bacteria, are also able to activate the bradykinin generating cascade-involving activation of Hageman factor as mentioned above.	teichoic/	139-148	kininogen 1	Homo sapiens	223-233
8737987-8	1996	It is also noteworthy that bacterial cell wall components themselves, i.e. endotoxin (or lipopolysaccharide) of gram negative bacteria and teichoic/lipoteichoic acid of gram positive bacteria, are also able to activate the bradykinin generating cascade-involving activation of Hageman factor as mentioned above.	lipoteichoic acid	148-165	kininogen 1	Homo sapiens	223-233
8601640-8	1996	Glucose extraction by skeletal muscle was 44% higher in the control (2.6+/-0.2 mmol/liter) than the bradykinin-infused leg (1.8+/-0.2 mmol/liter, P&lt;0.01).	Glucose	0-7	kininogen 1	Homo sapiens	100-110
8601640-9	1996	When bradykinin was infused in the basal state, flow was 98% higher in the bradykinin-infused (58+/-12 ml/kg muscle x min) than the control leg (28+/-6 ml/kg muscle x min, P&lt;0.01) but rates of muscle glucose uptake were identical in both legs (10.1+/-0.9 vs. 10.6+/-0.8 micromol/kg x min).	Glucose	203-210	kininogen 1	Homo sapiens	5-15
8601640-9	1996	When bradykinin was infused in the basal state, flow was 98% higher in the bradykinin-infused (58+/-12 ml/kg muscle x min) than the control leg (28+/-6 ml/kg muscle x min, P&lt;0.01) but rates of muscle glucose uptake were identical in both legs (10.1+/-0.9 vs. 10.6+/-0.8 micromol/kg x min).	Glucose	203-210	kininogen 1	Homo sapiens	75-85
8613709-0	1996	Bradykinin stimulates phosphoinositide turnover and phospholipase C but not phospholipase D and NADPH oxidase in human neutrophils.	Phosphatidylinositols	22-38	kininogen 1	Homo sapiens	0-10
8613709-13	1996	Our results show that BK activated a PIP2-PLC measured as the release of [3H]IP3.	Phosphatidylinositol 4,5-Diphosphate	37-41	kininogen 1	Homo sapiens	22-24
8613709-13	1996	Our results show that BK activated a PIP2-PLC measured as the release of [3H]IP3.	[3h]ip3	73-80	kininogen 1	Homo sapiens	22-24
8613709-15	1996	The fact that BK induced PLC activity but neither that of PLD nor NADPH oxidase, whereas fMLP triggered the activation of both phospholipases and evoked the PMN respiratory burst, suggests that diacylglycerol (DAG) from PIP2 as well as PA or PA-derived DAG, synergize to trigger the PMN oxidative response.	Diglycerides	194-208	kininogen 1	Homo sapiens	14-16
8613709-16	1996	Finally, BK inhibited O2- production by fMLP-activated PMN in a time-dependent manner.	Superoxides	22-24	kininogen 1	Homo sapiens	9-11
8632435-0	1996	An NMR, CD, molecular dynamics, and fluorometric study of the conformation of the bradykinin antagonist B-9340 in water and in aqueous micellar solutions.	Water	114-119	kininogen 1	Homo sapiens	82-92
8632435-1	1996	A detailed NMR, CD, fluorometry, and molecular modeling study of a novel bradykinin antagonist B-9340, containing a novel amino acid D-Igl (alpha-(2-indanyl)glycine) at position 7, was carried out.	2-indanylglycine	140-164	kininogen 1	Homo sapiens	73-83
8659776-8	1996	The effect of pretreatment with ketorolac on bradykinin-induced hyperalgesia was not achieved after bradykinin injection at sites pretreated with saline as well as ketorolac.	Ketorolac	32-41	kininogen 1	Homo sapiens	45-55
8766249-6	1996	One of these epitopes is probably associated with the C-terminal sequence of B (with tachykinin-like activity) and seems to be present in other neuropeptides such as SP ; another epitope would be the N-terminal sequence of SP (with bradykinin-like activity).	TFF2 protein, human	166-168	kininogen 1	Homo sapiens	232-242
8900488-8	1996	The effects of both kinase systems are blocked by serine/threonine (Ser/Thr) protein kinase inhibitors, indicating a role for phosphorylation at Ser or Thr residues in determining the cellular expression of bradykinin B2 receptor affinity forms.	Serine	50-56	kininogen 1	Homo sapiens	207-217
8900488-8	1996	The effects of both kinase systems are blocked by serine/threonine (Ser/Thr) protein kinase inhibitors, indicating a role for phosphorylation at Ser or Thr residues in determining the cellular expression of bradykinin B2 receptor affinity forms.	Threonine	57-66	kininogen 1	Homo sapiens	207-217
8900488-8	1996	The effects of both kinase systems are blocked by serine/threonine (Ser/Thr) protein kinase inhibitors, indicating a role for phosphorylation at Ser or Thr residues in determining the cellular expression of bradykinin B2 receptor affinity forms.	Serine	68-71	kininogen 1	Homo sapiens	207-217
8900488-8	1996	The effects of both kinase systems are blocked by serine/threonine (Ser/Thr) protein kinase inhibitors, indicating a role for phosphorylation at Ser or Thr residues in determining the cellular expression of bradykinin B2 receptor affinity forms.	Threonine	72-75	kininogen 1	Homo sapiens	207-217
8900488-8	1996	The effects of both kinase systems are blocked by serine/threonine (Ser/Thr) protein kinase inhibitors, indicating a role for phosphorylation at Ser or Thr residues in determining the cellular expression of bradykinin B2 receptor affinity forms.	Serine	145-148	kininogen 1	Homo sapiens	207-217
8900488-8	1996	The effects of both kinase systems are blocked by serine/threonine (Ser/Thr) protein kinase inhibitors, indicating a role for phosphorylation at Ser or Thr residues in determining the cellular expression of bradykinin B2 receptor affinity forms.	Threonine	152-155	kininogen 1	Homo sapiens	207-217
8833191-0	1996	Potentiation of bradykinin-induced inositol phosphates production by cyclic AMP elevating agents and endothelin-1 in cultured astrocytes.	Inositol Phosphates	35-54	kininogen 1	Homo sapiens	16-26
8833191-0	1996	Potentiation of bradykinin-induced inositol phosphates production by cyclic AMP elevating agents and endothelin-1 in cultured astrocytes.	Cyclic AMP	69-79	kininogen 1	Homo sapiens	16-26
8833191-1	1996	Cultured astrocytes express bradykinin (BK) receptors, which are coupled to phospholipase C (PLC) through G-protein to mediate phosphoinositide (PI) hydrolysis.	Phosphatidylinositols	127-143	kininogen 1	Homo sapiens	28-38
8833191-1	1996	Cultured astrocytes express bradykinin (BK) receptors, which are coupled to phospholipase C (PLC) through G-protein to mediate phosphoinositide (PI) hydrolysis.	Phosphatidylinositols	127-143	kininogen 1	Homo sapiens	40-42
8833191-3	1996	Short-term treatment of cells with dBcAMP had no effect on BK-induced PI hydrolysis; however, long-term treatment resulted in potentiation of the BK response.	Bucladesine	35-41	kininogen 1	Homo sapiens	146-148
8833191-7	1996	Cycloheximide (0.5 mu M) blocked the increase in (3H)BK binding, indicating that new synthesis of receptor protein might occur during 24 h pretreatment with dBcAMP.	Cycloheximide	0-13	kininogen 1	Homo sapiens	53-55
8833191-7	1996	Cycloheximide (0.5 mu M) blocked the increase in (3H)BK binding, indicating that new synthesis of receptor protein might occur during 24 h pretreatment with dBcAMP.	Bucladesine	157-163	kininogen 1	Homo sapiens	53-55
8833191-10	1996	(3H)BK binding and AlF(4)--induced but not A23187- or ionomycin-induced PI hydrolysis were increased, indicating that the site of action of long-term ET-1 treatment was the BK receptor and G protein; Scatchard analysis showed an increase in Bmax but no effect on Kd.	Tritium	1-3	kininogen 1	Homo sapiens	4-6
8967444-1	1996	Bradykinin (BK) stimulates protein tyrosine phosphorylation in human foreskin fibroblasts (K.-M. Lee, K. Toscas, and M. L. Villereal, J. Biol.	Tyrosine	35-43	kininogen 1	Homo sapiens	0-10
8967444-1	1996	Bradykinin (BK) stimulates protein tyrosine phosphorylation in human foreskin fibroblasts (K.-M. Lee, K. Toscas, and M. L. Villereal, J. Biol.	Tyrosine	35-43	kininogen 1	Homo sapiens	12-14
8967444-6	1996	The BK-stimulated pp125FAK tyrosine phosphorylation level is well correlated with increased kinase activity, as assessed by in vitro immune complex kinase assays.	Tyrosine	27-35	kininogen 1	Homo sapiens	4-6
8967444-8	1996	In addition to identifying the two proteins responsible for the major phosphotyrosine bands, we also report that pp60c-src is tyrosine phosphorylated and activated in response to BK, as analyzed by immunoblotting and in vitro kinase assays, respectively.	Tyrosine	77-85	kininogen 1	Homo sapiens	179-181
8821546-4	1996	3 Inhibition of prostaglandin E2 formation in MC3T3-E1 cells was not observed with thapsigargin after stimulation with arachidonic acid, A23187 or melittin, whereas bradykinin-induced prostaglandin E2 biosynthesis was blocked.	Dinoprostone	16-32	kininogen 1	Homo sapiens	165-175
8769870-0	1996	Differential regulation of histamine- and bradykinin-stimulated phospholipase C in adrenal chromaffin cells: evidence for involvement of different protein kinase C isoforms.	chromaffin	91-101	kininogen 1	Homo sapiens	42-52
8769870-1	1996	In this report we investigate the isoforms of protein kinase C (PKC) present in cultured adrenal chromaffin cells with respect to their modulation by treatment with phorbol ester and their possible differential involvement in the regulation of responses to histamine and bradykinin.	Histamine	257-266	kininogen 1	Homo sapiens	271-281
8769870-9	1996	The accumulation of total 3H-inositol (poly) phosphates in response to bradykinin or histamine was essentially abolished by prior treatment with 10-min PMA treatment (1 microM).	3h-inositol (poly) phosphates	26-55	kininogen 1	Homo sapiens	71-81
8769870-9	1996	The accumulation of total 3H-inositol (poly) phosphates in response to bradykinin or histamine was essentially abolished by prior treatment with 10-min PMA treatment (1 microM).	Tetradecanoylphorbol Acetate	152-155	kininogen 1	Homo sapiens	71-81
8769870-10	1996	However, with 12-h exposure to PMA, the bradykinin response was restored to the level seen with no prior PMA exposure.	Tetradecanoylphorbol Acetate	31-34	kininogen 1	Homo sapiens	40-50
8852584-6	1996	By measuring the concentration of Evans blue dye extravasation into the joint perfusate following its intravenous injection, bradykinin-induced plasma extravasation in the knee joint cavity was determined spectrophotometrically.	Evans Blue	34-44	kininogen 1	Homo sapiens	125-135
8644056-4	1996	ACEI, however, may not completely inhibit the production of angiotensin II and its effects, and adverse effects like cough and rise in creatinine have been associated with ACEI and reduced degradation of bradykinin.	Creatinine	135-145	kininogen 1	Homo sapiens	204-214
8779918-0	1996	Flow- and bradykinin-induced nitric oxide production by endothelial cells is independent of membrane potential.	Nitric Oxide	29-41	kininogen 1	Homo sapiens	10-20
8779918-5	1996	With control medium, 30 s, 2 min, and 3 h of treatment with flow or 2 min of treatment with BK resulted in an approximately threefold increase in cGMP over stationary cultures.	Cyclic GMP	146-150	kininogen 1	Homo sapiens	92-94
8821546-4	1996	3 Inhibition of prostaglandin E2 formation in MC3T3-E1 cells was not observed with thapsigargin after stimulation with arachidonic acid, A23187 or melittin, whereas bradykinin-induced prostaglandin E2 biosynthesis was blocked.	Dinoprostone	184-200	kininogen 1	Homo sapiens	165-175
8777276-12	1996	BK potentiated cytokine induced amplification of the PGE2 response to arachidonic acid.	Arachidonic Acid	70-86	kininogen 1	Homo sapiens	0-2
8573025-3	1996	RESULTS: The vascular endothelial cell may produce nitric oxide, endothelins, prostaglandins, and renin-angiotension products in response to chemical stimuli such as acetylcholine and bradykinin, to changes in blood pressure and vessel wall stress, to changes in local oxygen levels, and to other local stimuli.	Nitric Oxide	51-63	kininogen 1	Homo sapiens	184-194
8573025-3	1996	RESULTS: The vascular endothelial cell may produce nitric oxide, endothelins, prostaglandins, and renin-angiotension products in response to chemical stimuli such as acetylcholine and bradykinin, to changes in blood pressure and vessel wall stress, to changes in local oxygen levels, and to other local stimuli.	Prostaglandins	78-92	kininogen 1	Homo sapiens	184-194
8573025-3	1996	RESULTS: The vascular endothelial cell may produce nitric oxide, endothelins, prostaglandins, and renin-angiotension products in response to chemical stimuli such as acetylcholine and bradykinin, to changes in blood pressure and vessel wall stress, to changes in local oxygen levels, and to other local stimuli.	Oxygen	269-275	kininogen 1	Homo sapiens	184-194
8777276-0	1996	Bradykinin and thrombin synergistically potentiate interleukin 1 and tumour necrosis factor induced prostanoid biosynthesis in human dental pulp fibroblasts.	Prostaglandins	100-110	kininogen 1	Homo sapiens	0-10
8777276-3	1996	The onset of action was delayed 1-2 h and maximal response was seen after 24 h. In contrast, BK and thrombin caused a burst of PGE2 formation with maximal response after 10 min.	Dinoprostone	127-131	kininogen 1	Homo sapiens	93-95
8777276-4	1996	BK (1 microM) and thrombin (3 U/ml) synergistically potentiated IL-1 alpha and IL-1 beta stimulated PGE2 formation in 24 h cultures.	Dinoprostone	100-104	kininogen 1	Homo sapiens	0-2
8777276-5	1996	The effect of BK and thrombin on IL-1 beta enhanced PGE2 formation was seen both at suboptimal and optimal concentrations of IL-1 beta without affecting the sensitivity to IL-1 beta.	Dinoprostone	52-56	kininogen 1	Homo sapiens	14-16
8777276-6	1996	BK and thrombin also synergistically potentiated the stimulatory effect of TNF-alpha and TNF-beta on PGE2 formation.	Dinoprostone	101-105	kininogen 1	Homo sapiens	0-2
8777276-8	1996	BK analogues with affinity to BK B2-receptors, but not to BK B1-receptors, were able to synergistically potentiate IL-1 beta and TNF-alpha-enhanced PGE2 production.	Dinoprostone	148-152	kininogen 1	Homo sapiens	0-2
8777276-9	1996	The synergistic stimulation of PGE2 formation by IL-1, TNF and BK was abolished by indomethacin and flurbiprofen.	Dinoprostone	31-35	kininogen 1	Homo sapiens	63-65
8777276-9	1996	The synergistic stimulation of PGE2 formation by IL-1, TNF and BK was abolished by indomethacin and flurbiprofen.	Indomethacin	83-95	kininogen 1	Homo sapiens	63-65
8777276-9	1996	The synergistic stimulation of PGE2 formation by IL-1, TNF and BK was abolished by indomethacin and flurbiprofen.	Flurbiprofen	100-112	kininogen 1	Homo sapiens	63-65
8777276-10	1996	Preincubation with IL-1 beta and TNF-alpha for 24 h resulted in a substantial amplification of the PGE2 response to a subsequent 24 h challenge with BK in the absence of cytokine.	Dinoprostone	99-103	kininogen 1	Homo sapiens	149-151
8777276-12	1996	BK potentiated cytokine induced amplification of the PGE2 response to arachidonic acid.	Dinoprostone	53-57	kininogen 1	Homo sapiens	0-2
8714715-11	1996	Anaphylactoid reaction which is tentatively explained as a result of release of bradykinin in contact of blood with polyanionic material of the adsorbent, dextran sulphate, develops, in particular, while an angiotensin-converting enzyme inhibitor is administered as a depressant.	Dextran Sulfate	155-171	kininogen 1	Homo sapiens	80-90
9213428-1	1996	The [(3)H]inositol incorporation into the membrane fraction of A-431 human epidermoid carcinoma cells was markedly increased by stimulation of the cells with either epidermal growth factor (EGF), ATP, bradykinin, or a calcium ionophore A23187 in the presence of 1 mM extracellular calcium ions; most incorporated [(3)H]inositol was found to have accumulated as phosphatidylinositol (PI).	Tritium	5-9	kininogen 1	Homo sapiens	201-211
9213428-1	1996	The [(3)H]inositol incorporation into the membrane fraction of A-431 human epidermoid carcinoma cells was markedly increased by stimulation of the cells with either epidermal growth factor (EGF), ATP, bradykinin, or a calcium ionophore A23187 in the presence of 1 mM extracellular calcium ions; most incorporated [(3)H]inositol was found to have accumulated as phosphatidylinositol (PI).	Inositol	10-18	kininogen 1	Homo sapiens	201-211
9213428-1	1996	The [(3)H]inositol incorporation into the membrane fraction of A-431 human epidermoid carcinoma cells was markedly increased by stimulation of the cells with either epidermal growth factor (EGF), ATP, bradykinin, or a calcium ionophore A23187 in the presence of 1 mM extracellular calcium ions; most incorporated [(3)H]inositol was found to have accumulated as phosphatidylinositol (PI).	[(3)h]inositol	4-18	kininogen 1	Homo sapiens	201-211
8900488-11	1996	Regulated expression of this repertoire of bradykinin B2 receptors at the level of receptor number and concurrent activity allows fibroblasts a sensitive means to adjust their responses to their cellular environment utilizing Ser/Thr phosphorylation events.	Serine	226-229	kininogen 1	Homo sapiens	43-53
8900488-11	1996	Regulated expression of this repertoire of bradykinin B2 receptors at the level of receptor number and concurrent activity allows fibroblasts a sensitive means to adjust their responses to their cellular environment utilizing Ser/Thr phosphorylation events.	Threonine	230-233	kininogen 1	Homo sapiens	43-53
8664052-2	1996	Here, we demonstrate that tyrphostin inhibits in vitro colony growth of the H-345 and H-69 small cell lung cancer (SCLC) cell lines stimulated by the neuropeptides, bombesin and bradykinin, respectively.	Tyrphostins	26-36	kininogen 1	Homo sapiens	178-188
8655636-0	1996	Estrogen pretreatment increases arachidonic acid release by bradykinin stimulated normal human osteoblast-like cells.	Arachidonic Acid	32-48	kininogen 1	Homo sapiens	60-70
8913543-6	1996	Vasodilator responses to bradykinin are antagonized by the B2-receptor icatibant and are blunted (but not abolished) by inhibition of the L-arginine/NO pathway with L-NG-monomethyl arginine.	Arginine	138-148	kininogen 1	Homo sapiens	25-35
8913543-6	1996	Vasodilator responses to bradykinin are antagonized by the B2-receptor icatibant and are blunted (but not abolished) by inhibition of the L-arginine/NO pathway with L-NG-monomethyl arginine.	omega-N-Methylarginine	165-189	kininogen 1	Homo sapiens	25-35
8689766-16	1996	Given that BK is known to cause histamine release it appears possible that the responses to both compounds may be modified by conventional antihistamines.	Histamine	32-41	kininogen 1	Homo sapiens	11-13
8689766-19	1996	The aim of this study was to compare the effects of terfenadine (an H1-antagonist) and cimetidine (an H2-antagonist) on PAF- and BK-induced weal and flare responses in healthy, non-atopic human volunteers.	Terfenadine	52-63	kininogen 1	Homo sapiens	129-131
8689766-19	1996	The aim of this study was to compare the effects of terfenadine (an H1-antagonist) and cimetidine (an H2-antagonist) on PAF- and BK-induced weal and flare responses in healthy, non-atopic human volunteers.	Cimetidine	87-97	kininogen 1	Homo sapiens	129-131
8529790-8	1996	This is of interest, because in recent studies insulin has been suggested to elicit its actions on MBF and MGU via the accelerated release of endothelium-derived nitric oxide, the generation of which is also stimulated by BK in a concentration-dependent manner.	Nitric Oxide	162-174	kininogen 1	Homo sapiens	222-224
8529791-14	1996	Bradykinin-induced tyrosine phosphorylation of proteins of approximately 130 and 70 kDa was inhibited by insulin treatment of rat-1 fibroblasts.	Tyrosine	19-27	kininogen 1	Homo sapiens	0-10
8529791-15	1996	These data suggest that signals from the insulin receptor modify signaling from the bradykinin receptor to tyrosine phosphorylation of different cellular proteins.	Tyrosine	107-115	kininogen 1	Homo sapiens	84-94
8529805-6	1996	Indeed, this mediator, which seems to be an endothelium-derived, cytochrome P450-derived metabolite of arachidonic acid, would now appear to represent a substantial constitutive component of the vasodilator response to bradykinin.	Arachidonic Acid	103-119	kininogen 1	Homo sapiens	219-229
8777276-14	1996	These data show that proinflammatory mediators such as BK and thrombin act in concert with IL-1 and TNF in stimulating prostanoid formation in human pulpal fibroblasts and that the action of BK is linked to BK B2-receptors.	Prostaglandins	119-129	kininogen 1	Homo sapiens	55-57
8777276-15	1996	The results are compatible with the view that enhanced metabolism of arachidonic acid, probably due to increased activation or de novo synthesis of cyclooxy-genase(s), is involved in the mechanism by which IL-1, TNF, BK and thrombin interact.	Arachidonic Acid	69-85	kininogen 1	Homo sapiens	217-219
8745290-2	1996	We have investigated whether changes in extracellular ion composition and substrate deprivation modulate basal and/or bradykinin-stimulated L-arginine transport and release of nitric oxide (NO) and prostacyclin (PGI2) in porcine aortic endothelial cells cultured and superfused on microcarriers.	Arginine	140-150	kininogen 1	Homo sapiens	118-128
8803517-2	1996	We have investigated the effect of a neurokinin receptor antagonist, FK-224, on bradykinin (BK)-induced bronchoconstriction, and have compared its effect with the spontaneous variability of BK responsiveness.	FK 224	69-75	kininogen 1	Homo sapiens	80-90
8803517-2	1996	We have investigated the effect of a neurokinin receptor antagonist, FK-224, on bradykinin (BK)-induced bronchoconstriction, and have compared its effect with the spontaneous variability of BK responsiveness.	FK 224	69-75	kininogen 1	Homo sapiens	92-94
8803517-10	1996	We observed a significant fall in FEV1 after inhalation of saline plus ethanol, which was the diluent for BK (mean decrease 4.2%).	Sodium Chloride	59-65	kininogen 1	Homo sapiens	106-108
8803517-10	1996	We observed a significant fall in FEV1 after inhalation of saline plus ethanol, which was the diluent for BK (mean decrease 4.2%).	Ethanol	71-78	kininogen 1	Homo sapiens	106-108
8689766-2	1996	The aim of this study was to compare the effects of terfenadine (an H1-antagonist) and cimetidine (an H2-antagonist) on weal and flare responses to PAF and BK in healthy non-atopic human volunteers.	Terfenadine	52-63	kininogen 1	Homo sapiens	156-158
8689766-2	1996	The aim of this study was to compare the effects of terfenadine (an H1-antagonist) and cimetidine (an H2-antagonist) on weal and flare responses to PAF and BK in healthy non-atopic human volunteers.	Cimetidine	87-97	kininogen 1	Homo sapiens	156-158
8689766-4	1996	Terfenadine significantly reduced weal and flare responses to PAF (mean reduction 53 and 73%, respectively) and flare responses to BK (mean reduction 78%) but had no effect on weal responses to BK.	Terfenadine	0-11	kininogen 1	Homo sapiens	131-133
8689766-7	1996	These findings suggest that the flare response to intradermal BK is mediated via histamine release while the weal response is not.	Histamine	81-90	kininogen 1	Homo sapiens	62-64
8791263-3	1996	The kinin antagonist Hoe 140 and codeine both produced dose-related inhibition of cough responses to inhalation of citric acid or bradykinin aerosols by conscious guinea pigs.	Codeine	33-40	kininogen 1	Homo sapiens	130-140
8890934-0	1996	Regulation of bradykinin-induced Ins(1,4,5)P3 formation by protein kinase C in human fibroblasts.	Inositol 1,4,5-Trisphosphate	33-45	kininogen 1	Homo sapiens	14-24
8890934-1	1996	To better understand the molecular mechanisms that underlie the exaggerated bradykinin (BK)-stimulated release of Ins(1,4,5)P3 in fibroblasts from Alzheimer patients, the role of G-proteins, protein kinase C (PKC) and cyclic AMP in BK-induced Ins(1,4,5)P3 formation was determined.	Inositol 1,4,5-Trisphosphate	114-126	kininogen 1	Homo sapiens	76-86
8890934-1	1996	To better understand the molecular mechanisms that underlie the exaggerated bradykinin (BK)-stimulated release of Ins(1,4,5)P3 in fibroblasts from Alzheimer patients, the role of G-proteins, protein kinase C (PKC) and cyclic AMP in BK-induced Ins(1,4,5)P3 formation was determined.	Inositol 1,4,5-Trisphosphate	114-126	kininogen 1	Homo sapiens	88-90
8890934-2	1996	A role for G-proteins in the coupling of the BK receptor to intracellular signals was indicated by guanosine 5"-(3-O-thio)triphosphate (GTP gamma S) enhanced BK-stimulated Ins(1,4,5)P3 release.	Guanosine 5'-O-(3-Thiotriphosphate)	99-134	kininogen 1	Homo sapiens	45-47
8890934-2	1996	A role for G-proteins in the coupling of the BK receptor to intracellular signals was indicated by guanosine 5"-(3-O-thio)triphosphate (GTP gamma S) enhanced BK-stimulated Ins(1,4,5)P3 release.	Guanosine 5'-O-(3-Thiotriphosphate)	136-147	kininogen 1	Homo sapiens	45-47
8890934-2	1996	A role for G-proteins in the coupling of the BK receptor to intracellular signals was indicated by guanosine 5"-(3-O-thio)triphosphate (GTP gamma S) enhanced BK-stimulated Ins(1,4,5)P3 release.	Inositol 1,4,5-Trisphosphate	172-184	kininogen 1	Homo sapiens	45-47
8890934-4	1996	The inhibition by CTX appeared to be secondary to its ability to increase cyclic AMP, because forskolin also inhibited the BK-mediated Ins (1,4,5)P3 release.	Cyclic AMP	74-84	kininogen 1	Homo sapiens	123-125
8890934-4	1996	The inhibition by CTX appeared to be secondary to its ability to increase cyclic AMP, because forskolin also inhibited the BK-mediated Ins (1,4,5)P3 release.	Colforsin	94-103	kininogen 1	Homo sapiens	123-125
8890934-4	1996	The inhibition by CTX appeared to be secondary to its ability to increase cyclic AMP, because forskolin also inhibited the BK-mediated Ins (1,4,5)P3 release.	Inositol 1,4,5-Trisphosphate	135-148	kininogen 1	Homo sapiens	123-125
8890934-5	1996	Activation of PKC with TPA diminished the number of BK receptors by 33% and proportionally decreased BK-mediated Ins(1,4,5)P3 formation by 28%.	Tetradecanoylphorbol Acetate	23-26	kininogen 1	Homo sapiens	52-54
8890934-5	1996	Activation of PKC with TPA diminished the number of BK receptors by 33% and proportionally decreased BK-mediated Ins(1,4,5)P3 formation by 28%.	Tetradecanoylphorbol Acetate	23-26	kininogen 1	Homo sapiens	101-103
8890934-5	1996	Activation of PKC with TPA diminished the number of BK receptors by 33% and proportionally decreased BK-mediated Ins(1,4,5)P3 formation by 28%.	Inositol 1,4,5-Trisphosphate	113-125	kininogen 1	Homo sapiens	101-103
8950280-0	1996	Stimulation of Rb+ influx by bradykinin through Na+/K+/Cl- cotransport and Na+/K(+)-ATPase in NIH-3T3 fibroblasts.	Rubidium	15-18	kininogen 1	Homo sapiens	29-39
8950280-2	1996	Using Rb+ as a tracer for K+, we have studied the mechanisms involved in bradykinin-stimulated Rb+ influx in NIH-3T3 fibroblasts.	Rubidium	95-98	kininogen 1	Homo sapiens	73-83
8950280-4	1996	Bradykinin stimulated Rb+ influx (+82.6%) through both systems without changing their ratio (r = 0.72).	Rubidium	22-25	kininogen 1	Homo sapiens	0-10
8950280-6	1996	PKC inhibition by H-7, and PKC down-regulation by 24-h PMA (10(-6) M) treatment decreased the bradykinin-induced stimulation of Rb+ influx (+31% and +14.9% above control, respectively).	Rubidium	128-131	kininogen 1	Homo sapiens	94-104
8950280-7	1996	Both down-regulation and inhibition of PKC dramatically reduced the furosemide-sensitive Na+/K+/Cl- cotransport, as r fell to 0.239 and 0.032 in bradykinin-stimulated cells after H-7 and 24-h PMA treatments, respectively.	Furosemide	68-78	kininogen 1	Homo sapiens	145-155
8950280-8	1996	BAPTA/AM pretreatment (10(-4) M, 60 min), which complexed with [Ca2+]i, not only prevented the bradykinin-induced [Ca2+]i raise, but also partially inhibited bradykinin-induced Rb+ influx stimulation (+39% above control), without modifying r (0.76).	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	0-5	kininogen 1	Homo sapiens	95-105
8950280-8	1996	BAPTA/AM pretreatment (10(-4) M, 60 min), which complexed with [Ca2+]i, not only prevented the bradykinin-induced [Ca2+]i raise, but also partially inhibited bradykinin-induced Rb+ influx stimulation (+39% above control), without modifying r (0.76).	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	0-5	kininogen 1	Homo sapiens	158-168
8950280-8	1996	BAPTA/AM pretreatment (10(-4) M, 60 min), which complexed with [Ca2+]i, not only prevented the bradykinin-induced [Ca2+]i raise, but also partially inhibited bradykinin-induced Rb+ influx stimulation (+39% above control), without modifying r (0.76).	Rubidium	177-180	kininogen 1	Homo sapiens	95-105
8950280-9	1996	We conclude that stimulation of PKC is a major pathway involved in bradykinin stimulation of Rb+ influx in NIH-3T3 fibroblasts, and that rises in [Ca2+]i participate in bradykinin signalling, possibly through PKC activation.	Rubidium	93-96	kininogen 1	Homo sapiens	67-77
9238655-1	1996	Bradykinin is a nonapeptide inflammatory agent that in the endometrium stimulates stromal cell proliferation, prostaglandin synthesis and electrogenic ion transport.	Prostaglandins	110-123	kininogen 1	Homo sapiens	0-10
9238655-2	1996	The expression of bradykinin type II (B2) receptor mRNA was examined by in-situ hybridization using 35S-labelled riboprobe in human endometrium to determine its temporal and spatial pattern of distribution throughout the menstrual cycle.	Sulfur-35	100-103	kininogen 1	Homo sapiens	18-28
8745290-15	1996	Bradykinin-stimulated L-arginine transport was insensitive to removal of Ca2+, whereas agonist-induced NO release was abolished.	Arginine	22-32	kininogen 1	Homo sapiens	0-10
8804078-1	1996	Stimulation of small cell lung cancer (SCLC) cells with neuropeptides bombesin, bradykinin, gastrin, and neurotensin resulted in increased tyrosine kinase activity and tyrosine phosphorylation of a number of polypeptides including a p120 kDa polypeptide identified by immunoblotting as focal adhesion kinase (p125FAK).	Tyrosine	139-147	kininogen 1	Homo sapiens	80-90
9085350-7	1996	Nitric oxide production was induced by the action of different physical agents (shear stress, stretching) as well as various chemical substances agonists (bradykinin, acetylcholine, ATP).	Nitric Oxide	0-12	kininogen 1	Homo sapiens	155-165
8865464-4	1996	Evidence for a role for bradykinin and nitric oxide in pancreatitis has been conflicting with some studies suggesting these agents might ameliorate pancreatic dysfunction by enhancing pancreatic blood flow and secretion in response to bradykinin-stimulated generation of nitric oxide from endothelium, while other studies suggest that nitric oxide potentiates pancreatic oxidative stress.	Nitric Oxide	271-283	kininogen 1	Homo sapiens	235-245
8865464-4	1996	Evidence for a role for bradykinin and nitric oxide in pancreatitis has been conflicting with some studies suggesting these agents might ameliorate pancreatic dysfunction by enhancing pancreatic blood flow and secretion in response to bradykinin-stimulated generation of nitric oxide from endothelium, while other studies suggest that nitric oxide potentiates pancreatic oxidative stress.	Nitric Oxide	271-283	kininogen 1	Homo sapiens	235-245
8750710-0	1995	Effects of prostaglandin E2 on the intensity of bradykinin-evoked pain from skin and veins of humans.	Dinoprostone	11-27	kininogen 1	Homo sapiens	48-58
8750710-1	1995	Prostaglandin E2 increases bradykinin-induced spike activity from polymodal nociceptors of the skin and deep tissues in animals, suggesting sensitization of these receptors.	Dinoprostone	0-16	kininogen 1	Homo sapiens	27-37
8750710-2	1995	To see whether these neurophysiological observations in animals correspond with increased pain intensity in humans, and whether also vascular nociceptors are sensitized, we studied in humans the effects of prostaglandin E2 on the intensity of pain evoked by bradykinin via the nociceptive systems of skin and veins.	Dinoprostone	206-222	kininogen 1	Homo sapiens	258-268
8750710-5	1995	Prostaglandin E2 alone never elicited pain, but without exception increased the intensity of bradykinin-induced pain in a concentration-related manner at concentrations from 10(-9) to 10(-6) M, both in skin and veins.	Dinoprostone	0-16	kininogen 1	Homo sapiens	93-103
8750710-6	1995	Thus, bradykinin is more painful after pretreatment with prostaglandin E2, suggesting sensitization of nociceptors of the skin, but also of hand veins in humans.	Dinoprostone	57-73	kininogen 1	Homo sapiens	6-16
8521563-1	1995	BACKGROUND: Bradykinin is a potent vasodilator that acts through B2 kinin receptors to stimulate the release of endothelium-derived nitric oxide, prostacyclin, and hyperpolarizing factor.	Nitric Oxide	132-144	kininogen 1	Homo sapiens	12-22
8521563-1	1995	BACKGROUND: Bradykinin is a potent vasodilator that acts through B2 kinin receptors to stimulate the release of endothelium-derived nitric oxide, prostacyclin, and hyperpolarizing factor.	Epoprostenol	146-158	kininogen 1	Homo sapiens	12-22
8521563-3	1995	METHODS AND RESULTS: The selective bradykinin B2 receptor antagonist HOE 140 was infused into the left main coronary artery (200 micrograms/min for 15 minutes) in 15 patients without significant coronary stenoses.	4-hydroxy-2-octenal	69-72	kininogen 1	Homo sapiens	35-45
8521563-8	1995	After bradykinin B2 receptor blockade, there was a reduction in flow-dependent dilation (23.4 +/- 6.9% to 3.9 +/- 6.0%, P &lt; .001), the extent of which correlated with the degree of basal vasoconstriction after HOE 140 in the same vessel segment (P &lt; .05).	4-hydroxy-2-octenal	213-216	kininogen 1	Homo sapiens	6-16
8521575-4	1995	METHODS AND RESULTS: EDHF was evaluated as the bradykinin- or A23187-induced relaxation of the porcine coronary artery contracted by prostaglandin F2 alpha in the presence of NNA and IM.	edhf	21-25	kininogen 1	Homo sapiens	47-57
8521575-4	1995	METHODS AND RESULTS: EDHF was evaluated as the bradykinin- or A23187-induced relaxation of the porcine coronary artery contracted by prostaglandin F2 alpha in the presence of NNA and IM.	Dinoprost	133-155	kininogen 1	Homo sapiens	47-57
8521575-7	1995	At concentrations of 0 to 20 mumol/L, LPC dose-dependently inhibited the NNA/IM-resistant EDR induced by bradykinin and A23187, and the relaxation was reversible after the absorption of LPC with albumin.	Lysophosphatidylcholines	38-41	kininogen 1	Homo sapiens	105-115
8554523-0	1995	Potentiated bradykinin-induced increase of 1,2-diacylglycerol generation and phospholipase D activity in human senescent fibroblasts.	1,2-diacylglycerol	43-61	kininogen 1	Homo sapiens	12-22
8554523-3	1995	BK-induced activation of phospholipase D (PLD), the major enzyme involved in sustained 1,2-DAG generation, was 2.5-fold higher in old cells, strongly suggesting that it is involved in the potentiated increase of 1,2-DAG formation.	1,2-diacylglycerol	87-94	kininogen 1	Homo sapiens	0-2
8554523-3	1995	BK-induced activation of phospholipase D (PLD), the major enzyme involved in sustained 1,2-DAG generation, was 2.5-fold higher in old cells, strongly suggesting that it is involved in the potentiated increase of 1,2-DAG formation.	1,2-diacylglycerol	212-219	kininogen 1	Homo sapiens	0-2
8554523-7	1995	BK was also able to increase the release of [14C]ethanolamine, a water-soluble product of hydrolysis of phosphatidylethanolamine (PtdEtn), through PLD activation in young and old cells.	[14c]ethanolamine	44-61	kininogen 1	Homo sapiens	0-2
8603131-6	1996	This NTG tolerance significantly attenuated vasorelaxation to either ISDN, SNP or EDRF stimulated by bradykinin.	Nitroglycerin	5-8	kininogen 1	Homo sapiens	101-111
8749030-6	1995	Captopril, the angiotensin-converting enzyme inhibitor, decreased pulmonary vasoconstrictor responses to angiotensin I and enhanced vasodilator responses to bradykinin, but did not significantly change pressor responses to L-163,491.	Captopril	0-9	kininogen 1	Homo sapiens	157-167
8554523-7	1995	BK was also able to increase the release of [14C]ethanolamine, a water-soluble product of hydrolysis of phosphatidylethanolamine (PtdEtn), through PLD activation in young and old cells.	Water	65-70	kininogen 1	Homo sapiens	0-2
8554523-7	1995	BK was also able to increase the release of [14C]ethanolamine, a water-soluble product of hydrolysis of phosphatidylethanolamine (PtdEtn), through PLD activation in young and old cells.	phosphatidylethanolamine	104-128	kininogen 1	Homo sapiens	0-2
8554523-7	1995	BK was also able to increase the release of [14C]ethanolamine, a water-soluble product of hydrolysis of phosphatidylethanolamine (PtdEtn), through PLD activation in young and old cells.	phosphatidylethanolamine	130-136	kininogen 1	Homo sapiens	0-2
8554523-11	1995	It remains to be established whether the increased generation of DAG upon BK stimulation plays any role in the altered PKC signalling pathway which characterizes old fibroblasts.	1,2-diacylglycerol	65-68	kininogen 1	Homo sapiens	74-76
8594917-4	1995	Responses to kallidin were decreased by the kinin B2 antagonist, HOE 140, whereas responses to DABK and DAK were reduced by des-Arg9[Leu8]BK, a kinin B1-receptor antagonist.	des-arg9	124-132	kininogen 1	Homo sapiens	97-99
8519653-8	1995	In the absence of added arachidonate, bradykinin (BK) and endothelin-1 (ET-1), potentiated PGE2 production in IL-1 beta-treated fibroblasts, possibly by mobilising endogenous substrate.	Dinoprostone	91-95	kininogen 1	Homo sapiens	38-48
8519653-8	1995	In the absence of added arachidonate, bradykinin (BK) and endothelin-1 (ET-1), potentiated PGE2 production in IL-1 beta-treated fibroblasts, possibly by mobilising endogenous substrate.	Dinoprostone	91-95	kininogen 1	Homo sapiens	50-52
8565149-0	1995	Release of arachidonic acid via Ca2+ increase stimulated by pyrophosphonucleotides and bradykinin in mammary tumour cells.	Arachidonic Acid	11-27	kininogen 1	Homo sapiens	87-97
8565149-1	1995	The relationship between the increase of intracellular Ca2+ and the release of arachidonic acid by bradykinin and pyrophosphonucleotides was studied in cultured mammary tumour cells, MMT060562.	Arachidonic Acid	79-95	kininogen 1	Homo sapiens	99-109
8565149-2	1995	Bradykinin, ATP, UTP and UDP induced an increase of intracellular Ca2+ and the release of arachidonic acid from phospholipids into the extracellular fluid.	Arachidonic Acid	90-106	kininogen 1	Homo sapiens	0-10
8565149-2	1995	Bradykinin, ATP, UTP and UDP induced an increase of intracellular Ca2+ and the release of arachidonic acid from phospholipids into the extracellular fluid.	Phospholipids	112-125	kininogen 1	Homo sapiens	0-10
8565149-4	1995	Liberation of arachidonic acid by bradykinin and ATP was reduced by mepacrine, a blocker of phospholipase A2 and W-7, a calmodulin antagonist.	Arachidonic Acid	14-30	kininogen 1	Homo sapiens	34-44
8565149-4	1995	Liberation of arachidonic acid by bradykinin and ATP was reduced by mepacrine, a blocker of phospholipase A2 and W-7, a calmodulin antagonist.	Quinacrine	68-77	kininogen 1	Homo sapiens	34-44
8565149-4	1995	Liberation of arachidonic acid by bradykinin and ATP was reduced by mepacrine, a blocker of phospholipase A2 and W-7, a calmodulin antagonist.	W 7	113-116	kininogen 1	Homo sapiens	34-44
8683414-10	1995	BK and HIS increased PGE2 release in both HPDL cells and HGF.	Dinoprostone	21-25	kininogen 1	Homo sapiens	0-2
8531115-1	1995	The effect of tenidap, (+/-)-5-chloro-2,3-dihydro-3-(hydroxy-2- thienylmethylene)-2-oxo-1H-indole-1-carboxamide, a new anti-inflammatory agent, was investigated on intracellular free Ca++ concentration ([Ca++]i) responses evoked by bradykinin and thapsigargin in gingival fibroblasts.	tenidap	23-111	kininogen 1	Homo sapiens	232-242
7484881-7	1995	It is conceivable that these beneficial effects of chronic ACE inhibition are due, in part, to blockade of bradykinin degradation by the ACE and the increased endothelial synthesis of prostaglandins and/or the release of nitric oxide by enhanced tissue levels of bradykinin.	Nitric Oxide	221-233	kininogen 1	Homo sapiens	263-273
7495221-4	1995	The neurohumoral response in hypertensive heart disease, after myocardial infarction with overall deterioration of left ventricular function or congestive heart failure leads to an activation of either the cardiac or the circulating RAS, which closely interacts with the bradykinin-prostaglandin system.	Prostaglandins	282-295	kininogen 1	Homo sapiens	271-281
7503261-3	1995	However, Ro 24-9981 significantly potentiated bradykinin-induced increases in leaky site formation and clearance of fluorescein-isothiocyanate-dextran (P &lt; 0.05).	fluorescein isothiocyanate dextran	116-150	kininogen 1	Homo sapiens	46-56
7503261-6	1995	NG-nitro-L-arginine methyl ester, a selective inhibitor of nitric oxide synthase, but not NG-nitro-D-arginine methyl ester, significantly attenuated the effects of both bradykinin and Ro 24-9981 with bradykinin (P &lt; 0.05).	NG-Nitroarginine Methyl Ester	0-32	kininogen 1	Homo sapiens	169-179
7503261-6	1995	NG-nitro-L-arginine methyl ester, a selective inhibitor of nitric oxide synthase, but not NG-nitro-D-arginine methyl ester, significantly attenuated the effects of both bradykinin and Ro 24-9981 with bradykinin (P &lt; 0.05).	NG-Nitroarginine Methyl Ester	0-32	kininogen 1	Homo sapiens	200-210
7503261-6	1995	NG-nitro-L-arginine methyl ester, a selective inhibitor of nitric oxide synthase, but not NG-nitro-D-arginine methyl ester, significantly attenuated the effects of both bradykinin and Ro 24-9981 with bradykinin (P &lt; 0.05).	nitric	59-65	kininogen 1	Homo sapiens	169-179
8541641-0	1995	Efficient production of casoxin D, a bradykinin agonist peptide derived from human casein, by Bacillus brevis.	casoxin D	24-33	kininogen 1	Homo sapiens	37-47
8703645-12	1995	After stopping enalapril there was a highly significant reduction in wheal area produced by intradermal bradykinin, with the majority of the effect seen by day 3 (P &lt; 0.0005).	Enalapril	15-24	kininogen 1	Homo sapiens	104-114
7586370-9	1995	In the presence of captopril, bradykinin (0.1 nmol/L, n = 6) markedly accelerated LV relaxation (significantly more than captopril alone), whereas bradykinin alone (0.1 nmol/L, n = 6) had no effect.	Captopril	19-28	kininogen 1	Homo sapiens	30-40
7586370-10	1995	CONCLUSIONS: These data indicate that the ACE inhibitor captopril causes an acute and selective enhancement of LV relaxation independent of changes in coronary flow, probably via an endogenous bradykinin/nitric oxide pathway.	Captopril	56-65	kininogen 1	Homo sapiens	193-203
8608658-0	1995	Plasma bradykinin levels during hemodialysis with PAN DX and polysulfone membranes with and without concurrent ACE inhibitor.	polysulfone P 1700	61-72	kininogen 1	Homo sapiens	7-17
7498312-1	1995	High affinity [3H]bradykinin binding sites have been identified in human skin cryosections by in vitro autoradiography.	Tritium	15-17	kininogen 1	Homo sapiens	18-28
7595498-3	1995	Pretreatment of cells with a maximal effective concentration (5 microM) of BK did not affect the subsequent carbachol (CCh)-induced [Ca2+]i rise, but CCh (1 mM) pretreatment completely abolished the BK-induced [Ca2+]i rise without inhibition of BK-induced inositol 1,4,5-trisphosphate (IP3) generation.	Carbachol	150-153	kininogen 1	Homo sapiens	199-201
7595498-3	1995	Pretreatment of cells with a maximal effective concentration (5 microM) of BK did not affect the subsequent carbachol (CCh)-induced [Ca2+]i rise, but CCh (1 mM) pretreatment completely abolished the BK-induced [Ca2+]i rise without inhibition of BK-induced inositol 1,4,5-trisphosphate (IP3) generation.	Carbachol	150-153	kininogen 1	Homo sapiens	199-201
7595498-3	1995	Pretreatment of cells with a maximal effective concentration (5 microM) of BK did not affect the subsequent carbachol (CCh)-induced [Ca2+]i rise, but CCh (1 mM) pretreatment completely abolished the BK-induced [Ca2+]i rise without inhibition of BK-induced inositol 1,4,5-trisphosphate (IP3) generation.	Inositol 1,4,5-Trisphosphate	256-284	kininogen 1	Homo sapiens	75-77
7595498-3	1995	Pretreatment of cells with a maximal effective concentration (5 microM) of BK did not affect the subsequent carbachol (CCh)-induced [Ca2+]i rise, but CCh (1 mM) pretreatment completely abolished the BK-induced [Ca2+]i rise without inhibition of BK-induced inositol 1,4,5-trisphosphate (IP3) generation.	Inositol 1,4,5-Trisphosphate	286-289	kininogen 1	Homo sapiens	75-77
7595498-4	1995	Thapsigargin (1 microM) pretreatment abolished the subsequent BK- and CCh-induced [Ca2+]i rise, though it did not affect agonist-induced IP3 generation.	Thapsigargin	0-12	kininogen 1	Homo sapiens	62-64
7595498-5	1995	However, the addition of atropine at plateau phases of CCh-induced [Ca2+]i rise and IP3 production caused a rapid decline to the basal levels and then restored the [Ca2+]i rise by BK.	Atropine	25-33	kininogen 1	Homo sapiens	180-182
7595498-5	1995	However, the addition of atropine at plateau phases of CCh-induced [Ca2+]i rise and IP3 production caused a rapid decline to the basal levels and then restored the [Ca2+]i rise by BK.	Carbachol	55-58	kininogen 1	Homo sapiens	180-182
8851034-4	1995	markedly inhibits skin reactions induced by BK challenge (intradermal injection of 212 micrograms BK in 10 microL saline and prick test with a solution of 21.2 micrograms/microL).	Sodium Chloride	114-120	kininogen 1	Homo sapiens	44-46
8851034-4	1995	markedly inhibits skin reactions induced by BK challenge (intradermal injection of 212 micrograms BK in 10 microL saline and prick test with a solution of 21.2 micrograms/microL).	Sodium Chloride	114-120	kininogen 1	Homo sapiens	98-100
8851034-7	1995	New data in the literature suggest the existence of various pharmacological mediators possibly involved in the BK-induced reaction: neuromediators, nitric oxyde and PAF.	nitric oxyde	148-160	kininogen 1	Homo sapiens	111-113
8851034-7	1995	New data in the literature suggest the existence of various pharmacological mediators possibly involved in the BK-induced reaction: neuromediators, nitric oxyde and PAF.	Platelet Activating Factor	165-168	kininogen 1	Homo sapiens	111-113
8801862-4	1995	NO-dependent cGMP production in the cells (passage 1; preincubated in L-arginine-free medium for 24 h) was stimulated for 3 min with bradykinin (BK 1 nM) or the calcium-ionophore A23187 (100 nM) or by a 20 min incubation with L-arginine (L-Arg 0.1 mM, 20 min).	Cyclic GMP	13-17	kininogen 1	Homo sapiens	133-143
8801862-4	1995	NO-dependent cGMP production in the cells (passage 1; preincubated in L-arginine-free medium for 24 h) was stimulated for 3 min with bradykinin (BK 1 nM) or the calcium-ionophore A23187 (100 nM) or by a 20 min incubation with L-arginine (L-Arg 0.1 mM, 20 min).	Arginine	70-80	kininogen 1	Homo sapiens	133-143
8801862-4	1995	NO-dependent cGMP production in the cells (passage 1; preincubated in L-arginine-free medium for 24 h) was stimulated for 3 min with bradykinin (BK 1 nM) or the calcium-ionophore A23187 (100 nM) or by a 20 min incubation with L-arginine (L-Arg 0.1 mM, 20 min).	Arginine	226-236	kininogen 1	Homo sapiens	133-143
8801862-4	1995	NO-dependent cGMP production in the cells (passage 1; preincubated in L-arginine-free medium for 24 h) was stimulated for 3 min with bradykinin (BK 1 nM) or the calcium-ionophore A23187 (100 nM) or by a 20 min incubation with L-arginine (L-Arg 0.1 mM, 20 min).	Arginine	238-243	kininogen 1	Homo sapiens	133-143
8801862-9	1995	n-LDL reduced the cGMP-levels in unstimulated cells as well as the cGMP increase in response to bradykinin (-10%) and the calcium-ionophore A23187 (-80%).	Nitrogen	0-1	kininogen 1	Homo sapiens	96-106
8801862-9	1995	n-LDL reduced the cGMP-levels in unstimulated cells as well as the cGMP increase in response to bradykinin (-10%) and the calcium-ionophore A23187 (-80%).	Cyclic GMP	67-71	kininogen 1	Homo sapiens	96-106
7578941-1	1995	The conformation of the head-to-tail cyclic analogue of bradykinin in DMSO was investigated by nmr.	Dimethyl Sulfoxide	70-74	kininogen 1	Homo sapiens	56-66
7590107-7	1995	Activation of protein kinase C decreases the changes in intracellular calcium evoked by carbachol, bradykinin and 100 mM K+.	Calcium	70-77	kininogen 1	Homo sapiens	99-109
7558231-1	1995	In porcine coronary artery endothelium-dependent relaxation to bradykinin is in part attributed to a chemically unidentified factor, termed endothelium-derived hyperpolarizing factor (EDHF).	endothelium-derived hyperpolarizing factor	140-182	kininogen 1	Homo sapiens	63-73
7558231-1	1995	In porcine coronary artery endothelium-dependent relaxation to bradykinin is in part attributed to a chemically unidentified factor, termed endothelium-derived hyperpolarizing factor (EDHF).	edhf	184-188	kininogen 1	Homo sapiens	63-73
7558231-4	1995	The phospholipase C inhibitor U73122 (1 mumol/L) abolished bradykinin-induced, nitric oxide-mediated relaxation but did not inhibit either bradykinin-induced, EDHF-mediated relaxation or prostaglandin I2 production.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	30-36	kininogen 1	Homo sapiens	59-69
7558231-4	1995	The phospholipase C inhibitor U73122 (1 mumol/L) abolished bradykinin-induced, nitric oxide-mediated relaxation but did not inhibit either bradykinin-induced, EDHF-mediated relaxation or prostaglandin I2 production.	Nitric Oxide	79-91	kininogen 1	Homo sapiens	59-69
7558231-5	1995	However, when given at a larger dose (20 mumol/L) U73122 abolished both bradykinin-induced, EDHF-mediated relaxation and prostaglandin I2 production.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	50-56	kininogen 1	Homo sapiens	72-82
7558231-5	1995	However, when given at a larger dose (20 mumol/L) U73122 abolished both bradykinin-induced, EDHF-mediated relaxation and prostaglandin I2 production.	edhf	92-96	kininogen 1	Homo sapiens	72-82
7558231-6	1995	Similarly, the calcium-ATPase inhibitor thapsigargin, given at a dose (1 mumol/L) that abolished bradykinin-induced increases in intracellular calcium concentration in cultured porcine coronary artery endothelial cells, eliminated both bradykinin-induced.	Thapsigargin	40-52	kininogen 1	Homo sapiens	97-107
7558231-6	1995	Similarly, the calcium-ATPase inhibitor thapsigargin, given at a dose (1 mumol/L) that abolished bradykinin-induced increases in intracellular calcium concentration in cultured porcine coronary artery endothelial cells, eliminated both bradykinin-induced.	Thapsigargin	40-52	kininogen 1	Homo sapiens	236-246
7558231-6	1995	Similarly, the calcium-ATPase inhibitor thapsigargin, given at a dose (1 mumol/L) that abolished bradykinin-induced increases in intracellular calcium concentration in cultured porcine coronary artery endothelial cells, eliminated both bradykinin-induced.	Calcium	15-22	kininogen 1	Homo sapiens	97-107
7558231-6	1995	Similarly, the calcium-ATPase inhibitor thapsigargin, given at a dose (1 mumol/L) that abolished bradykinin-induced increases in intracellular calcium concentration in cultured porcine coronary artery endothelial cells, eliminated both bradykinin-induced.	Calcium	15-22	kininogen 1	Homo sapiens	236-246
7558231-8	1995	Although thapsigargin abolished bradykinin-induced prostaglandin I2 production, the basal production of prostaglandin I2 was enhanced and contraction of endothelium-intact rings was attenuated.	Thapsigargin	9-21	kininogen 1	Homo sapiens	32-42
7558231-8	1995	Although thapsigargin abolished bradykinin-induced prostaglandin I2 production, the basal production of prostaglandin I2 was enhanced and contraction of endothelium-intact rings was attenuated.	Epoprostenol	51-67	kininogen 1	Homo sapiens	32-42
7558231-10	1995	These observations suggest that phospholipase C activation and increased intracellular calcium concentration are required for both bradykinin-induced arachidonic acid release and EDHF production in porcine coronary artery.	Calcium	87-94	kininogen 1	Homo sapiens	131-141
7558231-10	1995	These observations suggest that phospholipase C activation and increased intracellular calcium concentration are required for both bradykinin-induced arachidonic acid release and EDHF production in porcine coronary artery.	Arachidonic Acid	150-166	kininogen 1	Homo sapiens	131-141
7560662-3	1995	OBJECTIVE: We postulated that repeated bradykinin and hypertonic saline bronchial challenges might reduce the airway response to subsequent hypertonic saline and bradykinin challenges, respectively.	Sodium Chloride	65-71	kininogen 1	Homo sapiens	162-172
7560662-3	1995	OBJECTIVE: We postulated that repeated bradykinin and hypertonic saline bronchial challenges might reduce the airway response to subsequent hypertonic saline and bradykinin challenges, respectively.	Sodium Chloride	151-157	kininogen 1	Homo sapiens	39-49
7560662-14	1995	CONCLUSION: Refractoriness produced by repeated exposure of the airways to bradykinin and hypertonic saline results in loss of responsiveness to hypertonic saline and bradykinin respectively, suggesting a shared mechanism for refractoriness produced by these stimuli.	Sodium Chloride	101-107	kininogen 1	Homo sapiens	167-177
7498312-3	1995	Competition experiments revealed a rank order of potency with bradykinin being most effective (bradykinin = [Lys]bradykinin &gt; [Met- Lys]bradykinin &gt; [Tyr]bradykinin &gt; [des-Arg9]bradykinin), whereas [des-Arg9]bradykinin was ineffective.	Tyrosine	156-159	kininogen 1	Homo sapiens	62-72
7498312-3	1995	Competition experiments revealed a rank order of potency with bradykinin being most effective (bradykinin = [Lys]bradykinin &gt; [Met- Lys]bradykinin &gt; [Tyr]bradykinin &gt; [des-Arg9]bradykinin), whereas [des-Arg9]bradykinin was ineffective.	des-arg9	177-185	kininogen 1	Homo sapiens	62-72
7498312-3	1995	Competition experiments revealed a rank order of potency with bradykinin being most effective (bradykinin = [Lys]bradykinin &gt; [Met- Lys]bradykinin &gt; [Tyr]bradykinin &gt; [des-Arg9]bradykinin), whereas [des-Arg9]bradykinin was ineffective.	des-arg9	208-216	kininogen 1	Homo sapiens	62-72
7595498-6	1995	Treatment of cells with both CCh and BK at the same time showed additive effects in IP3 production.	Inositol 1,4,5-Trisphosphate	84-87	kininogen 1	Homo sapiens	37-39
8610212-5	1995	The inhibition by L-NAME was reversed by the addition of L-arginine in both MCh- and BK-induced secretions from isolated glands.	NG-Nitroarginine Methyl Ester	18-24	kininogen 1	Homo sapiens	85-87
8610212-5	1995	The inhibition by L-NAME was reversed by the addition of L-arginine in both MCh- and BK-induced secretions from isolated glands.	Arginine	57-67	kininogen 1	Homo sapiens	85-87
8560418-4	1995	The functional defect in LKd was not merely due to bradykinin loss because two preparations of bradykinin-free LK blocked biotin-HK binding.	Biotin	122-128	kininogen 1	Homo sapiens	95-105
8560418-6	1995	These data suggested that LKd had an altered conformation which exposed the amino terminal arginine of bradykinin to antigenic detection.	Arginine	91-99	kininogen 1	Homo sapiens	103-113
7548185-0	1995	Regulation of bradykinin-stimulated phospholipase C and arachidonic acid release by protein kinase A in MDCK-D1 cells.	Arachidonic Acid	56-72	kininogen 1	Homo sapiens	14-24
7498312-2	1995	Equilibrium binding studies were performed with increasing concentrations of [3H]bradykinin for 120 min in the presence of protease inhibitors at 4 degrees C. In saturation experiments a single class of high affinity binding sites was identified with a dissociation constant Kd of 1.2 +/- 0.8 nM (mean +/- S.E.M., n = 3) and a maximal binding capacity Bmax of 33 +/- 8 fmol [3H]bradykinin specifically bound/mg protein (mean +/- S.E.M., n = 3).	Tritium	78-80	kininogen 1	Homo sapiens	81-91
7498312-2	1995	Equilibrium binding studies were performed with increasing concentrations of [3H]bradykinin for 120 min in the presence of protease inhibitors at 4 degrees C. In saturation experiments a single class of high affinity binding sites was identified with a dissociation constant Kd of 1.2 +/- 0.8 nM (mean +/- S.E.M., n = 3) and a maximal binding capacity Bmax of 33 +/- 8 fmol [3H]bradykinin specifically bound/mg protein (mean +/- S.E.M., n = 3).	Tritium	375-377	kininogen 1	Homo sapiens	81-91
8592247-5	1995	Some of the effects of bradykinin in particular may be due to secondary activation of prostaglandins (PG), especially PGE2 and PGI2.	Prostaglandins	86-100	kininogen 1	Homo sapiens	23-33
8592247-5	1995	Some of the effects of bradykinin in particular may be due to secondary activation of prostaglandins (PG), especially PGE2 and PGI2.	Prostaglandins	102-104	kininogen 1	Homo sapiens	23-33
8592247-5	1995	Some of the effects of bradykinin in particular may be due to secondary activation of prostaglandins (PG), especially PGE2 and PGI2.	Dinoprostone	118-122	kininogen 1	Homo sapiens	23-33
8592247-5	1995	Some of the effects of bradykinin in particular may be due to secondary activation of prostaglandins (PG), especially PGE2 and PGI2.	Epoprostenol	127-131	kininogen 1	Homo sapiens	23-33
8588976-2	1995	In [3H]myristate-labelled endometrial stromal cells, bradykinin and tetradecanoylphorbol acetate (TPA) mediated activation of phospholipase D (PLD) as measured by the accumulation of [3H]phosphatidylbutanol ([3H]PtdBut).	Tritium	4-6	kininogen 1	Homo sapiens	53-63
7548185-3	1995	When cells were preincubated for 20 min with 10 microM FSK + 0.5 mM IBMX, and subsequently treated with 1 microM BDK or control medium for 40 min, the basal and BDK-stimulated PLC activity, measured as accumulated labelled inositol phosphate (InsP) after 40 min and inositol trisphosphate (InsP3) after 10 s, were significantly inhibited.	Colforsin	55-58	kininogen 1	Homo sapiens	161-164
7548185-4	1995	In a parallel manner, FSK + IBMX also significantly decreased both basal and BDK-stimulated diacylglycerol (DAG) production.	Colforsin	22-25	kininogen 1	Homo sapiens	77-80
7548185-4	1995	In a parallel manner, FSK + IBMX also significantly decreased both basal and BDK-stimulated diacylglycerol (DAG) production.	Diglycerides	92-106	kininogen 1	Homo sapiens	77-80
7548185-4	1995	In a parallel manner, FSK + IBMX also significantly decreased both basal and BDK-stimulated diacylglycerol (DAG) production.	Diglycerides	108-111	kininogen 1	Homo sapiens	77-80
7548185-5	1995	The basal and BDK-enhanced AA release into the media was also significantly inhibited by pretreatment with FSK + IBMX.	Colforsin	107-110	kininogen 1	Homo sapiens	14-17
7548185-6	1995	In parallel experiments, H-89, a specific inhibitor of PKA, was preincubated for 60 min prior to addition of BDK and this resulted in a reversal of FSK+IBMX-induced inhibition of basal and BDK-stimulated PLC activity and AA release.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	25-29	kininogen 1	Homo sapiens	109-112
7548185-6	1995	In parallel experiments, H-89, a specific inhibitor of PKA, was preincubated for 60 min prior to addition of BDK and this resulted in a reversal of FSK+IBMX-induced inhibition of basal and BDK-stimulated PLC activity and AA release.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	25-29	kininogen 1	Homo sapiens	189-192
7548185-6	1995	In parallel experiments, H-89, a specific inhibitor of PKA, was preincubated for 60 min prior to addition of BDK and this resulted in a reversal of FSK+IBMX-induced inhibition of basal and BDK-stimulated PLC activity and AA release.	Colforsin	148-151	kininogen 1	Homo sapiens	109-112
7548185-6	1995	In parallel experiments, H-89, a specific inhibitor of PKA, was preincubated for 60 min prior to addition of BDK and this resulted in a reversal of FSK+IBMX-induced inhibition of basal and BDK-stimulated PLC activity and AA release.	Colforsin	148-151	kininogen 1	Homo sapiens	189-192
7548185-7	1995	An inhibitor of inositide-hydrolysing PLC, U73122, (1 microM) was also found to blunt BDK-stimulated PLC activity and BDK-enhanced AA release which indicated that stimulation of AA release by the nonapeptide was second to PLC activation.	inositide	16-25	kininogen 1	Homo sapiens	86-89
7548185-7	1995	An inhibitor of inositide-hydrolysing PLC, U73122, (1 microM) was also found to blunt BDK-stimulated PLC activity and BDK-enhanced AA release which indicated that stimulation of AA release by the nonapeptide was second to PLC activation.	inositide	16-25	kininogen 1	Homo sapiens	118-121
7548185-7	1995	An inhibitor of inositide-hydrolysing PLC, U73122, (1 microM) was also found to blunt BDK-stimulated PLC activity and BDK-enhanced AA release which indicated that stimulation of AA release by the nonapeptide was second to PLC activation.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	43-49	kininogen 1	Homo sapiens	86-89
7548185-7	1995	An inhibitor of inositide-hydrolysing PLC, U73122, (1 microM) was also found to blunt BDK-stimulated PLC activity and BDK-enhanced AA release which indicated that stimulation of AA release by the nonapeptide was second to PLC activation.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	43-49	kininogen 1	Homo sapiens	118-121
7626288-7	1995	By contrast, bradykinin, which evoked comparable increases in cytosolic calcium and phosphoinositide turnover, did not stimulate airway smooth muscle cell growth.	Calcium	72-79	kininogen 1	Homo sapiens	13-23
7626288-7	1995	By contrast, bradykinin, which evoked comparable increases in cytosolic calcium and phosphoinositide turnover, did not stimulate airway smooth muscle cell growth.	Phosphatidylinositols	84-100	kininogen 1	Homo sapiens	13-23
7631960-10	1995	NG-methyl-L-arginine or indomethacin (antagonists of NO or PGI2) inhibited the bradykinin-evoked antiaggregation (10.3 +/- 2.1% and 13.6 +/- 3.7%, respectively; n = 6).	ng-methyl-l-arginine	0-20	kininogen 1	Homo sapiens	79-89
7631960-10	1995	NG-methyl-L-arginine or indomethacin (antagonists of NO or PGI2) inhibited the bradykinin-evoked antiaggregation (10.3 +/- 2.1% and 13.6 +/- 3.7%, respectively; n = 6).	Indomethacin	24-36	kininogen 1	Homo sapiens	79-89
7631960-10	1995	NG-methyl-L-arginine or indomethacin (antagonists of NO or PGI2) inhibited the bradykinin-evoked antiaggregation (10.3 +/- 2.1% and 13.6 +/- 3.7%, respectively; n = 6).	Epoprostenol	59-63	kininogen 1	Homo sapiens	79-89
7631960-12	1995	Lidocaine failed to influence basal antiaggregation, but it inhibited bradykinin-stimulated antiaggregation in a concentration-dependent manner (concentration causing 50% inhibition = 108 +/- 41 microM; n = 6).	Lidocaine	0-9	kininogen 1	Homo sapiens	70-80
7550072-1	1995	In fura-2-loaded human periodontal ligament (HPDL) cells, bradykinin induced a rapidly transient increase and subsequently sustained increase in cytosolic Ca2+ ([Ca2+]i).	Fura-2	3-9	kininogen 1	Homo sapiens	58-68
7550072-4	1995	After depletion of the intracellular Ca2+ pool by thapsigargin, the increase in [Ca2+]i induced by bradykinin was obviously reduced.	Thapsigargin	50-62	kininogen 1	Homo sapiens	99-109
7550072-5	1995	Bradykinin also stimulated formation of inositol polyphosphates including 1,4,5-IP3.	inositol polyphosphates	40-63	kininogen 1	Homo sapiens	0-10
7550072-5	1995	Bradykinin also stimulated formation of inositol polyphosphates including 1,4,5-IP3.	Inositol 1,4,5-Trisphosphate	74-83	kininogen 1	Homo sapiens	0-10
7550072-6	1995	These results suggest that bradykinin stimulates intracellular Ca2+ release from the 1,4,5-IP3-sensitive Ca2+ pool.	Inositol 1,4,5-Trisphosphate	85-94	kininogen 1	Homo sapiens	27-37
7550072-7	1995	Bradykinin stimulated prostaglandin E2 (PGE2) release in the presence of external Ca2+, but not in the absence of external Ca2+.	Dinoprostone	22-38	kininogen 1	Homo sapiens	0-10
7550072-7	1995	Bradykinin stimulated prostaglandin E2 (PGE2) release in the presence of external Ca2+, but not in the absence of external Ca2+.	Dinoprostone	40-44	kininogen 1	Homo sapiens	0-10
7550072-9	1995	These results indicate that bradykinin induces Ca2+ mobilization via activation of phospholipase C and PGE2 release caused by the Ca2+ influx in HPDL cells.	Dinoprostone	103-107	kininogen 1	Homo sapiens	28-38
7544228-3	1995	METHODS: We examined the effect of procaterol, a beta 2-adrenoceptor agonist, on skin whealing responses to histamine, platelet-activating factor (PAF), substance P, or bradykinin in eight asthmatic children in a double-blind, randomized, cross-over study.	Procaterol	35-45	kininogen 1	Homo sapiens	169-179
7544228-4	1995	Two hours after taking procaterol (50 micrograms) or placebo orally, the subjects were given these mediators intradermally at a concentration of 10(-5) M. RESULTS: Procaterol has a small but significant inhibitory effect on wheal formation following the intradermal injection of histamine and PAF by an average of 15% (P &lt; .05) and 18% (P &lt; .05) respectively but not against substance P or bradykinin.	Procaterol	164-174	kininogen 1	Homo sapiens	396-406
8566312-0	1995	Regulation of bradykinin responses by PKC epsilon and histamine responses by PKC alpha in adrenal chromaffin cells.	Histamine	54-63	kininogen 1	Homo sapiens	14-24
8566312-0	1995	Regulation of bradykinin responses by PKC epsilon and histamine responses by PKC alpha in adrenal chromaffin cells.	chromaffin	98-108	kininogen 1	Homo sapiens	14-24
8588976-2	1995	In [3H]myristate-labelled endometrial stromal cells, bradykinin and tetradecanoylphorbol acetate (TPA) mediated activation of phospholipase D (PLD) as measured by the accumulation of [3H]phosphatidylbutanol ([3H]PtdBut).	Myristic Acid	7-16	kininogen 1	Homo sapiens	53-63
8588976-2	1995	In [3H]myristate-labelled endometrial stromal cells, bradykinin and tetradecanoylphorbol acetate (TPA) mediated activation of phospholipase D (PLD) as measured by the accumulation of [3H]phosphatidylbutanol ([3H]PtdBut).	[3h]phosphatidylbutanol	183-206	kininogen 1	Homo sapiens	53-63
7582546-2	1995	The contribution of sarco-endoplasmic reticulum Ca(2+)-ATPases (SERCA)-regulated Ca2+ stores to the increase in intracellular free calcium ([Ca2+]i) induced by bradykinin (BK) was investigated in fura-2 loaded human tracheal smooth muscle cells (TSMC).	Calcium	131-138	kininogen 1	Homo sapiens	160-170
8588976-2	1995	In [3H]myristate-labelled endometrial stromal cells, bradykinin and tetradecanoylphorbol acetate (TPA) mediated activation of phospholipase D (PLD) as measured by the accumulation of [3H]phosphatidylbutanol ([3H]PtdBut).	[3h]ptdbut	208-218	kininogen 1	Homo sapiens	53-63
7582546-2	1995	The contribution of sarco-endoplasmic reticulum Ca(2+)-ATPases (SERCA)-regulated Ca2+ stores to the increase in intracellular free calcium ([Ca2+]i) induced by bradykinin (BK) was investigated in fura-2 loaded human tracheal smooth muscle cells (TSMC).	Fura-2	196-202	kininogen 1	Homo sapiens	160-170
7582546-2	1995	The contribution of sarco-endoplasmic reticulum Ca(2+)-ATPases (SERCA)-regulated Ca2+ stores to the increase in intracellular free calcium ([Ca2+]i) induced by bradykinin (BK) was investigated in fura-2 loaded human tracheal smooth muscle cells (TSMC).	tsmc	246-250	kininogen 1	Homo sapiens	160-170
7582546-11	1995	The transient phase induced by BK, histamine and carbachol was inhibited in a time-dependent way by preincubation of the cells with thapsigargin.	Thapsigargin	132-144	kininogen 1	Homo sapiens	31-33
8588976-7	1995	Staurosporine, an inhibitor of protein kinase C, strongly inhibited (IC50 96 nM) TPA-induced [3H]PtdBut formation, but bradykinin-stimulated [3H]PtdBut accumulation was only partially inhibited (IC50 65 microM).	phosphatidylbutanol	145-151	kininogen 1	Homo sapiens	119-129
8588976-4	1995	Bradykinin induced a dose-dependent (EC50 0.11 nM) [3H]PtdBut accumulation at concentrations at which it stimulated DNA synthesis.	Tritium	52-54	kininogen 1	Homo sapiens	0-10
8588976-4	1995	Bradykinin induced a dose-dependent (EC50 0.11 nM) [3H]PtdBut accumulation at concentrations at which it stimulated DNA synthesis.	phosphatidylbutanol	55-61	kininogen 1	Homo sapiens	0-10
8588976-5	1995	In [3H]inositol-labelled cells, bradykinin evoked a rapid increase in inositol phosphates which preceded the increase in [3H]PtdBut formation.	Tritium	4-6	kininogen 1	Homo sapiens	32-42
8588976-5	1995	In [3H]inositol-labelled cells, bradykinin evoked a rapid increase in inositol phosphates which preceded the increase in [3H]PtdBut formation.	Inositol	7-15	kininogen 1	Homo sapiens	32-42
8588976-5	1995	In [3H]inositol-labelled cells, bradykinin evoked a rapid increase in inositol phosphates which preceded the increase in [3H]PtdBut formation.	Inositol Phosphates	70-89	kininogen 1	Homo sapiens	32-42
8588976-5	1995	In [3H]inositol-labelled cells, bradykinin evoked a rapid increase in inositol phosphates which preceded the increase in [3H]PtdBut formation.	Tritium	122-124	kininogen 1	Homo sapiens	32-42
8588976-5	1995	In [3H]inositol-labelled cells, bradykinin evoked a rapid increase in inositol phosphates which preceded the increase in [3H]PtdBut formation.	phosphatidylbutanol	125-131	kininogen 1	Homo sapiens	32-42
8588976-6	1995	Chronic pretreatment with 400 nM TPA abolished PLD activation to subsequent treatment with either TPA and bradykinin.	Tetradecanoylphorbol Acetate	33-36	kininogen 1	Homo sapiens	106-116
8588976-7	1995	Staurosporine, an inhibitor of protein kinase C, strongly inhibited (IC50 96 nM) TPA-induced [3H]PtdBut formation, but bradykinin-stimulated [3H]PtdBut accumulation was only partially inhibited (IC50 65 microM).	Tritium	142-144	kininogen 1	Homo sapiens	119-129
7631812-6	1995	Molecular-sieve column chromatography by Sephadex G-75 revealed that BK induced a single low-molecular-weight peak (approximately 400 Da) for both NCA and MCA.	sephadex	41-54	kininogen 1	Homo sapiens	69-71
7626667-4	1995	Among the factors of the second group that were tested (heparin, ADP, histamine, bradykinin), histamine was found to stimulate glucose transport in CEC by 10-50%.	Histamine	94-103	kininogen 1	Homo sapiens	81-91
7626667-4	1995	Among the factors of the second group that were tested (heparin, ADP, histamine, bradykinin), histamine was found to stimulate glucose transport in CEC by 10-50%.	Glucose	127-134	kininogen 1	Homo sapiens	81-91
7600649-8	1995	The magnitudes of bradykinin-induced dilation at the site with acetylcholine-induced dilation (mean +/- SD: 6 +/- 6%, 11 +/- 9%, and 15 +/- 9%) were comparable to that (3 +/- 6%, 8 +/- 8%, and 13 +/- 9%) at the site with acetylcholine-induced constriction.	Acetylcholine	63-76	kininogen 1	Homo sapiens	18-28
7600649-16	1995	CONCLUSIONS: These results suggest that bradykinin causes vasodilation of human epicardial coronary arteries in vivo and that bradykinin-induced endothelium-dependent vasodilation is impaired at the stenotic site but is preserved at the angiographically normal site where endothelium-dependent vasodilation by acetylcholine is impaired and at the spastic site.	Acetylcholine	310-323	kininogen 1	Homo sapiens	126-136
8562468-8	1995	While ACE inhibitors inhibit activation of angiotensin I into angiotensin II and prevent the breakdown of bradykinin (which stimulates nitric oxide and prostacyclin formation), calcium antagonists inhibit the effects of vasoconstrictor hormones such as angiotensin II at the level of vascular smooth muscle by reducing calcium inflow and facilitating the vasodilator effects of nitric oxide.	Nitric Oxide	135-147	kininogen 1	Homo sapiens	106-116
8562468-8	1995	While ACE inhibitors inhibit activation of angiotensin I into angiotensin II and prevent the breakdown of bradykinin (which stimulates nitric oxide and prostacyclin formation), calcium antagonists inhibit the effects of vasoconstrictor hormones such as angiotensin II at the level of vascular smooth muscle by reducing calcium inflow and facilitating the vasodilator effects of nitric oxide.	Epoprostenol	152-164	kininogen 1	Homo sapiens	106-116
7475057-8	1995	However, epicardial but not intramyocardial vessels incubated with mibefradil exhibited enhanced relaxations to bradykinin (BK) and sodium nitroprusside (SNP) as compared with control.	Mibefradil	67-77	kininogen 1	Homo sapiens	112-122
7475057-8	1995	However, epicardial but not intramyocardial vessels incubated with mibefradil exhibited enhanced relaxations to bradykinin (BK) and sodium nitroprusside (SNP) as compared with control.	Mibefradil	67-77	kininogen 1	Homo sapiens	124-126
7631812-11	1995	These data suggest that BK and histamine may stimulate BEC to release NCA and MCA and may modulate neutrophil and monocyte recruitment into the airways in patients with asthma.	(2-boronoethyl)-cysteine	55-58	kininogen 1	Homo sapiens	24-26
7790881-7	1995	Capsaicin pretreatment of neuronal DRG cultures, which destroys capsaicin-sensitive (small diameter) afferent neurons, attenuated capsaicin- and bradykinin-stimulated cyclic GMP production but did not affect basal or sodium nitroprusside-stimulated cyclic GMP production.	Capsaicin	0-9	kininogen 1	Homo sapiens	145-155
8846418-6	1995	The most likely is the generation of cyclic GMP within the ischemic myocardium following bradykinin-stimulated nitric oxide generation and release from endothelial cells.	Nitric Oxide	111-123	kininogen 1	Homo sapiens	89-99
8564529-5	1995	The bradykinin B2 receptor antagonist icatebant (HOE 140) inhibited the bradykinin-induced IL-2 and IL-6 release.	icatebant	38-47	kininogen 1	Homo sapiens	4-14
8564529-5	1995	The bradykinin B2 receptor antagonist icatebant (HOE 140) inhibited the bradykinin-induced IL-2 and IL-6 release.	icatebant	38-47	kininogen 1	Homo sapiens	72-82
7790881-7	1995	Capsaicin pretreatment of neuronal DRG cultures, which destroys capsaicin-sensitive (small diameter) afferent neurons, attenuated capsaicin- and bradykinin-stimulated cyclic GMP production but did not affect basal or sodium nitroprusside-stimulated cyclic GMP production.	Capsaicin	64-73	kininogen 1	Homo sapiens	145-155
7623773-0	1995	Role of protein kinase C subtypes alpha and delta in the regulation of bradykinin-stimulated phosphoinositide breakdown in astrocytes.	Phosphatidylinositols	93-109	kininogen 1	Homo sapiens	71-81
7623773-1	1995	Cultured astrocytes express bradykinin (BK) receptors coupled to phospholipase C (PLC)-mediated phosphoinositide (PI) hydrolysis.	Phosphatidylinositols	96-112	kininogen 1	Homo sapiens	28-38
7631443-2	1995	Inhibition of bradykinin degradation by ACE inhibitors alters the kinin-kallikrein arachidonic acid system leading to increased concentrations of inflammatory metabolites.	Arachidonic Acid	83-99	kininogen 1	Homo sapiens	14-24
15714750-5	1995	Preincubation of endothelial cells with bradykinin and superoxide dismutase (SOD) synergistically potentiated the increase in platelet cGMP, but was attenuated by Nomega-nitro-L-arginine, with partial restoration by L-arginine but not by D-arginine.	Cyclic GMP	135-139	kininogen 1	Homo sapiens	40-50
15714750-5	1995	Preincubation of endothelial cells with bradykinin and superoxide dismutase (SOD) synergistically potentiated the increase in platelet cGMP, but was attenuated by Nomega-nitro-L-arginine, with partial restoration by L-arginine but not by D-arginine.	Nitroarginine	163-186	kininogen 1	Homo sapiens	40-50
15714750-5	1995	Preincubation of endothelial cells with bradykinin and superoxide dismutase (SOD) synergistically potentiated the increase in platelet cGMP, but was attenuated by Nomega-nitro-L-arginine, with partial restoration by L-arginine but not by D-arginine.	Arginine	176-186	kininogen 1	Homo sapiens	40-50
15714750-5	1995	Preincubation of endothelial cells with bradykinin and superoxide dismutase (SOD) synergistically potentiated the increase in platelet cGMP, but was attenuated by Nomega-nitro-L-arginine, with partial restoration by L-arginine but not by D-arginine.	D-Arginine	238-248	kininogen 1	Homo sapiens	40-50
8572285-1	1995	Bradykinin (BK) and kallidin (KAL) derivatives containing a Cys residue instead of a Ser residue at positions 6 and 7, respectively [BK(Cys6), KAL(Cys7)], were synthesized.	Cysteine	60-63	kininogen 1	Homo sapiens	0-10
7772029-9	1995	An accumulation of [3H]PEth was measured in the plasma-membrane (PM)-enriched fractions of both HeLa and 3T3 Li cells after incubation with PMA and bradykinin respectively.	Tritium	20-22	kininogen 1	Homo sapiens	148-158
7772029-9	1995	An accumulation of [3H]PEth was measured in the plasma-membrane (PM)-enriched fractions of both HeLa and 3T3 Li cells after incubation with PMA and bradykinin respectively.	PEth	23-27	kininogen 1	Homo sapiens	148-158
7541954-10	1995	The SNP-, ACh-, and BK-induced decrease in [K+]i was significantly blunted by Ba2+ by 85, 92, and 89%, respectively (n &gt; 4 for each agonist examined, P &lt; 0.0001).	N-methyl-valyl-amiclenomycin	78-82	kininogen 1	Homo sapiens	20-22
7541954-11	1995	NG-monomethyl-L-arginine (L-NMMA) and methylene blue inhibited the [K+]i-lowering effect of ACh and BK by 94 and 85% for L-NMMA (n = 5 for each agonist, P &lt; 0.0001) and by 67 and 72% for methylene blue (n = 5 for each agonist, P &lt; 0.001).	omega-N-Methylarginine	0-24	kininogen 1	Homo sapiens	100-102
7541954-11	1995	NG-monomethyl-L-arginine (L-NMMA) and methylene blue inhibited the [K+]i-lowering effect of ACh and BK by 94 and 85% for L-NMMA (n = 5 for each agonist, P &lt; 0.0001) and by 67 and 72% for methylene blue (n = 5 for each agonist, P &lt; 0.001).	omega-N-Methylarginine	26-32	kininogen 1	Homo sapiens	100-102
7541954-11	1995	NG-monomethyl-L-arginine (L-NMMA) and methylene blue inhibited the [K+]i-lowering effect of ACh and BK by 94 and 85% for L-NMMA (n = 5 for each agonist, P &lt; 0.0001) and by 67 and 72% for methylene blue (n = 5 for each agonist, P &lt; 0.001).	Methylene Blue	38-52	kininogen 1	Homo sapiens	100-102
7541954-11	1995	NG-monomethyl-L-arginine (L-NMMA) and methylene blue inhibited the [K+]i-lowering effect of ACh and BK by 94 and 85% for L-NMMA (n = 5 for each agonist, P &lt; 0.0001) and by 67 and 72% for methylene blue (n = 5 for each agonist, P &lt; 0.001).	omega-N-Methylarginine	121-127	kininogen 1	Homo sapiens	100-102
7541954-11	1995	NG-monomethyl-L-arginine (L-NMMA) and methylene blue inhibited the [K+]i-lowering effect of ACh and BK by 94 and 85% for L-NMMA (n = 5 for each agonist, P &lt; 0.0001) and by 67 and 72% for methylene blue (n = 5 for each agonist, P &lt; 0.001).	Methylene Blue	190-204	kininogen 1	Homo sapiens	100-102
7756645-9	1995	Fifth, the nonpermeable dye, crystal violet, almost completely quenched the fluorescence signal emitted by HUVEC-associated fluorescein isothiocyanate (FITC) HK.	Gentian Violet	29-43	kininogen 1	Homo sapiens	158-160
7756645-9	1995	Fifth, the nonpermeable dye, crystal violet, almost completely quenched the fluorescence signal emitted by HUVEC-associated fluorescein isothiocyanate (FITC) HK.	Fluorescein-5-isothiocyanate	124-150	kininogen 1	Homo sapiens	158-160
7756645-9	1995	Fifth, the nonpermeable dye, crystal violet, almost completely quenched the fluorescence signal emitted by HUVEC-associated fluorescein isothiocyanate (FITC) HK.	Fluorescein-5-isothiocyanate	152-156	kininogen 1	Homo sapiens	158-160
7756645-12	1995	Membrane-bound HK contributed to the anticoagulant nature of endothelial cells by blocking human alpha-thrombin binding and its resultant induction of prostacyclin formation.	Epoprostenol	151-163	kininogen 1	Homo sapiens	15-17
7562331-7	1995	Examination of the interactions between bradykinin and EGF signal transduction pathways revealed that PGE2 release was increased in the presence of bradykinin and EGF (167 +/- 33% to 317 +/- 29%).	Dinoprostone	102-106	kininogen 1	Homo sapiens	40-50
7562331-7	1995	Examination of the interactions between bradykinin and EGF signal transduction pathways revealed that PGE2 release was increased in the presence of bradykinin and EGF (167 +/- 33% to 317 +/- 29%).	Dinoprostone	102-106	kininogen 1	Homo sapiens	148-158
7562331-8	1995	The bradykinin-stimulated PGE2 release was completely abolished by indomethacin.	Dinoprostone	26-30	kininogen 1	Homo sapiens	4-14
7562331-8	1995	The bradykinin-stimulated PGE2 release was completely abolished by indomethacin.	Indomethacin	67-79	kininogen 1	Homo sapiens	4-14
7562331-9	1995	Indomethacin also was found to block the bradykinin inhibition of EGF-induced DNA synthesis.	Indomethacin	0-12	kininogen 1	Homo sapiens	41-51
7644562-2	1995	The effect of the NO synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) on the plasma exudation induced by histamine and bradykinin was also studied.	NG-Nitroarginine Methyl Ester	80-86	kininogen 1	Homo sapiens	137-147
7644562-5	1995	PGE1 (0.1 nmol/site) significantly potentiated both histamine- and bradykinin-induced edema.	Alprostadil	0-4	kininogen 1	Homo sapiens	67-77
7644562-8	1995	L-NAME (50-400 nmol/site, but not its enantiomer D-NAME, dose-dependently reduced the edema formation induced by a combination of either histamine or bradykinin with PGE1.	NG-Nitroarginine Methyl Ester	0-6	kininogen 1	Homo sapiens	150-160
7644562-10	1995	Our results thus demonstrate that PGE1, but not nitrovasodilators, can actually potentiate histamine- and bradykinin-induced edema in rabbit skin.	Alprostadil	34-38	kininogen 1	Homo sapiens	106-116
7646841-9	1995	Likewise, in the human coronary artery, the hyperpolarization elicited by bradykinin, which is also mediated by EDHF, is augmented in the presence of perindoprilat and prevented by potassium-induced depolarization.	edhf	112-116	kininogen 1	Homo sapiens	74-84
7539258-0	1995	Bradykinin induces tyrosine phosphorylation of epidermal growth factor-receptor and focal adhesion proteins in human keratinocytes.	Tyrosine	19-27	kininogen 1	Homo sapiens	0-10
7539258-1	1995	Bradykinin is an inflammatory mediator which activates signalling pathways in human keratinocytes via a receptor linked to a GTP-binding protein.	Guanosine Triphosphate	125-128	kininogen 1	Homo sapiens	0-10
7539258-2	1995	In the HaCaT human keratinocyte cell line, we observed bradykinin-stimulated tyrosine phosphorylation of several cellular proteins with peak response at 15 min.	Tyrosine	77-85	kininogen 1	Homo sapiens	55-65
7539258-3	1995	The focal adhesion proteins paxillin and p125FAK were tyrosine phosphorylated in response to bradykinin but not in response to epidermal growth factor.	Tyrosine	54-62	kininogen 1	Homo sapiens	93-103
7539258-4	1995	Interestingly, we identified the epidermal growth factor receptor as a novel target for bradykinin-induced tyrosine phosphorylation.	Tyrosine	107-115	kininogen 1	Homo sapiens	88-98
7539258-5	1995	The tyrosine kinase inhibitor genistein and the protein kinase C inhibitors staurosporine and Ro31-7549, all blocked bradykinin-induced tyrosine phosphorylation.	Genistein	30-39	kininogen 1	Homo sapiens	117-127
7539258-5	1995	The tyrosine kinase inhibitor genistein and the protein kinase C inhibitors staurosporine and Ro31-7549, all blocked bradykinin-induced tyrosine phosphorylation.	Staurosporine	76-89	kininogen 1	Homo sapiens	117-127
7539258-5	1995	The tyrosine kinase inhibitor genistein and the protein kinase C inhibitors staurosporine and Ro31-7549, all blocked bradykinin-induced tyrosine phosphorylation.	Ro 31-7549	94-103	kininogen 1	Homo sapiens	117-127
7539258-5	1995	The tyrosine kinase inhibitor genistein and the protein kinase C inhibitors staurosporine and Ro31-7549, all blocked bradykinin-induced tyrosine phosphorylation.	Tyrosine	4-12	kininogen 1	Homo sapiens	117-127
7589163-0	1995	Furosemide inhibits bradykinin-induced contraction of human bronchi: role of thromboxane A2 receptor antagonism.	Furosemide	0-10	kininogen 1	Homo sapiens	20-30
7589163-1	1995	Bradykinin contracts human isolated small bronchi through prostanoid release and subsequent TP receptor stimulation.	Prostaglandins	58-68	kininogen 1	Homo sapiens	0-10
7589163-2	1995	Furosemide 10(-4) to 10(-3) M concentration dependently inhibited bradykinin- and the stable TP receptor agonist U-46619-induced contraction of human isolated small airways.	Furosemide	0-10	kininogen 1	Homo sapiens	66-76
7589163-4	1995	Such an inhibition of TP receptors could a least partly explain the inhibitory effect of furosemide on bradykinin-induced contraction, and could be one of the mechanisms of the protective effect of furosemide in asthma.	Furosemide	89-99	kininogen 1	Homo sapiens	103-113
7589163-4	1995	Such an inhibition of TP receptors could a least partly explain the inhibitory effect of furosemide on bradykinin-induced contraction, and could be one of the mechanisms of the protective effect of furosemide in asthma.	Furosemide	198-208	kininogen 1	Homo sapiens	103-113
7646841-9	1995	Likewise, in the human coronary artery, the hyperpolarization elicited by bradykinin, which is also mediated by EDHF, is augmented in the presence of perindoprilat and prevented by potassium-induced depolarization.	perindoprilat	150-163	kininogen 1	Homo sapiens	74-84
7646841-9	1995	Likewise, in the human coronary artery, the hyperpolarization elicited by bradykinin, which is also mediated by EDHF, is augmented in the presence of perindoprilat and prevented by potassium-induced depolarization.	Potassium	181-190	kininogen 1	Homo sapiens	74-84
7669485-9	1995	This effect of bradykinin was significantly inhibited by indomethacin (3 x 10(-7) M).	Indomethacin	57-69	kininogen 1	Homo sapiens	15-25
7545124-1	1995	We previously demonstrated that the bradykinin-induced contraction of human isolated small bronchi is inhibited by indomethacin, capsaicin (N-methyl-N-6-nonenamide) and ruthenium red but not by tachykinin receptor antagonists.	Indomethacin	115-127	kininogen 1	Homo sapiens	36-46
7545124-1	1995	We previously demonstrated that the bradykinin-induced contraction of human isolated small bronchi is inhibited by indomethacin, capsaicin (N-methyl-N-6-nonenamide) and ruthenium red but not by tachykinin receptor antagonists.	Capsaicin	129-138	kininogen 1	Homo sapiens	36-46
7545124-1	1995	We previously demonstrated that the bradykinin-induced contraction of human isolated small bronchi is inhibited by indomethacin, capsaicin (N-methyl-N-6-nonenamide) and ruthenium red but not by tachykinin receptor antagonists.	n-methyl-n-6-nonenamide	140-163	kininogen 1	Homo sapiens	36-46
7545124-1	1995	We previously demonstrated that the bradykinin-induced contraction of human isolated small bronchi is inhibited by indomethacin, capsaicin (N-methyl-N-6-nonenamide) and ruthenium red but not by tachykinin receptor antagonists.	Ruthenium Red	169-182	kininogen 1	Homo sapiens	36-46
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	vapiprost	30-37	kininogen 1	Homo sapiens	60-70
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	vapiprost	30-37	kininogen 1	Homo sapiens	139-149
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	vapiprost	30-37	kininogen 1	Homo sapiens	139-149
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	Indomethacin	115-127	kininogen 1	Homo sapiens	60-70
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	4-hydroxy-2-octenal	173-176	kininogen 1	Homo sapiens	60-70
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	4-hydroxy-2-octenal	173-176	kininogen 1	Homo sapiens	139-149
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	4-hydroxy-2-octenal	173-176	kininogen 1	Homo sapiens	139-149
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	d-arg0	182-188	kininogen 1	Homo sapiens	60-70
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	d-arg0	182-188	kininogen 1	Homo sapiens	139-149
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	d-arg0	182-188	kininogen 1	Homo sapiens	139-149
7669485-11	1995	Captopril (10(-7) M) significantly potentiated the pressor effect of bradykinin on the human placental circulation (n = 6).	Captopril	0-9	kininogen 1	Homo sapiens	69-79
7669485-17	1995	We suggest that the toxic effects of captopril on the foetus, rather than reflecting an inhibition of angiotensin II formation, may instead be related to a potentiation of the vasoconstrictor effect of bradykinin on the foetal placental circulation, thereby reducing blood flow and causing foetal damage.	Captopril	37-46	kininogen 1	Homo sapiens	202-212
7473001-4	1995	Similar to BK, two phorbol esters, phorbol 12,13 dibutyrate (PDBu) and phorbol 12-myristate-13-acetate (PMA) which are known to stimulate protein kinase C (PKC), synergistically enhanced the TNF alpha induced IL-1 beta production in the gingival fibroblasts.	Phorbol 12,13-Dibutyrate	35-59	kininogen 1	Homo sapiens	11-13
7556274-6	1995	However, in the presence of exogenous Bk, kallidin, or one of the slowly degradable Bk2-receptor agonists D-Arg(Hyp3)-Bk or [Hyp3-Tyr(Me)8]-Bk they elicited potent concentration-dependent relaxations.	D-Arginine	106-111	kininogen 1	Homo sapiens	84-86
7556274-6	1995	However, in the presence of exogenous Bk, kallidin, or one of the slowly degradable Bk2-receptor agonists D-Arg(Hyp3)-Bk or [Hyp3-Tyr(Me)8]-Bk they elicited potent concentration-dependent relaxations.	D-Arginine	106-111	kininogen 1	Homo sapiens	84-86
7473001-4	1995	Similar to BK, two phorbol esters, phorbol 12,13 dibutyrate (PDBu) and phorbol 12-myristate-13-acetate (PMA) which are known to stimulate protein kinase C (PKC), synergistically enhanced the TNF alpha induced IL-1 beta production in the gingival fibroblasts.	Tetradecanoylphorbol Acetate	104-107	kininogen 1	Homo sapiens	11-13
7659783-0	1995	A bradykinin antagonist inhibited nitric oxide generation and thromboxane biosynthesis in acute pancreatitis.	Nitric Oxide	34-46	kininogen 1	Homo sapiens	2-12
7637260-5	1995	Bradykinin, adenosine and angiotensin increased intracellular calcium concentration ([Ca2+]i).	Calcium	62-69	kininogen 1	Homo sapiens	0-10
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	thi-5,d-tic7	194-206	kininogen 1	Homo sapiens	60-70
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	thi-5,d-tic7	194-206	kininogen 1	Homo sapiens	139-149
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	thi-5,d-tic7	194-206	kininogen 1	Homo sapiens	139-149
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	oic8	207-211	kininogen 1	Homo sapiens	60-70
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	oic8	207-211	kininogen 1	Homo sapiens	139-149
7545124-3	1995	With higher concentrations of GR32191 (10(-7) and 10(-6) M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B2 receptor antagonist Hoe 140 (D-Arg0[Hyp3,Thi-5,D-Tic7,Oic8]bradykinin).	oic8	207-211	kininogen 1	Homo sapiens	139-149
7545124-4	1995	The thromboxane A2 synthase inhibitor dazoxiben (4-(-2-(1H-imidazol-1-yl)ethoxy) benzoic acid hydrochloride) 10(-6) M inhibited the bradykinin-induced contraction, suggesting that thromboxane A2 was involved in TP receptor stimulation.	dazoxiben	38-47	kininogen 1	Homo sapiens	132-142
7545124-4	1995	The thromboxane A2 synthase inhibitor dazoxiben (4-(-2-(1H-imidazol-1-yl)ethoxy) benzoic acid hydrochloride) 10(-6) M inhibited the bradykinin-induced contraction, suggesting that thromboxane A2 was involved in TP receptor stimulation.	dazoxiben	49-107	kininogen 1	Homo sapiens	132-142
7545124-4	1995	The thromboxane A2 synthase inhibitor dazoxiben (4-(-2-(1H-imidazol-1-yl)ethoxy) benzoic acid hydrochloride) 10(-6) M inhibited the bradykinin-induced contraction, suggesting that thromboxane A2 was involved in TP receptor stimulation.	Thromboxanes	4-15	kininogen 1	Homo sapiens	132-142
7545124-7	1995	The inhibitory effect of ruthenium red and capsaicin on the bradykinin response may be due to inhibition of thromboxane A2 release or arachidonic mobilisation.	Ruthenium Red	25-38	kininogen 1	Homo sapiens	60-70
7545124-7	1995	The inhibitory effect of ruthenium red and capsaicin on the bradykinin response may be due to inhibition of thromboxane A2 release or arachidonic mobilisation.	Capsaicin	43-52	kininogen 1	Homo sapiens	60-70
7659783-0	1995	A bradykinin antagonist inhibited nitric oxide generation and thromboxane biosynthesis in acute pancreatitis.	Thromboxanes	62-73	kininogen 1	Homo sapiens	2-12
7659783-1	1995	The effect of bradykinin on nitric oxide generation and eicosanoid production in the early stage of an experimental model of acute necrotizing pancreatitis induced by sodium taurocholate has been evaluated.	Nitric Oxide	28-40	kininogen 1	Homo sapiens	14-24
7659783-6	1995	Bradykinin seems to be involved in nitric oxide and thromboxane synthesis during the initial phases of acute necrohemorrhagic pancreatitis.	Nitric Oxide	35-47	kininogen 1	Homo sapiens	0-10
7659783-6	1995	Bradykinin seems to be involved in nitric oxide and thromboxane synthesis during the initial phases of acute necrohemorrhagic pancreatitis.	Thromboxanes	52-63	kininogen 1	Homo sapiens	0-10
7534659-6	1995	Addition of zymosan to human (10%) or porcine (10%) serum for 30 minutes significantly (P &lt; 0.05) increased the EC50 of BK-induced LAD relaxation from 4 +/- 1 to 418 +/- 159 nmol/L (n = 8) and from 9 +/- 3 to 281 +/- 132 nmol/L (n = 7), respectively.	Zymosan	12-19	kininogen 1	Homo sapiens	123-125
7667075-4	1995	Histamine (10 microM) and thrombin (10 U/ml) induced an abrupt and substantial decrease of TEER, bradykinin (1 microM) was less effective, PAF (380 nM) and LTC4 (1 microM) had no effect.	Histamine	0-9	kininogen 1	Homo sapiens	97-107
7650864-3	1995	On the other hand, when the inhibition of PGE2 production by T-614 was examined in the cultured fibroblasts stimulated with bradykinin, T-614 at 1 microgram/ml or less inhibited PGE2 release more effectively than that in the above cell-free system.	Dinoprostone	42-46	kininogen 1	Homo sapiens	124-134
7650864-3	1995	On the other hand, when the inhibition of PGE2 production by T-614 was examined in the cultured fibroblasts stimulated with bradykinin, T-614 at 1 microgram/ml or less inhibited PGE2 release more effectively than that in the above cell-free system.	T 614	61-66	kininogen 1	Homo sapiens	124-134
7741756-3	1995	In contrast, bradykinin (1 microM), 5-hydroxytryptamine (5-HT) (0.1 mM) and carbachol (1 mM) produced only a small (&lt; 1% of the response to 1 mM histamine) effect on [3H]inositol phosphate accumulation in these cells.	Histamine	148-157	kininogen 1	Homo sapiens	13-23
7741756-3	1995	In contrast, bradykinin (1 microM), 5-hydroxytryptamine (5-HT) (0.1 mM) and carbachol (1 mM) produced only a small (&lt; 1% of the response to 1 mM histamine) effect on [3H]inositol phosphate accumulation in these cells.	Tritium	170-172	kininogen 1	Homo sapiens	13-23
7741756-3	1995	In contrast, bradykinin (1 microM), 5-hydroxytryptamine (5-HT) (0.1 mM) and carbachol (1 mM) produced only a small (&lt; 1% of the response to 1 mM histamine) effect on [3H]inositol phosphate accumulation in these cells.	Inositol Phosphates	173-191	kininogen 1	Homo sapiens	13-23
7741756-4	1995	In human umbilical artery smooth muscle cells, histamine (EC50 16 microM), bradykinin (EC50 4.5 nM), 5-HT (EC50 0.7 microM) and carbachol (EC50 21 microM) produced substantial effects (&gt; 20% of the response to 1 mM histamine) on inositol phospholipid hydrolysis while ATP (1 mM) and thrombin (1 U/mL) were much less effective.	Histamine	218-227	kininogen 1	Homo sapiens	75-85
7741756-4	1995	In human umbilical artery smooth muscle cells, histamine (EC50 16 microM), bradykinin (EC50 4.5 nM), 5-HT (EC50 0.7 microM) and carbachol (EC50 21 microM) produced substantial effects (&gt; 20% of the response to 1 mM histamine) on inositol phospholipid hydrolysis while ATP (1 mM) and thrombin (1 U/mL) were much less effective.	Phosphatidylinositols	232-253	kininogen 1	Homo sapiens	75-85
7741756-4	1995	In human umbilical artery smooth muscle cells, histamine (EC50 16 microM), bradykinin (EC50 4.5 nM), 5-HT (EC50 0.7 microM) and carbachol (EC50 21 microM) produced substantial effects (&gt; 20% of the response to 1 mM histamine) on inositol phospholipid hydrolysis while ATP (1 mM) and thrombin (1 U/mL) were much less effective.	Adenosine Triphosphate	271-274	kininogen 1	Homo sapiens	75-85
7702566-3	1995	Therefore, activation of Gs (by cholera-toxin pre-treatment) amplified the bradykinin-stimulated cyclic AMP signal and concurrently attenuated the partial activation of extracellular-signal-regulated kinase-2 (ERK-2) by bradykinin.	Cyclic AMP	97-107	kininogen 1	Homo sapiens	75-85
7597662-8	1995	RESULTS: Phosphoramidon administration caused a transient fall in FEV1 from baseline, FEV1 values decreasing 6.3% and 5.3% on the bradykinin and histamine study days, respectively.	phosphoramidon	9-23	kininogen 1	Homo sapiens	130-140
7597662-9	1995	When compared with placebo, phosphoramidon elicited a small enhancement of the airways response to bradykinin, the geometric mean PC20 value (range) decreasing from 0.281 (0.015-5.575) to 0.136 (0.006-2.061) mg/ml.	phosphoramidon	28-42	kininogen 1	Homo sapiens	99-109
7597662-11	1995	CONCLUSIONS: The small increase in bronchial reactivity to bradykinin after phosphoramidon exposure suggests that endogenous airway NEP may play a modulatory role in the airways response to inflammatory peptides in human asthma.	phosphoramidon	76-90	kininogen 1	Homo sapiens	59-69
7895328-3	1995	Stimulation of endothelial cells with either bradykinin (100 nmol/L), histamine (1 mumol/L), or the Ca(2+)-ATPase inhibitor thapsigargin (30 nmol/L) resulted in a slightly delayed but prolonged tyrosine phosphorylation of two low molecular weight proteins (approximately 42 and approximately 44 kD).	Tyrosine	194-202	kininogen 1	Homo sapiens	45-55
7895328-6	1995	In fura 2-loaded endothelial cells, inhibition of tyrosine kinases attenuated Ca2+ signaling after stimulation with either bradykinin (30 nmol/L) or thapsigargin (30 nmol/L).	Fura-2	3-9	kininogen 1	Homo sapiens	123-133
7535766-4	1995	Bradykinin-induced translocation and activation of PKC alpha, but not translocation of PKC epsilon, was blocked in SF 3271 cells which had been incubated with 1-O-hexadecylglycerol (1-O-HDG; 20 micrograms/ml) for 24 h and then incubated in the absence of 1-O-HDG and serum for a further 24 h. Supplementation with 1-O-HDG increased the mass of ether-linked phospholipid.	chimyl alcohol	159-180	kininogen 1	Homo sapiens	0-10
7535766-4	1995	Bradykinin-induced translocation and activation of PKC alpha, but not translocation of PKC epsilon, was blocked in SF 3271 cells which had been incubated with 1-O-hexadecylglycerol (1-O-HDG; 20 micrograms/ml) for 24 h and then incubated in the absence of 1-O-HDG and serum for a further 24 h. Supplementation with 1-O-HDG increased the mass of ether-linked phospholipid.	chimyl alcohol	182-189	kininogen 1	Homo sapiens	0-10
7535766-4	1995	Bradykinin-induced translocation and activation of PKC alpha, but not translocation of PKC epsilon, was blocked in SF 3271 cells which had been incubated with 1-O-hexadecylglycerol (1-O-HDG; 20 micrograms/ml) for 24 h and then incubated in the absence of 1-O-HDG and serum for a further 24 h. Supplementation with 1-O-HDG increased the mass of ether-linked phospholipid.	chimyl alcohol	255-262	kininogen 1	Homo sapiens	0-10
7535766-4	1995	Bradykinin-induced translocation and activation of PKC alpha, but not translocation of PKC epsilon, was blocked in SF 3271 cells which had been incubated with 1-O-hexadecylglycerol (1-O-HDG; 20 micrograms/ml) for 24 h and then incubated in the absence of 1-O-HDG and serum for a further 24 h. Supplementation with 1-O-HDG increased the mass of ether-linked phospholipid.	chimyl alcohol	255-262	kininogen 1	Homo sapiens	0-10
7535766-4	1995	Bradykinin-induced translocation and activation of PKC alpha, but not translocation of PKC epsilon, was blocked in SF 3271 cells which had been incubated with 1-O-hexadecylglycerol (1-O-HDG; 20 micrograms/ml) for 24 h and then incubated in the absence of 1-O-HDG and serum for a further 24 h. Supplementation with 1-O-HDG increased the mass of ether-linked phospholipid.	ether-linked phospholipid	344-369	kininogen 1	Homo sapiens	0-10
7535766-5	1995	Bradykinin initiated a transient increase in cytosolic Ca2+ concentration in both control and 1-O-HDG supplemented cells, indicating that the initial receptor linked events were not affected by 1-O-HDG supplementation.	1-hexadecyl-2-acetyl-glycero-3-phosphocholine	94-97	kininogen 1	Homo sapiens	0-10
7535766-6	1995	Bradykinin also caused a rapid activation of phospholipase D (PLD), measured by phosphatidylbutanol accumulation, and mitogen-activated protein kinase (MAPK) determined by myelin basic protein phosphorylation of Mono Q fractions.	phosphatidylbutanol	80-99	kininogen 1	Homo sapiens	0-10
7781710-2	1995	Sevoflurane alone did not change resting [Ca2+]i, but diminished bradykinin-induced transient increase in [Ca2+]i in a concentration-dependent manner.	Sevoflurane	0-11	kininogen 1	Homo sapiens	65-75
7781710-3	1995	The inhibitory effect of sevoflurane on bradykinin-induced transient rise in [Ca2+]i was larger than that of a non-selective Ca2+ channel blocker (CO2+).	Sevoflurane	25-36	kininogen 1	Homo sapiens	40-50
7781710-3	1995	The inhibitory effect of sevoflurane on bradykinin-induced transient rise in [Ca2+]i was larger than that of a non-selective Ca2+ channel blocker (CO2+).	Cobalt(2+)	147-151	kininogen 1	Homo sapiens	40-50
7781710-4	1995	Application of sevoflurane following bradykinin-evoked [Ca2+]i transient diminished [Ca2+]i significantly, while bradykinin B2 receptor antagonist (D-Arg-[Hyp3, Thi5,8, D-Phe7] bradykinin) or CO2+ abolished it.	Sevoflurane	15-26	kininogen 1	Homo sapiens	37-47
7781710-4	1995	Application of sevoflurane following bradykinin-evoked [Ca2+]i transient diminished [Ca2+]i significantly, while bradykinin B2 receptor antagonist (D-Arg-[Hyp3, Thi5,8, D-Phe7] bradykinin) or CO2+ abolished it.	D-Arginine	148-153	kininogen 1	Homo sapiens	113-123
7781710-4	1995	Application of sevoflurane following bradykinin-evoked [Ca2+]i transient diminished [Ca2+]i significantly, while bradykinin B2 receptor antagonist (D-Arg-[Hyp3, Thi5,8, D-Phe7] bradykinin) or CO2+ abolished it.	D-Arginine	148-153	kininogen 1	Homo sapiens	113-123
7781710-4	1995	Application of sevoflurane following bradykinin-evoked [Ca2+]i transient diminished [Ca2+]i significantly, while bradykinin B2 receptor antagonist (D-Arg-[Hyp3, Thi5,8, D-Phe7] bradykinin) or CO2+ abolished it.	thi5	161-165	kininogen 1	Homo sapiens	113-123
7781710-4	1995	Application of sevoflurane following bradykinin-evoked [Ca2+]i transient diminished [Ca2+]i significantly, while bradykinin B2 receptor antagonist (D-Arg-[Hyp3, Thi5,8, D-Phe7] bradykinin) or CO2+ abolished it.	thi5	161-165	kininogen 1	Homo sapiens	113-123
7781710-5	1995	Sevoflurane impaired nitrite accumulation stimulated by bradykinin, and reduced the amount of NO released from endothelial cells.	Sevoflurane	0-11	kininogen 1	Homo sapiens	56-66
7534659-9	1995	Addition of soluble CR1 (sCR1, 10 nmol/L) to zymosan-activated HS preserved BK-induced relaxation (EC50) of the LAD rings (control, 4 +/- 1 nmol/L; sCR1 + zymosan+serum, 2 +/- 1 nmol/L; n = 6).	Zymosan	45-52	kininogen 1	Homo sapiens	76-78
7781710-5	1995	Sevoflurane impaired nitrite accumulation stimulated by bradykinin, and reduced the amount of NO released from endothelial cells.	Nitrites	21-28	kininogen 1	Homo sapiens	56-66
7781710-6	1995	Our results indicate that the negative effect of sevoflurane appears to be due to the inhibition of bradykinin-induced Ca2+ efflux from endoplasmic stores and Ca2+ influx through membrane Ca2+ channels.	Sevoflurane	49-60	kininogen 1	Homo sapiens	100-110
7882481-9	1995	A significant correlation was found between the maximal blood flow with acetylcholine and that with bradykinin (r = .89).	Acetylcholine	72-85	kininogen 1	Homo sapiens	100-110
7882481-11	1995	NG-monomethyl-L-arginine significantly blunted the response to bradykinin in control subjects (maximal blood flow decreased from 15.8 +/- 6 to 10.1 +/- 2 mL.min-1.100 mL-1, P &lt; .003).	omega-N-Methylarginine	0-24	kininogen 1	Homo sapiens	63-73
7605251-5	1995	Bradykinin analogues with affinity to the bradykinin B2 receptor, but not those with affinity to the B1 receptor, caused a burst of PGE2 formation.	Dinoprostone	132-136	kininogen 1	Homo sapiens	42-52
7702566-4	1995	We have previously demonstrated that, in order to induce full activation of ERK-2 with bradykinin, it is necessary to obliterate PKC-stimulated cyclic AMP formation.	Cyclic AMP	144-154	kininogen 1	Homo sapiens	87-97
7702566-8	1995	The present study indicates that the bradykinin-stimulated ERK-2 pathway is entirely cyclic AMP-sensitive, and suggests that coincident signal detection by adenylate cyclase may be an important physiological route for the modulation of early mitogenic signalling.	Cyclic AMP	85-95	kininogen 1	Homo sapiens	37-47
7605251-0	1995	Effects of bradykinin and thrombin on prostaglandin formation, cell proliferation and collagen biosynthesis in human dental-pulp fibroblasts.	Prostaglandins	38-51	kininogen 1	Homo sapiens	11-21
7605251-1	1995	Bradykinin and thrombin caused a time- and dose-dependent stimulation of prostanoid biosynthesis in human dental-pulp fibroblasts, as assessed by the release of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha (the stable breakdown product of prostacyclin).	Prostaglandins	73-83	kininogen 1	Homo sapiens	0-10
7605251-1	1995	Bradykinin and thrombin caused a time- and dose-dependent stimulation of prostanoid biosynthesis in human dental-pulp fibroblasts, as assessed by the release of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha (the stable breakdown product of prostacyclin).	Dinoprostone	161-177	kininogen 1	Homo sapiens	0-10
7605251-1	1995	Bradykinin and thrombin caused a time- and dose-dependent stimulation of prostanoid biosynthesis in human dental-pulp fibroblasts, as assessed by the release of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha (the stable breakdown product of prostacyclin).	Dinoprostone	179-183	kininogen 1	Homo sapiens	0-10
7605251-1	1995	Bradykinin and thrombin caused a time- and dose-dependent stimulation of prostanoid biosynthesis in human dental-pulp fibroblasts, as assessed by the release of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha (the stable breakdown product of prostacyclin).	6-Ketoprostaglandin F1 alpha	189-218	kininogen 1	Homo sapiens	0-10
7605251-1	1995	Bradykinin and thrombin caused a time- and dose-dependent stimulation of prostanoid biosynthesis in human dental-pulp fibroblasts, as assessed by the release of prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1 alpha (the stable breakdown product of prostacyclin).	Epoprostenol	252-264	kininogen 1	Homo sapiens	0-10
7605251-2	1995	The stimulatory effect of bradykinin and thrombin on PGE2 biosynthesis was maximal within 5-10 min.	Dinoprostone	53-57	kininogen 1	Homo sapiens	26-36
7605251-6	1995	The stimulatory action of bradykinin and thrombin on PGE2 biosynthesis was abolished by two structurally different cyclo-oxygenase inhibitors and significantly reduced by two corticosteroids.	Dinoprostone	53-57	kininogen 1	Homo sapiens	26-36
7605251-3	1995	The concentration of bradykinin producing half-maximal stimulation (EC50) of PGE2 and prostacyclin formation was 10 nM.	Dinoprostone	77-81	kininogen 1	Homo sapiens	21-31
7605251-11	1995	These data show that human dental-pulp fibroblasts are equipped with receptors for bradykinin and thrombin linked to enhanced prostanoid biosynthesis.	Prostaglandins	126-136	kininogen 1	Homo sapiens	83-93
7605251-3	1995	The concentration of bradykinin producing half-maximal stimulation (EC50) of PGE2 and prostacyclin formation was 10 nM.	Epoprostenol	86-98	kininogen 1	Homo sapiens	21-31
7605251-5	1995	Bradykinin analogues with affinity to the bradykinin B2 receptor, but not those with affinity to the B1 receptor, caused a burst of PGE2 formation.	Dinoprostone	132-136	kininogen 1	Homo sapiens	0-10
7620702-0	1995	Quantitative comparisons of muscarinic and bradykinin receptor-mediated Ins (1,4,5)P3 accumulation and Ca2+ signalling in human neuroblastoma cells.	Inositol 1,4,5-Trisphosphate	72-85	kininogen 1	Homo sapiens	43-53
7727181-8	1995	Converting enzyme inhibitors attenuate the breakdown of bradykinin and therefore enhance prostaglandin E2 synthesis mediated by bradykinin.	Dinoprostone	89-105	kininogen 1	Homo sapiens	56-66
7727181-8	1995	Converting enzyme inhibitors attenuate the breakdown of bradykinin and therefore enhance prostaglandin E2 synthesis mediated by bradykinin.	Dinoprostone	89-105	kininogen 1	Homo sapiens	128-138
17743549-6	1995	Similar agreement was obtained in initial studies that modeled experimental data for arginine-protonated bradykinin.	Arginine	85-93	kininogen 1	Homo sapiens	105-115
7620702-2	1995	Muscarinic and bradykinin receptor-mediated Ins(1,4,5)P3 accumulation, Ca2+ mobilization and Ca2+ entry have been examined in human SH-SY5Y neuroblastoma cells.	Inositol 1,4,5-Trisphosphate	44-56	kininogen 1	Homo sapiens	15-25
7620702-7	1995	Bradykinin also dose-dependently stimulated Ins(1,4,5)P3 accumulation but responses were smaller and not sustained.	Inositol 1,4,5-Trisphosphate	44-56	kininogen 1	Homo sapiens	0-10
7620702-10	1995	Peak Ins(1,4,5)P3 elevation in response to carbachol and bradykinin were lowered by an amount approximating this reduction over the entire dose-response curves.	Inositol 1,4,5-Trisphosphate	5-17	kininogen 1	Homo sapiens	57-67
7620702-27	1995	At this point accumulations were dose-related with a potency similar to that of sustained Ins(1,4,5)P3 accumulation.However, bradykinin produced a minor accumulation of [3H]-InsPs, maximal by 1 min.	Tritium	170-172	kininogen 1	Homo sapiens	125-135
7896012-0	1995	Captopril increases skin microvascular blood flow secondary to bradykinin, nitric oxide, and prostaglandins.	Captopril	0-9	kininogen 1	Homo sapiens	63-73
7775337-5	1995	Phosphoramidon (0.1 and 1 mM; 90 breaths), an NEP inhibitor, induced a dose-dependent increase in lung resistance to bradykinin without further enhancing BHR induced by IL-1 beta.	phosphoramidon	0-14	kininogen 1	Homo sapiens	117-127
7615583-4	1995	Fibrinogen, albumin, IgG, high molecular weight kininogen (HMWK), and lipoproteins ApoA-1 and ApoE were the major proteins adsorbed onto polyarylamide.	polyarylamide	137-150	kininogen 1	Homo sapiens	26-57
7890486-5	1995	However, enalaprilat or benazepril enhanced the relaxation of ciliary arteries to bradykinin (P &lt; 0.02).	Enalaprilat	9-20	kininogen 1	Homo sapiens	82-92
7890486-5	1995	However, enalaprilat or benazepril enhanced the relaxation of ciliary arteries to bradykinin (P &lt; 0.02).	benazepril	24-34	kininogen 1	Homo sapiens	82-92
7890486-6	1995	In the perfused porcine eye, enalaprilat (10(-5) M) augmented vasodilation to bradykinin (P &lt; 0.02).	Enalaprilat	29-40	kininogen 1	Homo sapiens	78-88
7890486-7	1995	The bradykinin antagonist Hoe 140 (3 x 10(-7) M) prevented the relaxation of ciliary arteries to bradykinin (P &lt; 0.001), but not to acetylcholine.	4-hydroxy-2-octenal	26-29	kininogen 1	Homo sapiens	4-14
7890486-7	1995	The bradykinin antagonist Hoe 140 (3 x 10(-7) M) prevented the relaxation of ciliary arteries to bradykinin (P &lt; 0.001), but not to acetylcholine.	4-hydroxy-2-octenal	26-29	kininogen 1	Homo sapiens	97-107
7890486-14	1995	ACE-inhibitors prevents the effects of Ang 1 and augment endothelium-dependent relaxation to bradykinin, which releases nitric oxide through B2 receptors.	Nitric Oxide	120-132	kininogen 1	Homo sapiens	93-103
7615583-4	1995	Fibrinogen, albumin, IgG, high molecular weight kininogen (HMWK), and lipoproteins ApoA-1 and ApoE were the major proteins adsorbed onto polyarylamide.	polyarylamide	137-150	kininogen 1	Homo sapiens	59-63
7772573-6	1995	Pretreatment with phorbol-12-myristate-13-acetate (PMA), a protein kinase C (PKC) activator, significantly resulted in reduction of the descending shoulder of BK-induced increase in [Ca2+]i.	Tetradecanoylphorbol Acetate	51-54	kininogen 1	Homo sapiens	159-161
7896012-2	1995	This study was designed to test whether the ACEI captopril increases skin microvascular blood flow by a bradykinin-dependent mechanism.	Captopril	49-58	kininogen 1	Homo sapiens	104-114
7896012-7	1995	The responses to bradykinin or captopril were abolished by coinjecting a bradykinin antagonist, a specific bradykinin B2 receptor antagonist, or inhibitors of NOS or cyclooxygenase.	Captopril	31-40	kininogen 1	Homo sapiens	73-83
7896012-10	1995	The results indicate that captopril increases skin microvascular blood flow in rabbits and humans secondary to an increase in endogenous tissue bradykinin; this stimulates B2 receptors with subsequent release of prostaglandins and nitric oxide.	Captopril	26-35	kininogen 1	Homo sapiens	144-154
7772573-7	1995	A 20-min pretreatment with PKC inhibitors, H-7 or staurosporine, reversed the decrease by PMA in the shoulder of BK-induced Ca2+ response.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	43-46	kininogen 1	Homo sapiens	113-115
7772573-7	1995	A 20-min pretreatment with PKC inhibitors, H-7 or staurosporine, reversed the decrease by PMA in the shoulder of BK-induced Ca2+ response.	Staurosporine	50-63	kininogen 1	Homo sapiens	113-115
7772573-8	1995	Furthermore, the BK-induced [45Ca] uptake was inhibited by EGTA and PMA.	Egtazic Acid	59-63	kininogen 1	Homo sapiens	17-19
7772573-8	1995	Furthermore, the BK-induced [45Ca] uptake was inhibited by EGTA and PMA.	Tetradecanoylphorbol Acetate	68-71	kininogen 1	Homo sapiens	17-19
7772573-9	1995	Ins(1,4,5)P3 generation induced by BK peaked at 20 s and returned to the basal level at 60 s. There were no significant differences in Ins(1,4,5)P3 levels at 20 and 60 s among the cells exposed to BK alone, BK with PMA pretreatment (20 min) and BK with PMA+H-7 pretreatment.	Inositol 1,4,5-Trisphosphate	0-12	kininogen 1	Homo sapiens	35-37
7700249-1	1995	Measurement of the intracellular Ca2+ concentration ([Ca2+]i) in fura-2-loaded single cells of the human neuroblastoma line SH-SY5Y indicated coexpression of muscarinic and bradykinin receptors linked to activation of phosphoinositidase C (PIC).	Fura-2	65-71	kininogen 1	Homo sapiens	173-183
7861149-0	1995	Mobilization of inositol 1,4,5-trisphosphate-sensitive Ca2+ stores supports bradykinin- and muscarinic-evoked release of [3H] noradrenaline from SH-SY5Y cells.	Inositol 1,4,5-Trisphosphate	16-44	kininogen 1	Homo sapiens	76-86
7861149-0	1995	Mobilization of inositol 1,4,5-trisphosphate-sensitive Ca2+ stores supports bradykinin- and muscarinic-evoked release of [3H] noradrenaline from SH-SY5Y cells.	[3h] noradrenaline	121-139	kininogen 1	Homo sapiens	76-86
7861149-1	1995	The human neuroblastoma cell line SH-SY5Y, maintained at confluence for 14 days, released [3H]-noradrenaline ([3H]NA) when stimulated with either the muscarinic receptor agonist methacholine or bradykinin.	3h]-noradrenaline	91-108	kininogen 1	Homo sapiens	194-204
7861149-4	1995	Methacholine and bradykinin also produced rapid elevations of both inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] and intracellular free [Ca2+] ([Ca2+]i).	Inositol 1,4,5-Trisphosphate	67-95	kininogen 1	Homo sapiens	17-27
7861149-4	1995	Methacholine and bradykinin also produced rapid elevations of both inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] and intracellular free [Ca2+] ([Ca2+]i).	Inositol 1,4,5-Trisphosphate	97-109	kininogen 1	Homo sapiens	17-27
7861149-7	1995	At low [Ca2+]e, thapsigargin abolished elevation of [Ca2+]i in response to methacholine and bradykinin and completely inhibited their stimulation of [3H]NA release.	Thapsigargin	16-28	kininogen 1	Homo sapiens	92-102
7861149-8	1995	It is proposed, therefore, that Ca2+ release from Ins (1,4,5)P3-sensitive stores is a major trigger of methacholine- and bradykinin-evoked [3H]NA release in SH-SY5Y cells.	Inositol 1,4,5-Trisphosphate	50-63	kininogen 1	Homo sapiens	121-131
7861149-8	1995	It is proposed, therefore, that Ca2+ release from Ins (1,4,5)P3-sensitive stores is a major trigger of methacholine- and bradykinin-evoked [3H]NA release in SH-SY5Y cells.	Tritium	140-142	kininogen 1	Homo sapiens	121-131
7700249-4	1995	Maximal (1 mM) carbachol concentrations abolished the elevation of [Ca2+]i produced by bradykinin but the muscarinic antagonist atropine (10 microM) restored the response, provided that extracellular Ca2+ was present throughout the experiment or was added before bradykinin.	Carbachol	15-24	kininogen 1	Homo sapiens	87-97
7700249-4	1995	Maximal (1 mM) carbachol concentrations abolished the elevation of [Ca2+]i produced by bradykinin but the muscarinic antagonist atropine (10 microM) restored the response, provided that extracellular Ca2+ was present throughout the experiment or was added before bradykinin.	Atropine	128-136	kininogen 1	Homo sapiens	263-273
7700249-5	1995	Carbachol also abolished bradykinin-mediated Ins(1,4,5)P3 elevation.	Carbachol	0-9	kininogen 1	Homo sapiens	25-35
7700249-5	1995	Carbachol also abolished bradykinin-mediated Ins(1,4,5)P3 elevation.	Inositol 1,4,5-Trisphosphate	45-57	kininogen 1	Homo sapiens	25-35
7700249-7	1995	In cells maintained at confluence for 2 weeks, the rapid peak elevations of [Ca2+]i and Ins(1,4,5)P3 levels induced by carbachol and bradykinin were approximately equivalent in magnitude.	Inositol 1,4,5-Trisphosphate	88-100	kininogen 1	Homo sapiens	133-143
7700249-8	1995	In these cells carbachol again abolished bradykinin-mediated elevation of [Ca2+]i but only attenuated, rather than abolished, the elevation of Ins(1,4,5)P3 levels.	Carbachol	15-24	kininogen 1	Homo sapiens	41-51
7700249-9	1995	The [Ca2+]i and Ins(1,4,5)P3 responses to bradykinin were fully restored 100 sec after atropine only in the presence of extracellular Ca2+.	Inositol 1,4,5-Trisphosphate	16-28	kininogen 1	Homo sapiens	42-52
7700249-9	1995	The [Ca2+]i and Ins(1,4,5)P3 responses to bradykinin were fully restored 100 sec after atropine only in the presence of extracellular Ca2+.	Atropine	87-95	kininogen 1	Homo sapiens	42-52
7700249-10	1995	Thus, depletion of an intracellular Ins(1,4,5)P3-sensitive Ca2+ store may underlie the ability of carbachol to produce not only heterologous desensitization of the [Ca2+]i elevation induced by bradykinin but also that of the Ins(1,4,5)P3 response.	Inositol 1,4,5-Trisphosphate	36-48	kininogen 1	Homo sapiens	193-203
7700249-10	1995	Thus, depletion of an intracellular Ins(1,4,5)P3-sensitive Ca2+ store may underlie the ability of carbachol to produce not only heterologous desensitization of the [Ca2+]i elevation induced by bradykinin but also that of the Ins(1,4,5)P3 response.	Carbachol	98-107	kininogen 1	Homo sapiens	193-203
7700249-12	1995	Furthermore, studies in which Ins(1,4,5)P3-sensitive stores were depleted with thapsigargin and cells were challenged in the presence or absence of extracellular Ca2+ indicated that Ca2+, irrespective of its origin (intra- or extracellular), potentiated the Ins(1,4,5)P3 response to bradykinin alone.	Inositol 1,4,5-Trisphosphate	30-42	kininogen 1	Homo sapiens	283-293
7836425-0	1995	Effects of bradykinin and endothelin-1 on the calcium homeostasis of mammalian cells.	Calcium	46-53	kininogen 1	Homo sapiens	11-21
7772573-0	1995	Involvement of protein kinase C in bradykinin-induced intracellular calcium increase in primary cultured human keratinocytes.	Calcium	68-75	kininogen 1	Homo sapiens	35-45
7772573-2	1995	We have previously demonstrated that BK induced the generation of inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) which caused Ca2+ mobilization in human keratinocytes.	Inositol 1,4,5-Trisphosphate	66-94	kininogen 1	Homo sapiens	37-39
7772573-2	1995	We have previously demonstrated that BK induced the generation of inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) which caused Ca2+ mobilization in human keratinocytes.	Inositol 1,4,5-Trisphosphate	96-108	kininogen 1	Homo sapiens	37-39
7772573-3	1995	In this study, BK-induced Ca2+ responses were examined in primary cultured human keratinocytes by video imaging fluorescence microscopy using fura-2.	Fura-2	142-148	kininogen 1	Homo sapiens	15-17
7772573-4	1995	Intracellular calcium concentration ([Ca2+]i) level increased to a peak within 30 s after BK addition and decreased gradually to the basal level.	Calcium	14-21	kininogen 1	Homo sapiens	90-92
7772573-6	1995	Pretreatment with phorbol-12-myristate-13-acetate (PMA), a protein kinase C (PKC) activator, significantly resulted in reduction of the descending shoulder of BK-induced increase in [Ca2+]i.	Tetradecanoylphorbol Acetate	18-49	kininogen 1	Homo sapiens	159-161
7836425-4	1995	Bradykinin and endothelin-1 reduced total cell Ca by up to 56% in HF-15 cells, COS-7 cells, and CHO K1 cells transfected with the rat B2 receptor cDNA.	carbonyl sulfide	79-82	kininogen 1	Homo sapiens	0-10
7530714-7	1995	Importantly, pulse-chase experiments in endothelial cells biosynthetically labeled with [3H]palmitate show that bradykinin treatment promotes ecNOS depalmitoylation.	[3h]palmitate	88-101	kininogen 1	Homo sapiens	112-122
7768281-2	1995	A selective and potent antagonist of the bradykinin B2 receptor has recently been discovered (HOE 140: D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin).	D-Arginine	103-108	kininogen 1	Homo sapiens	41-51
7768281-2	1995	A selective and potent antagonist of the bradykinin B2 receptor has recently been discovered (HOE 140: D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin).	D-Arginine	103-108	kininogen 1	Homo sapiens	132-142
7768281-2	1995	A selective and potent antagonist of the bradykinin B2 receptor has recently been discovered (HOE 140: D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin).	thi5	115-119	kininogen 1	Homo sapiens	41-51
7768281-4	1995	Bradykinin induced contractions of the isolated human bronchus and umbilical artery and vein (the umbilical vessels were pretreated with indomethacin and L-nitro-arginine to inhibit prostaglandin and nitric oxide synthesis).	Indomethacin	137-149	kininogen 1	Homo sapiens	0-10
7768281-4	1995	Bradykinin induced contractions of the isolated human bronchus and umbilical artery and vein (the umbilical vessels were pretreated with indomethacin and L-nitro-arginine to inhibit prostaglandin and nitric oxide synthesis).	l-nitro-arginine	154-170	kininogen 1	Homo sapiens	0-10
7768281-4	1995	Bradykinin induced contractions of the isolated human bronchus and umbilical artery and vein (the umbilical vessels were pretreated with indomethacin and L-nitro-arginine to inhibit prostaglandin and nitric oxide synthesis).	Prostaglandins	182-195	kininogen 1	Homo sapiens	0-10
7768281-4	1995	Bradykinin induced contractions of the isolated human bronchus and umbilical artery and vein (the umbilical vessels were pretreated with indomethacin and L-nitro-arginine to inhibit prostaglandin and nitric oxide synthesis).	Nitric Oxide	200-212	kininogen 1	Homo sapiens	0-10
7830070-5	1995	The level of Ins(1,4,5)P3 increased rapidly and transiently in response to BK, peaked at 5 s, but still remained 116-132% above the basal level by 30 s. Although the temporal patterns were similar in both groups, the Ins(1,4,5)P3 concentrations in AD fibroblasts were 73 and 89% above levels in the age-matched controls at 5 and 10 s, respectively.	Inositol 1,4,5-Trisphosphate	13-25	kininogen 1	Homo sapiens	75-77
7830070-8	1995	These results indicate that the elevated Ins(1,4,5)P3 production in response to BK in AD fibroblasts is positively correlated with an increase in the receptor numbers.	Inositol 1,4,5-Trisphosphate	41-53	kininogen 1	Homo sapiens	80-82
7763192-0	1995	Effect of nafamostat mesilate on bradykinin generation and hemodynamics during LDL apheresis.	nafamostat	10-29	kininogen 1	Homo sapiens	33-43
7763192-3	1995	The effects on bradykinin generation were compared between heparin and NM.	Heparin	59-66	kininogen 1	Homo sapiens	15-25
7763192-6	1995	A distinct generation of bradykinin was observed by passing plasma through the DS column, and this led to the rise of bradykinin levels from 12 +/- 5 (mean +/- SE) to 72 +/- 14 pg/ml after treatment of 1,000 ml of plasma.	Dextran Sulfate	79-81	kininogen 1	Homo sapiens	25-35
7763192-6	1995	A distinct generation of bradykinin was observed by passing plasma through the DS column, and this led to the rise of bradykinin levels from 12 +/- 5 (mean +/- SE) to 72 +/- 14 pg/ml after treatment of 1,000 ml of plasma.	Dextran Sulfate	79-81	kininogen 1	Homo sapiens	118-128
7840273-4	1995	Each agent accelerated the time-dependent effects of t-BOOH on Ca2+ signaling in fura 2-loaded cells and potentiated the inhibition of bradykinin-stimulated 45Ca2+ efflux induced by t-BOOH.	t-booh	182-188	kininogen 1	Homo sapiens	135-145
7536247-15	1995	As with the bradykinin-stimulated Ca2+ entry pathway, the 5,6-EET-activated Ca2+ entry pathway was permeable to Mn2+ and Ba2+, sensitive to Ni2+, La3+ and membrane depolarization, and insensitive to the removal of extracellular Na+ or the organic Ca2+ antagonist, nitrendipine.	5,6-epoxy-8,11,14-eicosatrienoic acid	58-65	kininogen 1	Homo sapiens	12-22
7536247-15	1995	As with the bradykinin-stimulated Ca2+ entry pathway, the 5,6-EET-activated Ca2+ entry pathway was permeable to Mn2+ and Ba2+, sensitive to Ni2+, La3+ and membrane depolarization, and insensitive to the removal of extracellular Na+ or the organic Ca2+ antagonist, nitrendipine.	Manganese(2+)	112-116	kininogen 1	Homo sapiens	12-22
7536247-15	1995	As with the bradykinin-stimulated Ca2+ entry pathway, the 5,6-EET-activated Ca2+ entry pathway was permeable to Mn2+ and Ba2+, sensitive to Ni2+, La3+ and membrane depolarization, and insensitive to the removal of extracellular Na+ or the organic Ca2+ antagonist, nitrendipine.	N-methyl-valyl-amiclenomycin	121-125	kininogen 1	Homo sapiens	12-22
7536247-15	1995	As with the bradykinin-stimulated Ca2+ entry pathway, the 5,6-EET-activated Ca2+ entry pathway was permeable to Mn2+ and Ba2+, sensitive to Ni2+, La3+ and membrane depolarization, and insensitive to the removal of extracellular Na+ or the organic Ca2+ antagonist, nitrendipine.	Nickel(2+)	140-144	kininogen 1	Homo sapiens	12-22
7536247-15	1995	As with the bradykinin-stimulated Ca2+ entry pathway, the 5,6-EET-activated Ca2+ entry pathway was permeable to Mn2+ and Ba2+, sensitive to Ni2+, La3+ and membrane depolarization, and insensitive to the removal of extracellular Na+ or the organic Ca2+ antagonist, nitrendipine.	Nitrendipine	264-276	kininogen 1	Homo sapiens	12-22
7639622-9	1995	Furthermore, tracheal relaxation by, e.g., bradykinin or potassium chloride, is mediated by the release of nitric oxide.	Nitric Oxide	107-119	kininogen 1	Homo sapiens	43-53
8697901-4	1995	On the other hand, additive effects were observed in both [Ca2+]i rise and IP3 generation when leu-EK was simultaneously added with bradykinin.	Inositol 1,4,5-Trisphosphate	75-78	kininogen 1	Homo sapiens	132-142
7728221-3	1995	Fibroblasts from two independent families with FAD (OS-1, and OS-2 families) showed a suppressed calcium response after stimulation by 100 nM bradykinin (BK) 100 nM vasopressin (VP) or 10% FCS in Ca(2+)-free condition compared with control fibroblasts at 48 h after plating.	Calcium	97-104	kininogen 1	Homo sapiens	142-152
8582461-2	1995	The present study was undertaken to examine whether the effect of enalapril on plasma bradykinin (BK), substance P and prostaglandin E2 (PGE2), which are likely to be involved in the mechanism of enalapril-induced cough, might also be affected by its time of administration.	Enalapril	66-75	kininogen 1	Homo sapiens	86-96
8582461-2	1995	The present study was undertaken to examine whether the effect of enalapril on plasma bradykinin (BK), substance P and prostaglandin E2 (PGE2), which are likely to be involved in the mechanism of enalapril-induced cough, might also be affected by its time of administration.	Enalapril	66-75	kininogen 1	Homo sapiens	98-100
8582461-2	1995	The present study was undertaken to examine whether the effect of enalapril on plasma bradykinin (BK), substance P and prostaglandin E2 (PGE2), which are likely to be involved in the mechanism of enalapril-induced cough, might also be affected by its time of administration.	Enalapril	196-205	kininogen 1	Homo sapiens	86-96
8582461-2	1995	The present study was undertaken to examine whether the effect of enalapril on plasma bradykinin (BK), substance P and prostaglandin E2 (PGE2), which are likely to be involved in the mechanism of enalapril-induced cough, might also be affected by its time of administration.	Enalapril	196-205	kininogen 1	Homo sapiens	98-100
8582461-6	1995	Blood pressure 24 h after administration of enalapril was reduced at 22:00 h, but not at 10:00 h. Plasma BK tended to increase following enalapril administration at 10:00 h, but not at 22:00 h. Remarkable increases in plasma BK were observed in two patients in the day trial and one of them also complained of cough.	Enalapril	44-53	kininogen 1	Homo sapiens	225-227
8582461-6	1995	Blood pressure 24 h after administration of enalapril was reduced at 22:00 h, but not at 10:00 h. Plasma BK tended to increase following enalapril administration at 10:00 h, but not at 22:00 h. Remarkable increases in plasma BK were observed in two patients in the day trial and one of them also complained of cough.	Enalapril	137-146	kininogen 1	Homo sapiens	105-107
8582461-6	1995	Blood pressure 24 h after administration of enalapril was reduced at 22:00 h, but not at 10:00 h. Plasma BK tended to increase following enalapril administration at 10:00 h, but not at 22:00 h. Remarkable increases in plasma BK were observed in two patients in the day trial and one of them also complained of cough.	Enalapril	137-146	kininogen 1	Homo sapiens	225-227
8582461-9	1995	The results suggest that the response of BK to enalapril is affected by the time of administration.	Enalapril	47-56	kininogen 1	Homo sapiens	41-43
8835619-4	1995	In this study we have evaluated the effect of CyA administered to IDDM patients on blood pressure and serum angiotensin-converting enzyme (SACE), an endopeptidase that is an integral part of the renin-angiotensin and bradykinin systems.	Cyclosporine	46-49	kininogen 1	Homo sapiens	195-227
8619926-0	1995	Localisation of bradykinin-like immunoreactivity and modulation of bradykinin-evoked phospholipase D activity by 17 beta-oestradiol in human endometrium.	Estradiol	113-131	kininogen 1	Homo sapiens	67-77
8619926-6	1995	As phosphatidate, the product of phospholipase D pathway, may mediate cell proliferation, the effect of 17 beta-oestradiol on bradykinin-evoked phospholipase D activity assayed as accumulation of [3H]phosphatidylbutanol ([3H]PtdBut) was examined in [3H]myristic acid-labelled primary cultures of human endometrial stromal cells.	phosphatidate	3-16	kininogen 1	Homo sapiens	126-136
8619926-6	1995	As phosphatidate, the product of phospholipase D pathway, may mediate cell proliferation, the effect of 17 beta-oestradiol on bradykinin-evoked phospholipase D activity assayed as accumulation of [3H]phosphatidylbutanol ([3H]PtdBut) was examined in [3H]myristic acid-labelled primary cultures of human endometrial stromal cells.	Estradiol	104-122	kininogen 1	Homo sapiens	126-136
8619926-6	1995	As phosphatidate, the product of phospholipase D pathway, may mediate cell proliferation, the effect of 17 beta-oestradiol on bradykinin-evoked phospholipase D activity assayed as accumulation of [3H]phosphatidylbutanol ([3H]PtdBut) was examined in [3H]myristic acid-labelled primary cultures of human endometrial stromal cells.	[3h]phosphatidylbutanol	196-219	kininogen 1	Homo sapiens	126-136
8619926-6	1995	As phosphatidate, the product of phospholipase D pathway, may mediate cell proliferation, the effect of 17 beta-oestradiol on bradykinin-evoked phospholipase D activity assayed as accumulation of [3H]phosphatidylbutanol ([3H]PtdBut) was examined in [3H]myristic acid-labelled primary cultures of human endometrial stromal cells.	Tritium	197-199	kininogen 1	Homo sapiens	126-136
8619926-6	1995	As phosphatidate, the product of phospholipase D pathway, may mediate cell proliferation, the effect of 17 beta-oestradiol on bradykinin-evoked phospholipase D activity assayed as accumulation of [3H]phosphatidylbutanol ([3H]PtdBut) was examined in [3H]myristic acid-labelled primary cultures of human endometrial stromal cells.	phosphatidylbutanol	225-231	kininogen 1	Homo sapiens	126-136
8619926-6	1995	As phosphatidate, the product of phospholipase D pathway, may mediate cell proliferation, the effect of 17 beta-oestradiol on bradykinin-evoked phospholipase D activity assayed as accumulation of [3H]phosphatidylbutanol ([3H]PtdBut) was examined in [3H]myristic acid-labelled primary cultures of human endometrial stromal cells.	Tritium	222-224	kininogen 1	Homo sapiens	126-136
8619926-6	1995	As phosphatidate, the product of phospholipase D pathway, may mediate cell proliferation, the effect of 17 beta-oestradiol on bradykinin-evoked phospholipase D activity assayed as accumulation of [3H]phosphatidylbutanol ([3H]PtdBut) was examined in [3H]myristic acid-labelled primary cultures of human endometrial stromal cells.	Myristic Acid	253-266	kininogen 1	Homo sapiens	126-136
8619926-7	1995	Bradykinin induced a rapid accumulation of [3H]PtdBut in a time-dependent manner, indicating phospholipase D activation.	Tritium	44-46	kininogen 1	Homo sapiens	0-10
8619926-7	1995	Bradykinin induced a rapid accumulation of [3H]PtdBut in a time-dependent manner, indicating phospholipase D activation.	phosphatidylbutanol	47-53	kininogen 1	Homo sapiens	0-10
8619926-8	1995	Pretreatment of stromal cells with 17 beta-oestradiol enhanced the bradykinin-evoked phospholipase D activity.	Estradiol	35-53	kininogen 1	Homo sapiens	67-77
8619926-9	1995	These results suggest that bradykinin-like immunoreactivity is strongly associated with proliferative stromal cells undergoing mitosis, a process that may be mediated by phospholipase D activation as the magnitude of this enzyme"s activation in vitro appears to be regulated by 17 beta-oestradiol.	Estradiol	278-296	kininogen 1	Homo sapiens	27-37
8835628-0	1995	Degradation of bradykinin in human urine by carboxypeptidase Y-like exopeptidase and neutral endopeptidase and their inhibition by ebelactone B and phosphoramidon.	ebelactone B	131-143	kininogen 1	Homo sapiens	15-25
8835628-0	1995	Degradation of bradykinin in human urine by carboxypeptidase Y-like exopeptidase and neutral endopeptidase and their inhibition by ebelactone B and phosphoramidon.	phosphoramidon	148-162	kininogen 1	Homo sapiens	15-25
7529307-1	1995	NG-nitro-L-arginine methyl ester (L-NAME) has been reported to have variable effects on the vasodilator response to acetylcholine (ACh) and bradykinin (BK) in vivo.	NG-Nitroarginine Methyl Ester	0-32	kininogen 1	Homo sapiens	140-150
8835628-3	1995	The combination of phosphoramidon and ebelactone B completely (by 95%) inhibited bradykinin degradation in human urine.	phosphoramidon	19-33	kininogen 1	Homo sapiens	81-91
8835628-3	1995	The combination of phosphoramidon and ebelactone B completely (by 95%) inhibited bradykinin degradation in human urine.	ebelactone B	38-50	kininogen 1	Homo sapiens	81-91
7529307-0	1995	Differential effects of L-NAME on blood pressure and heart rate responses to acetylcholine and bradykinin in cynomolgus primates.	NG-Nitroarginine Methyl Ester	24-30	kininogen 1	Homo sapiens	95-105
7529307-1	1995	NG-nitro-L-arginine methyl ester (L-NAME) has been reported to have variable effects on the vasodilator response to acetylcholine (ACh) and bradykinin (BK) in vivo.	NG-Nitroarginine Methyl Ester	0-32	kininogen 1	Homo sapiens	152-154
7529307-1	1995	NG-nitro-L-arginine methyl ester (L-NAME) has been reported to have variable effects on the vasodilator response to acetylcholine (ACh) and bradykinin (BK) in vivo.	NG-Nitroarginine Methyl Ester	34-40	kininogen 1	Homo sapiens	140-150
7529307-1	1995	NG-nitro-L-arginine methyl ester (L-NAME) has been reported to have variable effects on the vasodilator response to acetylcholine (ACh) and bradykinin (BK) in vivo.	NG-Nitroarginine Methyl Ester	34-40	kininogen 1	Homo sapiens	152-154
7529307-11	1995	In pentobarbital-anesthetized monkeys, ACh-induced hypotensive responses were inhibited by 75% to 94% in the presence of L-NAME; BK (0.3-1 microgram/kg i.v.)	Acetylcholine	39-42	kininogen 1	Homo sapiens	129-131
7529307-11	1995	In pentobarbital-anesthetized monkeys, ACh-induced hypotensive responses were inhibited by 75% to 94% in the presence of L-NAME; BK (0.3-1 microgram/kg i.v.)	NG-Nitroarginine Methyl Ester	121-127	kininogen 1	Homo sapiens	129-131
8531498-8	1995	Results suggest that bradykinin stimulates PTSMC to produce PGE2 via the signal transduction system including Ca2+, and dexamethasone appeared to suppress PGE2 production by reducing the activity of cytosolic phospholipase A2 (cPLA2) and PGE2 synthase.	ptsmc	43-48	kininogen 1	Homo sapiens	21-31
8531498-3	1995	Bradykinin induced a dose-dependent increase in both the rise in [Ca2+]i and PGE2 production by PTSMC.	Dinoprostone	77-81	kininogen 1	Homo sapiens	0-10
8531498-8	1995	Results suggest that bradykinin stimulates PTSMC to produce PGE2 via the signal transduction system including Ca2+, and dexamethasone appeared to suppress PGE2 production by reducing the activity of cytosolic phospholipase A2 (cPLA2) and PGE2 synthase.	Dinoprostone	60-64	kininogen 1	Homo sapiens	21-31
8531498-3	1995	Bradykinin induced a dose-dependent increase in both the rise in [Ca2+]i and PGE2 production by PTSMC.	ptsmc	96-101	kininogen 1	Homo sapiens	0-10
8559491-1	1995	BACKGROUND: Anaphylactoid reactions occurring in uraemic patients haemodialysed with polyacrylonitrile haemodialysis (HD) membranes and being treated with ACE inhibitors have been attributed to an excessive generation of bradykinin.	polyacrylonitrile	85-102	kininogen 1	Homo sapiens	221-231
8531498-6	1995	Incubation of PTSMC with 10(-6)M dexamethasone for 24 h significantly suppressed both the rise in [Ca2+]i and PGE2 production by PTSMC in response to bradykinin, and also significantly suppressed bradykinin-stimulated release of radioactivity from PTSMC prelabeled with 3H-labeled arachidonic acid (3H-AA).	ptsmc	14-19	kininogen 1	Homo sapiens	150-160
8531498-6	1995	Incubation of PTSMC with 10(-6)M dexamethasone for 24 h significantly suppressed both the rise in [Ca2+]i and PGE2 production by PTSMC in response to bradykinin, and also significantly suppressed bradykinin-stimulated release of radioactivity from PTSMC prelabeled with 3H-labeled arachidonic acid (3H-AA).	ptsmc	14-19	kininogen 1	Homo sapiens	196-206
8531498-6	1995	Incubation of PTSMC with 10(-6)M dexamethasone for 24 h significantly suppressed both the rise in [Ca2+]i and PGE2 production by PTSMC in response to bradykinin, and also significantly suppressed bradykinin-stimulated release of radioactivity from PTSMC prelabeled with 3H-labeled arachidonic acid (3H-AA).	Dexamethasone	33-46	kininogen 1	Homo sapiens	150-160
8531498-6	1995	Incubation of PTSMC with 10(-6)M dexamethasone for 24 h significantly suppressed both the rise in [Ca2+]i and PGE2 production by PTSMC in response to bradykinin, and also significantly suppressed bradykinin-stimulated release of radioactivity from PTSMC prelabeled with 3H-labeled arachidonic acid (3H-AA).	Dexamethasone	33-46	kininogen 1	Homo sapiens	196-206
8531498-6	1995	Incubation of PTSMC with 10(-6)M dexamethasone for 24 h significantly suppressed both the rise in [Ca2+]i and PGE2 production by PTSMC in response to bradykinin, and also significantly suppressed bradykinin-stimulated release of radioactivity from PTSMC prelabeled with 3H-labeled arachidonic acid (3H-AA).	ptsmc	129-134	kininogen 1	Homo sapiens	150-160
8531498-6	1995	Incubation of PTSMC with 10(-6)M dexamethasone for 24 h significantly suppressed both the rise in [Ca2+]i and PGE2 production by PTSMC in response to bradykinin, and also significantly suppressed bradykinin-stimulated release of radioactivity from PTSMC prelabeled with 3H-labeled arachidonic acid (3H-AA).	ptsmc	129-134	kininogen 1	Homo sapiens	150-160
8559491-2	1995	METHODS: Here we tested in a prospective trial a new type of polyacrylonitrile membrane (SPAN) with respect to bradykinin generation in nine HD patients receiving either captopril or enalapril.	polyacrylonitrile	61-78	kininogen 1	Homo sapiens	111-121
7651903-3	1995	The primary structure of bowfin bradykinin was established as Ala-Pro-Pro-Gly-Trp-Ser-Pro-Phe-Arg.	Bradykinin[bowfin]	62-97	kininogen 1	Homo sapiens	32-42
7651903-4	1995	This amino acid sequence contains one amino acid substitution (Phe5 --&gt; Trp) compared with mammalian bradykinin.	Tryptophan	75-78	kininogen 1	Homo sapiens	104-114
8545250-1	1995	Endothelial neutral endopeptidase (EC 3.4.24.11, NEP) contributes to the inactivation of vasoactive and inflammatory peptides such as f-Met-Leu-Phe, substance P, atrial natriuretic peptide, and bradykinin.	N-Formylmethionine Leucyl-Phenylalanine	134-147	kininogen 1	Homo sapiens	194-204
7989355-6	1994	Human umbilical vein endothelial cells (HUVEC) in culture at 37 degrees C express 2-3-fold more binding sites for biotinylated high molecular weight kininogen (biotin-HK) containing BK than for biotin-HK from which BK has been liberated by plasma kallikrein.	Biotin	114-120	kininogen 1	Homo sapiens	127-158
7989355-6	1994	Human umbilical vein endothelial cells (HUVEC) in culture at 37 degrees C express 2-3-fold more binding sites for biotinylated high molecular weight kininogen (biotin-HK) containing BK than for biotin-HK from which BK has been liberated by plasma kallikrein.	Biotin	160-166	kininogen 1	Homo sapiens	127-158
7989355-6	1994	Human umbilical vein endothelial cells (HUVEC) in culture at 37 degrees C express 2-3-fold more binding sites for biotinylated high molecular weight kininogen (biotin-HK) containing BK than for biotin-HK from which BK has been liberated by plasma kallikrein.	Biotin	160-166	kininogen 1	Homo sapiens	182-184
7989355-7	1994	Binding of BK-free biotin-HK was not restored by preincubating HUVEC with BK, arguing against the possibility that BK released from biotin-HK stimulated expression of additional HK receptors.	Biotin	19-25	kininogen 1	Homo sapiens	11-13
7989355-8	1994	The extent of biotin-HK binding to HUVEC at 37 degrees C directly correlated with the amount of BK retained within the protein.	Biotin	14-20	kininogen 1	Homo sapiens	96-98
7989355-10	1994	First, monoclonal antibodies to the carboxyl terminus of BK (MBK3) and the common light chains of the kininogens (HKL6, HKL8) inhibited biotin-HK binding to HUVEC.	Biotin	136-142	kininogen 1	Homo sapiens	57-59
7989355-11	1994	Second, a synthetic, dimeric bradykinin receptor antagonist blocked biotin-HK (IC50 = 9 microM) binding to HUVEC as did two synthetic tissue kallikrein inhibitors modeled after the carboxyl-terminal sequence of BK.	Biotin	68-74	kininogen 1	Homo sapiens	29-39
7989355-12	1994	Third, synthetic peptides containing the carboxyl-terminal portion of BK and the amino terminus of kininogens" common light chain, MKRPPGFSPFRSSRIG and GFSPFRSSRIG, blocked binding of biotin-HK (IC50 = 2-3 mM), whereas an overlapping peptide, SPFRSSRIGEIKEETT, at 5 mM and a scrambled peptide, FSGPKRSPIMGRPSFR, did not.	Peptides	17-25	kininogen 1	Homo sapiens	70-72
7989355-12	1994	Third, synthetic peptides containing the carboxyl-terminal portion of BK and the amino terminus of kininogens" common light chain, MKRPPGFSPFRSSRIG and GFSPFRSSRIG, blocked binding of biotin-HK (IC50 = 2-3 mM), whereas an overlapping peptide, SPFRSSRIGEIKEETT, at 5 mM and a scrambled peptide, FSGPKRSPIMGRPSFR, did not.	Biotin	184-190	kininogen 1	Homo sapiens	70-72
7786135-2	1994	Its synthesis from L-arginine is assured by NO-synthase, the activity of which is dependent on intracellular calcium concentrations, which are themselves modulated by pharmacological (acetylcholine, serotonin, bradykinin...) or physical factors (shearing forces exerted by blood flow).	Arginine	19-29	kininogen 1	Homo sapiens	210-220
7998998-1	1994	Bradykinin activates adenylate cyclase via a pathway that involves the "up-stream" regulation of phospholipase D (PLD)-catalysed hydrolysis of phosphatidylcholine and activation of protein kinase C (PKC) in airway smooth muscle [Stevens, Pyne, Grady and Pyne (1994) Biochem.	Phosphatidylcholines	143-162	kininogen 1	Homo sapiens	0-10
7998998-10	1994	Deoxyadenosine (0.1 mM), a P-site inhibitor of adenylate cyclase, blocked bradykinin-stimulated cyclic AMP formation and converted the activation of ERK-2 into a sustained response.	2'-deoxyadenosine	0-14	kininogen 1	Homo sapiens	74-84
7998998-10	1994	Deoxyadenosine (0.1 mM), a P-site inhibitor of adenylate cyclase, blocked bradykinin-stimulated cyclic AMP formation and converted the activation of ERK-2 into a sustained response.	Cyclic AMP	96-106	kininogen 1	Homo sapiens	74-84
7998998-11	1994	Thus the PKC-stimulated cyclic AMP response can limit the activation of ERK-2 in response to bradykinin.	Cyclic AMP	24-34	kininogen 1	Homo sapiens	93-103
7889260-7	1994	Substance P, histamine, bradykinin and the Ca2+ ionophores ionomycin and A23187 all caused concentration- and endothelium-dependent relaxation in vessels pre-contracted with the thromboxane A2-mimetic, U46619 (3 nM) to an active force optimal for relaxation responses.	Thromboxanes	178-189	kininogen 1	Homo sapiens	24-34
7889260-16	1994	L-NMMA, but not L-NOARG,caused small but significant decreases in the maximum responses to substance P, bradykinin (18.5 +/- 6.9% and 27.6 +/- 10.9% relaxation with L-NMMA and L-NOARG, respectively), histamine and A23187 (P&lt;0.05).	omega-N-Methylarginine	0-6	kininogen 1	Homo sapiens	104-114
7889260-16	1994	L-NMMA, but not L-NOARG,caused small but significant decreases in the maximum responses to substance P, bradykinin (18.5 +/- 6.9% and 27.6 +/- 10.9% relaxation with L-NMMA and L-NOARG, respectively), histamine and A23187 (P&lt;0.05).	omega-N-Methylarginine	165-171	kininogen 1	Homo sapiens	104-114
7786135-2	1994	Its synthesis from L-arginine is assured by NO-synthase, the activity of which is dependent on intracellular calcium concentrations, which are themselves modulated by pharmacological (acetylcholine, serotonin, bradykinin...) or physical factors (shearing forces exerted by blood flow).	Calcium	109-116	kininogen 1	Homo sapiens	210-220
7697491-2	1994	In order to study these phenomena in a large cell population, calcium flux was measured in MRC-5 cell line expressing the B2 receptor for bradykinin using an ACAS 570 scanning cytometer.	Calcium	62-69	kininogen 1	Homo sapiens	138-148
7697491-7	1994	The intensity of the calcium peak after binding of bradykinin is independent of the concentration of extracellular calcium.	Calcium	21-28	kininogen 1	Homo sapiens	51-61
7955144-0	1994	des-Arg9-bradykinin produces tone-dependent kinin B1 receptor-mediated responses in the pulmonary vascular bed.	des-arg9	0-8	kininogen 1	Homo sapiens	9-19
7889285-2	1994	Experiments were designed to analyse the requirement of myoendothelial junctions by bradykinin-induced endothelium-dependent relaxations resistant to NG-nitro-L-arginine (L-NOARG) and indomethacin porcine coronary arteries.	Nitroarginine	150-169	kininogen 1	Homo sapiens	84-94
7889285-2	1994	Experiments were designed to analyse the requirement of myoendothelial junctions by bradykinin-induced endothelium-dependent relaxations resistant to NG-nitro-L-arginine (L-NOARG) and indomethacin porcine coronary arteries.	Nitroarginine	171-178	kininogen 1	Homo sapiens	84-94
7889285-2	1994	Experiments were designed to analyse the requirement of myoendothelial junctions by bradykinin-induced endothelium-dependent relaxations resistant to NG-nitro-L-arginine (L-NOARG) and indomethacin porcine coronary arteries.	Indomethacin	184-196	kininogen 1	Homo sapiens	84-94
7889285-9	1994	In the presence of endothelium, bradykinin induced concentration-dependent relaxations with a mean EC50 of 3.2 nM and a maximum response of 95 +/- 1% of papaverine-induced relaxation (control curve).	Papaverine	153-163	kininogen 1	Homo sapiens	32-42
7889285-15	1994	Bradykinin-induced relaxations in endothelium-preserved rings were only slightly suppressed by L-NOARG (86% of control).	Nitroarginine	95-102	kininogen 1	Homo sapiens	0-10
7889285-17	1994	In the presence of L-NOARG, bradykinin failed to relax partially depolarized vessels.	Nitroarginine	19-26	kininogen 1	Homo sapiens	28-38
7889285-19	1994	In the presence of 2 mM -heptanol, 180 mM mannitol or 180 mM sucrose maximum relaxation to bradykinin was reduced to ~70%, i.e. to the same extent as in the presence of high [K+].	Heptanol	24-33	kininogen 1	Homo sapiens	91-101
7889285-19	1994	In the presence of 2 mM -heptanol, 180 mM mannitol or 180 mM sucrose maximum relaxation to bradykinin was reduced to ~70%, i.e. to the same extent as in the presence of high [K+].	Mannitol	42-50	kininogen 1	Homo sapiens	91-101
7889285-19	1994	In the presence of 2 mM -heptanol, 180 mM mannitol or 180 mM sucrose maximum relaxation to bradykinin was reduced to ~70%, i.e. to the same extent as in the presence of high [K+].	Sucrose	61-68	kininogen 1	Homo sapiens	91-101
7955144-3	1994	Vasoconstrictor responses to des-Arg9-bradykinin under low-tone conditions and vasodilator responses under elevated-tone conditions were antagonized by des-Arg9,[Leu8]-bradykinin, a kinin B1 receptor antagonist, whereas responses under low- and high-tone conditions were not altered by Hoe 140, a kinin B2 receptor antagonist.	des-arg9	29-37	kininogen 1	Homo sapiens	38-48
7955144-3	1994	Vasoconstrictor responses to des-Arg9-bradykinin under low-tone conditions and vasodilator responses under elevated-tone conditions were antagonized by des-Arg9,[Leu8]-bradykinin, a kinin B1 receptor antagonist, whereas responses under low- and high-tone conditions were not altered by Hoe 140, a kinin B2 receptor antagonist.	des-arg9	29-37	kininogen 1	Homo sapiens	168-178
7955144-3	1994	Vasoconstrictor responses to des-Arg9-bradykinin under low-tone conditions and vasodilator responses under elevated-tone conditions were antagonized by des-Arg9,[Leu8]-bradykinin, a kinin B1 receptor antagonist, whereas responses under low- and high-tone conditions were not altered by Hoe 140, a kinin B2 receptor antagonist.	4-hydroxy-2-octenal	286-289	kininogen 1	Homo sapiens	38-48
7955144-3	1994	Vasoconstrictor responses to des-Arg9-bradykinin under low-tone conditions and vasodilator responses under elevated-tone conditions were antagonized by des-Arg9,[Leu8]-bradykinin, a kinin B1 receptor antagonist, whereas responses under low- and high-tone conditions were not altered by Hoe 140, a kinin B2 receptor antagonist.	4-hydroxy-2-octenal	286-289	kininogen 1	Homo sapiens	168-178
7994806-16	1994	Cleavage of HK, larger after SK than after rTPA infusion, represents a condition enhancing the generation of bradykinin by kallikrein.	rtpa	43-47	kininogen 1	Homo sapiens	109-119
7955144-4	1994	Vasoconstrictor responses to des-Arg9-bradykinin under low-tone conditions were attenuated by phentolamine, prazosin, and reserpine but not by sodium meclofenamate, suggesting that release of catecholamines and activation of alpha-adrenergic receptors are involved.	Phentolamine	94-106	kininogen 1	Homo sapiens	38-48
7955144-4	1994	Vasoconstrictor responses to des-Arg9-bradykinin under low-tone conditions were attenuated by phentolamine, prazosin, and reserpine but not by sodium meclofenamate, suggesting that release of catecholamines and activation of alpha-adrenergic receptors are involved.	Prazosin	108-116	kininogen 1	Homo sapiens	38-48
7955144-4	1994	Vasoconstrictor responses to des-Arg9-bradykinin under low-tone conditions were attenuated by phentolamine, prazosin, and reserpine but not by sodium meclofenamate, suggesting that release of catecholamines and activation of alpha-adrenergic receptors are involved.	Reserpine	122-131	kininogen 1	Homo sapiens	38-48
7955144-4	1994	Vasoconstrictor responses to des-Arg9-bradykinin under low-tone conditions were attenuated by phentolamine, prazosin, and reserpine but not by sodium meclofenamate, suggesting that release of catecholamines and activation of alpha-adrenergic receptors are involved.	Catecholamines	192-206	kininogen 1	Homo sapiens	38-48
7955144-5	1994	Pulmonary vasodilator responses under elevated-tone conditions were inhibited by N omega-nitro-L-arginine methyl ester, suggesting that des-Arg9-bradykinin stimulates the release of nitric oxide, whereas meclofenamate and U-37883A, a nonsulfonylurea ATP-sensitive K+ channel antagonist, did not alter vasodilator responses to the B1 receptor agonist.	NG-Nitroarginine Methyl Ester	81-118	kininogen 1	Homo sapiens	145-155
7955144-5	1994	Pulmonary vasodilator responses under elevated-tone conditions were inhibited by N omega-nitro-L-arginine methyl ester, suggesting that des-Arg9-bradykinin stimulates the release of nitric oxide, whereas meclofenamate and U-37883A, a nonsulfonylurea ATP-sensitive K+ channel antagonist, did not alter vasodilator responses to the B1 receptor agonist.	Nitric Oxide	182-194	kininogen 1	Homo sapiens	145-155
7955144-5	1994	Pulmonary vasodilator responses under elevated-tone conditions were inhibited by N omega-nitro-L-arginine methyl ester, suggesting that des-Arg9-bradykinin stimulates the release of nitric oxide, whereas meclofenamate and U-37883A, a nonsulfonylurea ATP-sensitive K+ channel antagonist, did not alter vasodilator responses to the B1 receptor agonist.	Meclofenamic Acid	204-217	kininogen 1	Homo sapiens	145-155
7955144-5	1994	Pulmonary vasodilator responses under elevated-tone conditions were inhibited by N omega-nitro-L-arginine methyl ester, suggesting that des-Arg9-bradykinin stimulates the release of nitric oxide, whereas meclofenamate and U-37883A, a nonsulfonylurea ATP-sensitive K+ channel antagonist, did not alter vasodilator responses to the B1 receptor agonist.	U 37883A	222-230	kininogen 1	Homo sapiens	145-155
7955144-6	1994	These results suggest that vasoconstrictor responses to des-Arg9-bradykinin under low-tone conditions are mediated by the activation of kinin B1 receptors, the release of catecholamines within the lung, and the activation of alpha-adrenergic receptors, whereas vasodilator responses under elevated tone conditions are mediated by activation of B1 receptors and the release of nitric oxide from the endothelium.	Catecholamines	171-185	kininogen 1	Homo sapiens	65-75
7955144-6	1994	These results suggest that vasoconstrictor responses to des-Arg9-bradykinin under low-tone conditions are mediated by the activation of kinin B1 receptors, the release of catecholamines within the lung, and the activation of alpha-adrenergic receptors, whereas vasodilator responses under elevated tone conditions are mediated by activation of B1 receptors and the release of nitric oxide from the endothelium.	Nitric Oxide	376-388	kininogen 1	Homo sapiens	65-75
7874846-8	1994	Ethanol and subsequent petroleum ether extraction of 5-40 fmol of bradykinin added to plasma yielded recoveries of 39 +/- 16% (mean +/- SD); normal kinin levels in human plasma were 18.6 +/- 3.3 pmol/l (mean +/- SEM).	naphtha	23-38	kininogen 1	Homo sapiens	66-76
7882021-0	1994	Bradykinin excites tetrodotoxin-resistant primary afferent fibers.	Tetrodotoxin	19-31	kininogen 1	Homo sapiens	0-10
7882021-6	1994	The depolarizing effect of bradykinin on the dorsal root ganglion neurons and its synaptic excitatory effect on dorsal horn neurons was abolished by pretreatment of the same segment of sensory neurons by a B2 bradykinin receptor antagonist (D-Arg0,Hyp3,beta-Thi5,8,D-Phe7)-bradykinin (5 microM).	d-arg0	241-247	kininogen 1	Homo sapiens	27-37
7882021-6	1994	The depolarizing effect of bradykinin on the dorsal root ganglion neurons and its synaptic excitatory effect on dorsal horn neurons was abolished by pretreatment of the same segment of sensory neurons by a B2 bradykinin receptor antagonist (D-Arg0,Hyp3,beta-Thi5,8,D-Phe7)-bradykinin (5 microM).	d-arg0	241-247	kininogen 1	Homo sapiens	209-219
7882021-6	1994	The depolarizing effect of bradykinin on the dorsal root ganglion neurons and its synaptic excitatory effect on dorsal horn neurons was abolished by pretreatment of the same segment of sensory neurons by a B2 bradykinin receptor antagonist (D-Arg0,Hyp3,beta-Thi5,8,D-Phe7)-bradykinin (5 microM).	beta-thi5	253-262	kininogen 1	Homo sapiens	27-37
7882021-6	1994	The depolarizing effect of bradykinin on the dorsal root ganglion neurons and its synaptic excitatory effect on dorsal horn neurons was abolished by pretreatment of the same segment of sensory neurons by a B2 bradykinin receptor antagonist (D-Arg0,Hyp3,beta-Thi5,8,D-Phe7)-bradykinin (5 microM).	-phe7	266-271	kininogen 1	Homo sapiens	27-37
7882021-9	1994	Replacement of sodium ions with TRIS completely abolished the stimulatory effect of bradykinin on the sensory neurons.	Sodium	15-21	kininogen 1	Homo sapiens	84-94
7882021-9	1994	Replacement of sodium ions with TRIS completely abolished the stimulatory effect of bradykinin on the sensory neurons.	Tromethamine	32-36	kininogen 1	Homo sapiens	84-94
7882021-10	1994	Bradykinin potentiated the postsynaptic potentials induced by electrical stimulation of TTX-resistant afferent fibers.	Tetrodotoxin	88-91	kininogen 1	Homo sapiens	0-10
7523301-4	1994	The enzyme hydrolyzed (optimum pH 6.5) the Pro-pNA bond in carbobenzoxy-Gly-Pro-p-nitroanilide (Z-Gly-Pro-pNA) and bonds at the carboxyl side of proline in several human bioactive peptides, such as bradykinin, substance P, neurotensin, angiotensins, oxytocin, vasopressin, and human endothelin fragment 22-38.	carbobenzoxy-gly-pro-p-nitroanilide	59-94	kininogen 1	Homo sapiens	198-208
7523301-4	1994	The enzyme hydrolyzed (optimum pH 6.5) the Pro-pNA bond in carbobenzoxy-Gly-Pro-p-nitroanilide (Z-Gly-Pro-pNA) and bonds at the carboxyl side of proline in several human bioactive peptides, such as bradykinin, substance P, neurotensin, angiotensins, oxytocin, vasopressin, and human endothelin fragment 22-38.	Z-Gly-Pro-PNA	96-109	kininogen 1	Homo sapiens	198-208
7523301-4	1994	The enzyme hydrolyzed (optimum pH 6.5) the Pro-pNA bond in carbobenzoxy-Gly-Pro-p-nitroanilide (Z-Gly-Pro-pNA) and bonds at the carboxyl side of proline in several human bioactive peptides, such as bradykinin, substance P, neurotensin, angiotensins, oxytocin, vasopressin, and human endothelin fragment 22-38.	Proline	145-152	kininogen 1	Homo sapiens	198-208
7523301-8	1994	The hydrolysis of Z-Gly-Pro-pNA was potently inhibited by the following, with the Ki(app) (in micromolar) in parentheses: insulin B-chain (0.7), human endothelin-1 (0.5), neuropeptide Y (1.7), substance P (32.0), T-kinin (4.0), neurotensin (5.0), and bradykinin (16.0).	Z-Gly-Pro-PNA	18-31	kininogen 1	Homo sapiens	251-261
7946358-0	1994	The G protein G13 mediates inhibition of voltage-dependent calcium current by bradykinin.	Calcium	59-66	kininogen 1	Homo sapiens	78-88
7946358-1	1994	In neuroblastoma-glioma hybrid cells, bradykinin has dual modulatory effects on ion channels: it activates a K+ current as well as inhibits the voltage-dependent Ca2+ current (ICa,V).	isocyanic acid	176-179	kininogen 1	Homo sapiens	38-48
7946358-4	1994	Here, we show that the inhibition of ICa,V by bradykinin is suppressed selectively by intracellular application of antibodies specific for G13.	isocyanic acid	37-40	kininogen 1	Homo sapiens	46-56
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	Indomethacin	75-87	kininogen 1	Homo sapiens	37-47
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	Indomethacin	75-87	kininogen 1	Homo sapiens	49-51
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	Indomethacin	75-87	kininogen 1	Homo sapiens	308-310
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	Indomethacin	89-93	kininogen 1	Homo sapiens	37-47
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	Indomethacin	89-93	kininogen 1	Homo sapiens	49-51
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	Indomethacin	89-93	kininogen 1	Homo sapiens	308-310
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	Nitric Oxide	170-182	kininogen 1	Homo sapiens	37-47
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	Nitric Oxide	170-182	kininogen 1	Homo sapiens	49-51
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	Nitric Oxide	170-182	kininogen 1	Homo sapiens	308-310
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	NG-Nitroarginine Methyl Ester	208-245	kininogen 1	Homo sapiens	37-47
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	NG-Nitroarginine Methyl Ester	208-245	kininogen 1	Homo sapiens	49-51
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	NG-Nitroarginine Methyl Ester	247-253	kininogen 1	Homo sapiens	37-47
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	NG-Nitroarginine Methyl Ester	247-253	kininogen 1	Homo sapiens	49-51
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	Potassium Chloride	286-289	kininogen 1	Homo sapiens	37-47
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	Potassium Chloride	286-289	kininogen 1	Homo sapiens	49-51
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	NG-Nitroarginine Methyl Ester	291-297	kininogen 1	Homo sapiens	37-47
7977690-8	1994	In contrast, bradykinin transiently elevated [Ca2+]i, and its potentiation of the osmosensitive anion efflux was completely inhibited after BAPTA-AM loading.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	140-148	kininogen 1	Homo sapiens	13-23
7620517-1	1994	Endothelium-dependent relaxations to bradykinin (BK) in U46619-contracted, indomethacin (INDO)-treated porcine coronary artery (PCA) rings are modestly attenuated by the nitric oxide (NO) synthase inhibitor, N omega-nitro-l-arginine methyl ester (L-NAME); whereas, when contracted with KCl, L-NAME abolishes BK relaxations.	NG-Nitroarginine Methyl Ester	291-297	kininogen 1	Homo sapiens	49-51
7522486-5	1994	At high O2 (680 mm Hg), basal NO was detectable and NO increased 6- to 10-fold with bradykinin or A23187.	Oxygen	8-10	kininogen 1	Homo sapiens	84-94
7819601-4	1994	Two application examples of the method are given: the linear peptide bradykinin and desmopressin, a peptide with an internal S-S bond and a non-amino-acid constituent.	Sulfur	125-126	kininogen 1	Homo sapiens	69-79
7879699-5	1994	The ability of the cyclooxygenase inhibitors indomethacin and naproxen to decrease the response to bradykinin by approximately 68% indicates the effect is mediated, at least partially, through the generation of prostaglandins.	Indomethacin	45-57	kininogen 1	Homo sapiens	99-109
7879699-5	1994	The ability of the cyclooxygenase inhibitors indomethacin and naproxen to decrease the response to bradykinin by approximately 68% indicates the effect is mediated, at least partially, through the generation of prostaglandins.	Naproxen	62-70	kininogen 1	Homo sapiens	99-109
7879699-5	1994	The ability of the cyclooxygenase inhibitors indomethacin and naproxen to decrease the response to bradykinin by approximately 68% indicates the effect is mediated, at least partially, through the generation of prostaglandins.	Prostaglandins	211-225	kininogen 1	Homo sapiens	99-109
7712026-0	1995	Potentiation by tumour necrosis factor-alpha of calcium signals induced by bradykinin and carbachol in human tracheal smooth muscle cells.	Calcium	48-55	kininogen 1	Homo sapiens	75-85
7712026-1	1995	The effect of tumour necrosis factor-alpha (TNF alpha) on the increase in cytosolic free calcium ([Ca2+])i induced by carbachol and bradykinin (BK) was investigated in human tracheal smooth muscle cells in culture (TSMC).	Calcium	89-96	kininogen 1	Homo sapiens	132-142
7712026-1	1995	The effect of tumour necrosis factor-alpha (TNF alpha) on the increase in cytosolic free calcium ([Ca2+])i induced by carbachol and bradykinin (BK) was investigated in human tracheal smooth muscle cells in culture (TSMC).	Calcium	89-96	kininogen 1	Homo sapiens	144-146
7833219-0	1994	Local L-NG-monomethyl-arginine attenuates the vasodilator action of bradykinin in the human forearm.	omega-N-Methylarginine	6-30	kininogen 1	Homo sapiens	68-78
7921430-2	1994	Studies in vivo in the human suggest that BK causes cholinergic nerve activation, release of prostanoids, and local axon reflexes with release of tachykinins in the airways.	Prostaglandins	93-104	kininogen 1	Homo sapiens	42-44
7921430-4	1994	Responses to BK were recorded from airways with spontaneous intrinsic tone and from airways precontracted with methacholine.	Methacholine Chloride	111-123	kininogen 1	Homo sapiens	13-15
7921430-5	1994	Furthermore, we measured the BK-induced release of the prostanoids PGE2, PGI2, and TXA2 from airways with and without epithelium in the absence and presence of indomethacin by radioimmunoassay.	Prostaglandins	55-66	kininogen 1	Homo sapiens	29-31
7921430-5	1994	Furthermore, we measured the BK-induced release of the prostanoids PGE2, PGI2, and TXA2 from airways with and without epithelium in the absence and presence of indomethacin by radioimmunoassay.	Dinoprostone	67-71	kininogen 1	Homo sapiens	29-31
7921430-5	1994	Furthermore, we measured the BK-induced release of the prostanoids PGE2, PGI2, and TXA2 from airways with and without epithelium in the absence and presence of indomethacin by radioimmunoassay.	Epoprostenol	73-77	kininogen 1	Homo sapiens	29-31
7530473-2	1994	We compared effects of NG-monomethyl-L-arginine (L-NMMA), an NO synthase inhibitor, on vasodilator responses to intra-arterial infusion of bradykinin and substance P in the human forearm.	omega-N-Methylarginine	23-47	kininogen 1	Homo sapiens	139-149
7530473-2	1994	We compared effects of NG-monomethyl-L-arginine (L-NMMA), an NO synthase inhibitor, on vasodilator responses to intra-arterial infusion of bradykinin and substance P in the human forearm.	omega-N-Methylarginine	49-55	kininogen 1	Homo sapiens	139-149
7530473-7	1994	Co-infusion of L-NMMA (2 mumol min-1 and 4 mumol min-1) with bradykinin (100 pmol min-1) for 6 min produced respectively a 9 +/- 14% and 42 +/- 14% inhibition (compared with L-NMMA vehicle) in the response to bradykinin.	omega-N-Methylarginine	15-21	kininogen 1	Homo sapiens	61-71
7530473-7	1994	Co-infusion of L-NMMA (2 mumol min-1 and 4 mumol min-1) with bradykinin (100 pmol min-1) for 6 min produced respectively a 9 +/- 14% and 42 +/- 14% inhibition (compared with L-NMMA vehicle) in the response to bradykinin.	omega-N-Methylarginine	15-21	kininogen 1	Homo sapiens	209-219
7530473-7	1994	Co-infusion of L-NMMA (2 mumol min-1 and 4 mumol min-1) with bradykinin (100 pmol min-1) for 6 min produced respectively a 9 +/- 14% and 42 +/- 14% inhibition (compared with L-NMMA vehicle) in the response to bradykinin.	omega-N-Methylarginine	174-180	kininogen 1	Homo sapiens	61-71
7530473-13	1994	These results demonstrate that vasodilator responses to both bradykinin and substance P are mediated in part via the L-arginine/NO pathway.	Arginine	117-127	kininogen 1	Homo sapiens	61-71
7833219-5	1994	In this study the effects of a specific inhibitor of nitric oxide synthase, L-NG-monomethyl-arginine (L-NMMA) and noradrenaline on the vasodilator responses to bradykinin were examined in the forearm arterial bed of healthy volunteers.	omega-N-Methylarginine	76-100	kininogen 1	Homo sapiens	160-170
7833219-5	1994	In this study the effects of a specific inhibitor of nitric oxide synthase, L-NG-monomethyl-arginine (L-NMMA) and noradrenaline on the vasodilator responses to bradykinin were examined in the forearm arterial bed of healthy volunteers.	omega-N-Methylarginine	102-108	kininogen 1	Homo sapiens	160-170
7833219-5	1994	In this study the effects of a specific inhibitor of nitric oxide synthase, L-NG-monomethyl-arginine (L-NMMA) and noradrenaline on the vasodilator responses to bradykinin were examined in the forearm arterial bed of healthy volunteers.	Norepinephrine	114-127	kininogen 1	Homo sapiens	160-170
7833219-12	1994	The response to bradykinin, but not that to GTN, was attenuated by L-NMMA compared with noradrenaline (P &lt; 0.05; n = 6), suggesting that bradykinin-induced vasodilatation in the forearm is mediated, at least in part, by stimulating release of nitric oxide.	omega-N-Methylarginine	67-73	kininogen 1	Homo sapiens	16-26
7833219-12	1994	The response to bradykinin, but not that to GTN, was attenuated by L-NMMA compared with noradrenaline (P &lt; 0.05; n = 6), suggesting that bradykinin-induced vasodilatation in the forearm is mediated, at least in part, by stimulating release of nitric oxide.	omega-N-Methylarginine	67-73	kininogen 1	Homo sapiens	140-150
7833219-12	1994	The response to bradykinin, but not that to GTN, was attenuated by L-NMMA compared with noradrenaline (P &lt; 0.05; n = 6), suggesting that bradykinin-induced vasodilatation in the forearm is mediated, at least in part, by stimulating release of nitric oxide.	Norepinephrine	88-101	kininogen 1	Homo sapiens	140-150
7833219-12	1994	The response to bradykinin, but not that to GTN, was attenuated by L-NMMA compared with noradrenaline (P &lt; 0.05; n = 6), suggesting that bradykinin-induced vasodilatation in the forearm is mediated, at least in part, by stimulating release of nitric oxide.	Nitric Oxide	246-258	kininogen 1	Homo sapiens	16-26
7833219-12	1994	The response to bradykinin, but not that to GTN, was attenuated by L-NMMA compared with noradrenaline (P &lt; 0.05; n = 6), suggesting that bradykinin-induced vasodilatation in the forearm is mediated, at least in part, by stimulating release of nitric oxide.	Nitric Oxide	246-258	kininogen 1	Homo sapiens	140-150
7528837-1	1994	Cyclic GMP accumulation in endothelial cells-smooth muscle cells (EC-SMC) coculture induced by both receptor-dependent (thrombin, bradykinin, BK) and receptor-independent (Ca(2+)-ionophore A23187) stimulation, was inhibited by preincubation with low-density lipoprotein (LDL) in time- and concentration-dependent manner.	Cyclic GMP	0-10	kininogen 1	Homo sapiens	130-140
7867229-4	1994	Nitric oxide release occurs under basal conditions, in response to chemical stimuli (acetylcholine, bradykinin, thrombin, prostacyclin, serotonin, etc.)	Nitric Oxide	0-12	kininogen 1	Homo sapiens	100-110
7849248-8	1994	In the presence of 10 microM bradykinin, cellular cGMP increased by 1.75 +/- 0.6-fold versus control cells.	Cyclic GMP	50-54	kininogen 1	Homo sapiens	29-39
7849248-9	1994	However, unlike ANP, bradykinin-stimulated cGMP synthesis was significantly inhibited by prior treatment with oxyhemoglobin (10(-5) M), an inhibitor of soluble guanylate cyclase, and NG-nitro-L-arginine (NO2Arg), a specific inhibitor of endothelial-derived relaxing factor (EDRF).	Cyclic GMP	43-47	kininogen 1	Homo sapiens	21-31
7849248-9	1994	However, unlike ANP, bradykinin-stimulated cGMP synthesis was significantly inhibited by prior treatment with oxyhemoglobin (10(-5) M), an inhibitor of soluble guanylate cyclase, and NG-nitro-L-arginine (NO2Arg), a specific inhibitor of endothelial-derived relaxing factor (EDRF).	Nitroarginine	183-202	kininogen 1	Homo sapiens	21-31
7849248-9	1994	However, unlike ANP, bradykinin-stimulated cGMP synthesis was significantly inhibited by prior treatment with oxyhemoglobin (10(-5) M), an inhibitor of soluble guanylate cyclase, and NG-nitro-L-arginine (NO2Arg), a specific inhibitor of endothelial-derived relaxing factor (EDRF).	Nitroarginine	204-210	kininogen 1	Homo sapiens	21-31
7528372-7	1994	The stimulatory effect of bradykinin on bone resorption is completely lost when the prostaglandin response is abolished, whereas thrombin can stimulate bone resorption both via prostaglandin-dependent and independent mechanisms.	Prostaglandins	84-97	kininogen 1	Homo sapiens	26-36
7876356-2	1994	From resting concentration 138 +/- 13 nM, bradykinin (0.1 microM) produces an increase to a maximum of 835 +/- 195 nM, histamine (10 microM) to 352 +/- 51 nM, and ATP (5-500 microM) to more than 1500 nM.	Histamine	119-128	kininogen 1	Homo sapiens	42-52
7876356-2	1994	From resting concentration 138 +/- 13 nM, bradykinin (0.1 microM) produces an increase to a maximum of 835 +/- 195 nM, histamine (10 microM) to 352 +/- 51 nM, and ATP (5-500 microM) to more than 1500 nM.	Adenosine Triphosphate	163-166	kininogen 1	Homo sapiens	42-52
7528372-8	1994	In addition, bradykinin and thrombin act in concert with interleukin-1 to synergistically stimulate bone resorption and prostaglandin biosynthesis.	Prostaglandins	120-133	kininogen 1	Homo sapiens	13-23
8077670-0	1994	Bradykinin is a potent and relatively selective stimulus for cytosolic calcium elevation in human synovial cells.	Calcium	71-78	kininogen 1	Homo sapiens	0-10
8077670-1	1994	Previously, we have shown that bradykinin elicits the production of prostaglandin E2 (PGE2) in human synovial cells only after pre-exposure of the cells to IL-1.	Dinoprostone	68-84	kininogen 1	Homo sapiens	31-41
8077670-1	1994	Previously, we have shown that bradykinin elicits the production of prostaglandin E2 (PGE2) in human synovial cells only after pre-exposure of the cells to IL-1.	Dinoprostone	86-90	kininogen 1	Homo sapiens	31-41
8077670-2	1994	The observation that calcium ionophores, but not a variety of physiologic receptor-mediated agonists, can mimic bradykinin in its synergy with IL-1 led us to hypothesize that the ability of bradykinin to induce prostanoid synthesis was a result of its selective ability (among physiologic agonists) to raise the cytosolic free ionized calcium concentration ([Ca2+]i) levels of synovial cells.	Calcium	21-28	kininogen 1	Homo sapiens	112-122
8077670-2	1994	The observation that calcium ionophores, but not a variety of physiologic receptor-mediated agonists, can mimic bradykinin in its synergy with IL-1 led us to hypothesize that the ability of bradykinin to induce prostanoid synthesis was a result of its selective ability (among physiologic agonists) to raise the cytosolic free ionized calcium concentration ([Ca2+]i) levels of synovial cells.	Calcium	21-28	kininogen 1	Homo sapiens	190-200
8077670-2	1994	The observation that calcium ionophores, but not a variety of physiologic receptor-mediated agonists, can mimic bradykinin in its synergy with IL-1 led us to hypothesize that the ability of bradykinin to induce prostanoid synthesis was a result of its selective ability (among physiologic agonists) to raise the cytosolic free ionized calcium concentration ([Ca2+]i) levels of synovial cells.	Prostaglandins	211-221	kininogen 1	Homo sapiens	190-200
8077670-2	1994	The observation that calcium ionophores, but not a variety of physiologic receptor-mediated agonists, can mimic bradykinin in its synergy with IL-1 led us to hypothesize that the ability of bradykinin to induce prostanoid synthesis was a result of its selective ability (among physiologic agonists) to raise the cytosolic free ionized calcium concentration ([Ca2+]i) levels of synovial cells.	Calcium	335-342	kininogen 1	Homo sapiens	190-200
8077670-6	1994	Furthermore, the relative specificity and potency of the PGE2 response of bradykinin in IL-1-treated cells was paralleled, in resting cells, by a similar pattern in the [Ca2+]i response.	Dinoprostone	57-61	kininogen 1	Homo sapiens	74-84
8063797-5	1994	The cloned B1 bradykinin receptor expressed in mammalian cells exhibits high affinity binding for 3H-labeled [des-Arg10]kallidin and low affinity for bradykinin.	Tritium	98-100	kininogen 1	Homo sapiens	14-24
7522407-3	1994	Both bradykinin and substance P relaxed strips of both arteries precontracted with prostaglandin F2 alpha to similar extents.	Dinoprost	83-105	kininogen 1	Homo sapiens	5-15
7835634-2	1994	The present study was undertaken to determine whether endothelial nitric oxide (NO) is involved in the endothelium-dependent vasodilation elicited by bradykinin (BK) in rings of newborn (1-7-day-old) piglet cerebral arteries precontracted with KCl (25 mM).	Nitric Oxide	66-78	kininogen 1	Homo sapiens	150-160
7835634-2	1994	The present study was undertaken to determine whether endothelial nitric oxide (NO) is involved in the endothelium-dependent vasodilation elicited by bradykinin (BK) in rings of newborn (1-7-day-old) piglet cerebral arteries precontracted with KCl (25 mM).	Nitric Oxide	66-78	kininogen 1	Homo sapiens	162-164
7835634-5	1994	The preincubation with the precursor of NO synthesis, L-arginine (10(-4) M), reduced KCl-induced contraction and increased the BK relaxation.	Arginine	54-64	kininogen 1	Homo sapiens	127-129
7835634-6	1994	However, preincubation with the NO synthase inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME; 3 x 10(-5) M), increased KCl contraction and basal tone, and inhibited BK relaxation.	NG-Nitroarginine Methyl Ester	55-87	kininogen 1	Homo sapiens	168-170
7835634-6	1994	However, preincubation with the NO synthase inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME; 3 x 10(-5) M), increased KCl contraction and basal tone, and inhibited BK relaxation.	NG-Nitroarginine Methyl Ester	89-95	kininogen 1	Homo sapiens	168-170
8067439-5	1994	Administration of N omega-nitro-L-arginine and its methyl ester reduced vasodilator responses to bradykinin, acetylcholine, and substance P, whereas responses to endothelium-independent vasodilator agents were not attenuated.	Nitroarginine	18-42	kininogen 1	Homo sapiens	97-107
8067439-5	1994	Administration of N omega-nitro-L-arginine and its methyl ester reduced vasodilator responses to bradykinin, acetylcholine, and substance P, whereas responses to endothelium-independent vasodilator agents were not attenuated.	methyl ester	51-63	kininogen 1	Homo sapiens	97-107
8067439-6	1994	Decreases in systemic arterial pressure and in hindquarters perfusion pressure in response to bradykinin were enhanced by the angiotensin-converting enzyme inhibitors captopril and enalaprilat.	Captopril	167-176	kininogen 1	Homo sapiens	94-104
7749364-7	1994	Interestingly, the mouse B2 bradykinin receptor has a 60-80 fold higher affinity than the human B2 bradykinin receptor for the peptide antagonists D-Arg0[Hyp3,Thi5,8,D-Phe7]bradykinin and D-Arg0[Hyp3,D-Phe7]bradykinin.	d-arg0	147-153	kininogen 1	Homo sapiens	28-38
8067439-6	1994	Decreases in systemic arterial pressure and in hindquarters perfusion pressure in response to bradykinin were enhanced by the angiotensin-converting enzyme inhibitors captopril and enalaprilat.	Enalaprilat	181-192	kininogen 1	Homo sapiens	94-104
8067439-7	1994	These results suggest that hindquarters vasodilator responses to bradykinin are mediated by activation of kinin B2 receptors and in part by the release of nitric oxide.	Nitric Oxide	155-167	kininogen 1	Homo sapiens	65-75
7749364-7	1994	Interestingly, the mouse B2 bradykinin receptor has a 60-80 fold higher affinity than the human B2 bradykinin receptor for the peptide antagonists D-Arg0[Hyp3,Thi5,8,D-Phe7]bradykinin and D-Arg0[Hyp3,D-Phe7]bradykinin.	d-arg0	147-153	kininogen 1	Homo sapiens	99-109
7749364-7	1994	Interestingly, the mouse B2 bradykinin receptor has a 60-80 fold higher affinity than the human B2 bradykinin receptor for the peptide antagonists D-Arg0[Hyp3,Thi5,8,D-Phe7]bradykinin and D-Arg0[Hyp3,D-Phe7]bradykinin.	thi5	159-163	kininogen 1	Homo sapiens	28-38
7749364-7	1994	Interestingly, the mouse B2 bradykinin receptor has a 60-80 fold higher affinity than the human B2 bradykinin receptor for the peptide antagonists D-Arg0[Hyp3,Thi5,8,D-Phe7]bradykinin and D-Arg0[Hyp3,D-Phe7]bradykinin.	thi5	159-163	kininogen 1	Homo sapiens	99-109
7749364-7	1994	Interestingly, the mouse B2 bradykinin receptor has a 60-80 fold higher affinity than the human B2 bradykinin receptor for the peptide antagonists D-Arg0[Hyp3,Thi5,8,D-Phe7]bradykinin and D-Arg0[Hyp3,D-Phe7]bradykinin.	d-arg0	188-194	kininogen 1	Homo sapiens	28-38
7749371-12	1994	These data therefore suggest that physiological concentrations of P(i) and Zn(II) may be sufficient for a low-level turnover of the contact system in plasma which in turn may be responsible for the background levels of cleaved HK and BK found in normal plasma.	Phosphorus	66-68	kininogen 1	Homo sapiens	234-236
7749371-12	1994	These data therefore suggest that physiological concentrations of P(i) and Zn(II) may be sufficient for a low-level turnover of the contact system in plasma which in turn may be responsible for the background levels of cleaved HK and BK found in normal plasma.	Zinc	75-81	kininogen 1	Homo sapiens	234-236
7531489-2	1994	Enhanced, superimposed EDNO release can be stimulated by various local and circulating factors, such as bradykinin, ATP, etc., but also most importantly by viscous drag-induced shear stress of the bloodstream acting on the endothelial lining.	Nitric Oxide	23-27	kininogen 1	Homo sapiens	104-114
7982121-0	1994	Effects of ipratropium bromide on bradykinin nasal provocation in chronic allergic rhinitis.	Ipratropium	11-30	kininogen 1	Homo sapiens	34-44
8039606-3	1994	Pretreatment with high D-glucose (44 vs. 5 mM) enhanced release of intracellular Ca2+ by bradykinin as a result of a 2.0-fold increased formation of inositol 1,4,5-trisphosphate.	Glucose	23-32	kininogen 1	Homo sapiens	89-99
8039606-3	1994	Pretreatment with high D-glucose (44 vs. 5 mM) enhanced release of intracellular Ca2+ by bradykinin as a result of a 2.0-fold increased formation of inositol 1,4,5-trisphosphate.	Inositol 1,4,5-Trisphosphate	149-177	kininogen 1	Homo sapiens	89-99
8039606-5	1994	In high D-glucose preincubated cells, stimulation with bradykinin significantly increased transplasmalemmal 45Ca2+ flux (3.2-fold) and caused a 2.0-fold increase in permeability to Mn2+, a surrogate for endothelial plasma membrane Ca2+ channels.	Glucose	8-17	kininogen 1	Homo sapiens	55-65
8039606-5	1994	In high D-glucose preincubated cells, stimulation with bradykinin significantly increased transplasmalemmal 45Ca2+ flux (3.2-fold) and caused a 2.0-fold increase in permeability to Mn2+, a surrogate for endothelial plasma membrane Ca2+ channels.	Manganese(2+)	181-185	kininogen 1	Homo sapiens	55-65
8043027-0	1994	Bradykinin-evoked release of [3H]noradrenaline from the human neuroblastoma SH-SY5Y.	[3h]noradrenaline	29-46	kininogen 1	Homo sapiens	0-10
8043027-1	1994	Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min.	[3h]noradrenaline	23-40	kininogen 1	Homo sapiens	0-10
8043027-1	1994	Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min.	[3h]noradrenaline	23-40	kininogen 1	Homo sapiens	12-14
7921430-10	1994	Both contractile and relaxation responses to BK and the release of the prostanoids PGE2, PGI2, and TXA2 by the airway tissues were largely inhibited by indomethacin, whereas TTX had no effect.	Indomethacin	152-164	kininogen 1	Homo sapiens	45-47
8043027-1	1994	Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min.	Tritium	23-27	kininogen 1	Homo sapiens	0-10
8043027-1	1994	Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min.	Tritium	23-27	kininogen 1	Homo sapiens	12-14
8043027-1	1994	Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min.	Tetradecanoylphorbol Acetate	139-175	kininogen 1	Homo sapiens	0-10
8043027-1	1994	Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min.	Tetradecanoylphorbol Acetate	139-175	kininogen 1	Homo sapiens	12-14
8043027-1	1994	Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min.	Tetradecanoylphorbol Acetate	177-180	kininogen 1	Homo sapiens	0-10
8043027-1	1994	Bradykinin (BK) evoked [3H]noradrenaline ([3H]NA) release from the human neuroblastoma SH-SY5Y and this was enhanced by pre-treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA) for 8 min.	Tetradecanoylphorbol Acetate	177-180	kininogen 1	Homo sapiens	12-14
8043027-5	1994	BK acting at B2-receptors, also elevated intracellular calcium and depolarized SH-SY5Y cells.	Calcium	55-62	kininogen 1	Homo sapiens	0-2
8043027-6	1994	Although pre-treatment of SH-SY5Y cells with TPA enhanced BK-evoked [3H]NA release, the elevation of intracellular calcium [Ca2+]; was decreased by about 50%.	Tetradecanoylphorbol Acetate	45-48	kininogen 1	Homo sapiens	58-60
8043027-6	1994	Although pre-treatment of SH-SY5Y cells with TPA enhanced BK-evoked [3H]NA release, the elevation of intracellular calcium [Ca2+]; was decreased by about 50%.	Tritium	69-71	kininogen 1	Homo sapiens	58-60
8043027-7	1994	BK-evoked release of [3H]NA in cells not pre-treated with phorbol ester was only 23% dependent on extracellular calcium.	Tritium	22-24	kininogen 1	Homo sapiens	0-2
7970215-1	1994	Prostaglandin E2 augments bradykinin- and heat-induced discharges of polymodal receptors as studied in vitro preparations.	Dinoprostone	0-16	kininogen 1	Homo sapiens	26-36
8043027-7	1994	BK-evoked release of [3H]NA in cells not pre-treated with phorbol ester was only 23% dependent on extracellular calcium.	Phorbol Esters	58-71	kininogen 1	Homo sapiens	0-2
8043027-7	1994	BK-evoked release of [3H]NA in cells not pre-treated with phorbol ester was only 23% dependent on extracellular calcium.	Calcium	112-119	kininogen 1	Homo sapiens	0-2
8043027-10	1994	The results of this study showed that BK, acting at B2-receptors, activated [3H]NA release in SH-SY5Y.	Tritium	77-79	kininogen 1	Homo sapiens	38-40
7516822-9	1994	In contrast, the five substance P derivatives inhibited the calcium response to bombesin, AVP, bradykinin, and fetal bovine serum.	Calcium	60-67	kininogen 1	Homo sapiens	95-105
8026018-10	1994	NG-Monomethyl-L-arginine, an inhibitor of nitric oxide synthesis, reduced the maximum forearm vasodilation induced by bradykinin to the same extent in patients and in healthy subjects (-29 +/- 8% versus -32 +/- 6% reduction in peak flow, P = .80), with similar maximum flows in response to bradykinin (9.2 +/- 4.0 versus 10.4 +/- 2.6 mL.min-1 x 100 mL-1, P = .35).	omega-N-Methylarginine	0-24	kininogen 1	Homo sapiens	118-128
8026018-10	1994	NG-Monomethyl-L-arginine, an inhibitor of nitric oxide synthesis, reduced the maximum forearm vasodilation induced by bradykinin to the same extent in patients and in healthy subjects (-29 +/- 8% versus -32 +/- 6% reduction in peak flow, P = .80), with similar maximum flows in response to bradykinin (9.2 +/- 4.0 versus 10.4 +/- 2.6 mL.min-1 x 100 mL-1, P = .35).	omega-N-Methylarginine	0-24	kininogen 1	Homo sapiens	290-300
8026018-10	1994	NG-Monomethyl-L-arginine, an inhibitor of nitric oxide synthesis, reduced the maximum forearm vasodilation induced by bradykinin to the same extent in patients and in healthy subjects (-29 +/- 8% versus -32 +/- 6% reduction in peak flow, P = .80), with similar maximum flows in response to bradykinin (9.2 +/- 4.0 versus 10.4 +/- 2.6 mL.min-1 x 100 mL-1, P = .35).	Nitric Oxide	42-54	kininogen 1	Homo sapiens	118-128
8026018-11	1994	CONCLUSIONS: Hypercholesterolemic patients are capable of normal nitric oxide bioavailability in response to bradykinin.	Nitric Oxide	65-77	kininogen 1	Homo sapiens	109-119
21559559-6	1994	The inhibitory effect of BK on glioma invasion may be mediated by a calcium-independent mechanism.	Calcium	68-75	kininogen 1	Homo sapiens	25-27
8048578-6	1994	Endothelium-dependent relaxations to bradykinin and ET-1 were greater in pulmonary veins compared with arteries, inhibited by N omega-nitro-L-arginine, and reversed by L-arginine.	Nitroarginine	126-150	kininogen 1	Homo sapiens	37-47
8048578-6	1994	Endothelium-dependent relaxations to bradykinin and ET-1 were greater in pulmonary veins compared with arteries, inhibited by N omega-nitro-L-arginine, and reversed by L-arginine.	Arginine	140-150	kininogen 1	Homo sapiens	37-47
7960398-2	1994	Cyclization, by the diphenyl-phosphorazide method, of linear peptides prepared by the solid-phase procedure based on Fmoc chemistry, was used for preparing cyclo-bradykinin and cyclo-kallidin (cyclo-Lys-bradykinin).	diphenyl-phosphorazide	20-42	kininogen 1	Homo sapiens	162-172
7960398-2	1994	Cyclization, by the diphenyl-phosphorazide method, of linear peptides prepared by the solid-phase procedure based on Fmoc chemistry, was used for preparing cyclo-bradykinin and cyclo-kallidin (cyclo-Lys-bradykinin).	diphenyl-phosphorazide	20-42	kininogen 1	Homo sapiens	203-213
7960398-2	1994	Cyclization, by the diphenyl-phosphorazide method, of linear peptides prepared by the solid-phase procedure based on Fmoc chemistry, was used for preparing cyclo-bradykinin and cyclo-kallidin (cyclo-Lys-bradykinin).	Peptides	61-69	kininogen 1	Homo sapiens	162-172
7960398-2	1994	Cyclization, by the diphenyl-phosphorazide method, of linear peptides prepared by the solid-phase procedure based on Fmoc chemistry, was used for preparing cyclo-bradykinin and cyclo-kallidin (cyclo-Lys-bradykinin).	Peptides	61-69	kininogen 1	Homo sapiens	203-213
8027219-2	1994	We study here the regulation of the PiP2 cascade by TSH, ATP, NaF, and bradykinin.	Phosphatidylinositol 4,5-Diphosphate	36-40	kininogen 1	Homo sapiens	71-81
8027219-4	1994	Activation of the PiP2 cascade by TSH (10 mU/mL), NaF, bradykinin, ionomycin, and 12-O-tetradecanoylphorbol-13-acetate stimulates iodide organification.	Phosphatidylinositol 4,5-Diphosphate	18-22	kininogen 1	Homo sapiens	55-65
8027219-4	1994	Activation of the PiP2 cascade by TSH (10 mU/mL), NaF, bradykinin, ionomycin, and 12-O-tetradecanoylphorbol-13-acetate stimulates iodide organification.	Iodides	130-136	kininogen 1	Homo sapiens	55-65
7950978-2	1994	These cells also possess bradykinin B2 receptors coupled to phospholipase C and consequent increases in intracellular calcium and protein kinase C. Interleukin 1 beta causes an increase in c-fos, AP-1 transcriptional activity and an increased expression of several genes including NGF, but the initial signalling events are unknown.	Calcium	118-125	kininogen 1	Homo sapiens	25-35
8040274-4	1994	Bradykinin-stimulated Ca influx was reduced by dibutyryl cAMP, isoproterenol, and forskolin.	Bucladesine	47-61	kininogen 1	Homo sapiens	0-10
8040274-4	1994	Bradykinin-stimulated Ca influx was reduced by dibutyryl cAMP, isoproterenol, and forskolin.	Isoproterenol	63-76	kininogen 1	Homo sapiens	0-10
8040274-4	1994	Bradykinin-stimulated Ca influx was reduced by dibutyryl cAMP, isoproterenol, and forskolin.	Colforsin	82-91	kininogen 1	Homo sapiens	0-10
8040274-8	1994	Consequently, in bradykinin-stimulated cells, the adenylyl cyclase system regulates Ca influx through cAMP-dependent protein kinase, but not intracellular Ca release.	Cyclic AMP	102-106	kininogen 1	Homo sapiens	17-27
7950978-3	1994	Bradykinin causes a rapid decrease in A2B receptor mediated cAMP formation, via a mechanism that involves calcium, but not cGMP, and appears to depend upon a direct decrease in adenylyl cyclase.	Cyclic AMP	60-64	kininogen 1	Homo sapiens	0-10
7950978-3	1994	Bradykinin causes a rapid decrease in A2B receptor mediated cAMP formation, via a mechanism that involves calcium, but not cGMP, and appears to depend upon a direct decrease in adenylyl cyclase.	Calcium	106-113	kininogen 1	Homo sapiens	0-10
7950978-3	1994	Bradykinin causes a rapid decrease in A2B receptor mediated cAMP formation, via a mechanism that involves calcium, but not cGMP, and appears to depend upon a direct decrease in adenylyl cyclase.	Cyclic GMP	123-127	kininogen 1	Homo sapiens	0-10
7517647-5	1994	The similar inhibitory effects of L-NNA, L-NAME, and L-NABE on vasodilator responses to ACh, BK, and SP suggest that the L-arginine analogue, L-NNA, as well as the methyl and benzyl esters of L-NNA are useful probes for studying NO-mediated endothelium-dependent responses in the pulmonary vascular bed of the intact-chest cat.	N(w)-nitroarginine benzyl ester	53-59	kininogen 1	Homo sapiens	93-95
7911978-3	1994	Internal calcium was elevated and glutamate release stimulated by application of the neuroligand bradykinin to cultured astrocytes.	Calcium	9-16	kininogen 1	Homo sapiens	97-107
7911978-3	1994	Internal calcium was elevated and glutamate release stimulated by application of the neuroligand bradykinin to cultured astrocytes.	Glutamic Acid	34-43	kininogen 1	Homo sapiens	97-107
7911978-6	1994	Bradykinin significantly increased calcium levels in neurons co-cultured with astrocytes, but not in solitary neurons.	Calcium	35-42	kininogen 1	Homo sapiens	0-10
7911978-7	1994	The glutamate receptor antagonists D-2-amino-5-phosphonopentanoic acid and D-glutamylglycine prevented bradykinin-induced neuronal calcium elevation.	2-amino-4-oxo-5-phosphonopentanoic acid	35-70	kininogen 1	Homo sapiens	103-113
7911978-7	1994	The glutamate receptor antagonists D-2-amino-5-phosphonopentanoic acid and D-glutamylglycine prevented bradykinin-induced neuronal calcium elevation.	d-glutamylglycine	75-92	kininogen 1	Homo sapiens	103-113
7911978-7	1994	The glutamate receptor antagonists D-2-amino-5-phosphonopentanoic acid and D-glutamylglycine prevented bradykinin-induced neuronal calcium elevation.	Calcium	131-138	kininogen 1	Homo sapiens	103-113
8206938-1	1994	We have studied the cleavage of human high molecular weight kininogen (HK) by plasma kallikrein in the absence and presence of the surfaces, dextran sulfate (DxSO4) and sulfatides.	Dextran Sulfate	141-156	kininogen 1	Homo sapiens	38-74
8206938-1	1994	We have studied the cleavage of human high molecular weight kininogen (HK) by plasma kallikrein in the absence and presence of the surfaces, dextran sulfate (DxSO4) and sulfatides.	Sulfoglycosphingolipids	169-179	kininogen 1	Homo sapiens	38-74
8206938-2	1994	Using a combination of SDS-polyacrylamide gel electrophoresis, Western blotting with polyclonal antibodies that specifically recognize the COOH terminus of the bradykinin moiety, and high pressure liquid chromatography analyses of the cleavage reaction, we have identified two intermediates in the formation of bradykinin from intact kininogen and demonstrated that alternative cleavage pathways are followed in the absence and presence of surfaces.	Carbonic Acid	139-143	kininogen 1	Homo sapiens	160-170
8206938-3	1994	The COOH-terminal bradykinin cleavage occurred first both in the absence and presence of DxSO4, producing a 103-kDa HK intermediate consisting of disulfide-linked heavy and light chains that retained the kinin moiety.	dxso4	89-94	kininogen 1	Homo sapiens	18-28
8206938-3	1994	The COOH-terminal bradykinin cleavage occurred first both in the absence and presence of DxSO4, producing a 103-kDa HK intermediate consisting of disulfide-linked heavy and light chains that retained the kinin moiety.	dxso4	89-94	kininogen 1	Homo sapiens	116-118
8206938-3	1994	The COOH-terminal bradykinin cleavage occurred first both in the absence and presence of DxSO4, producing a 103-kDa HK intermediate consisting of disulfide-linked heavy and light chains that retained the kinin moiety.	Disulfides	146-155	kininogen 1	Homo sapiens	18-28
8206938-3	1994	The COOH-terminal bradykinin cleavage occurred first both in the absence and presence of DxSO4, producing a 103-kDa HK intermediate consisting of disulfide-linked heavy and light chains that retained the kinin moiety.	Disulfides	146-155	kininogen 1	Homo sapiens	116-118
8206938-4	1994	In the presence of DxSO4, this was followed exclusively by the NH2-terminal bradykinin cleavage and release of kinin with no apparent change in molecular mass.	dxso4	19-24	kininogen 1	Homo sapiens	76-86
8206938-7	1994	Comparison of the relative rates of the three kallikrein cleavages in the absence and presence of DxSO4 indicated that the surface enhanced the rates of both bradykinin cleavages 2-4-fold, but inhibited the light chain cleavage rate approximately 10-fold, thereby accounting for the change from a partially random to a sequential cleavage pattern in the presence of the surface.	dxso4	98-103	kininogen 1	Homo sapiens	158-168
8206938-8	1994	Steady-state kinetic analysis revealed that DxSO4 enhanced the kcat/KM for bradykinin release by the rate-limiting NH2-terminal bradykinin cleavage by approximately 2-fold due exclusively to an increase in kcat.	dxso4	44-49	kininogen 1	Homo sapiens	75-85
8206938-8	1994	Steady-state kinetic analysis revealed that DxSO4 enhanced the kcat/KM for bradykinin release by the rate-limiting NH2-terminal bradykinin cleavage by approximately 2-fold due exclusively to an increase in kcat.	dxso4	44-49	kininogen 1	Homo sapiens	128-138
8206938-9	1994	Sulfatides appeared to produce the same effects on the pattern of HK cleavages as DxSO4.	Sulfoglycosphingolipids	0-10	kininogen 1	Homo sapiens	66-68
8206938-10	1994	Blocking of the nonactive site, i.e. exosite, interaction between kallikrein and HK with excess prekallikrein or a synthetic peptide containing the region of HK that interacts with the kallikrein exosite significantly reduced the rate of bradykinin release as well as HK cleavages detected by SDS-polyacrylamide gel electrophoresis either in the absence or presence of DxSO4, indicating that the exosite interaction facilitates bradykinin cleavage.	Sodium Dodecyl Sulfate	293-296	kininogen 1	Homo sapiens	81-83
8206938-10	1994	Blocking of the nonactive site, i.e. exosite, interaction between kallikrein and HK with excess prekallikrein or a synthetic peptide containing the region of HK that interacts with the kallikrein exosite significantly reduced the rate of bradykinin release as well as HK cleavages detected by SDS-polyacrylamide gel electrophoresis either in the absence or presence of DxSO4, indicating that the exosite interaction facilitates bradykinin cleavage.	Sodium Dodecyl Sulfate	293-296	kininogen 1	Homo sapiens	158-160
8206938-10	1994	Blocking of the nonactive site, i.e. exosite, interaction between kallikrein and HK with excess prekallikrein or a synthetic peptide containing the region of HK that interacts with the kallikrein exosite significantly reduced the rate of bradykinin release as well as HK cleavages detected by SDS-polyacrylamide gel electrophoresis either in the absence or presence of DxSO4, indicating that the exosite interaction facilitates bradykinin cleavage.	Sodium Dodecyl Sulfate	293-296	kininogen 1	Homo sapiens	158-160
8206938-10	1994	Blocking of the nonactive site, i.e. exosite, interaction between kallikrein and HK with excess prekallikrein or a synthetic peptide containing the region of HK that interacts with the kallikrein exosite significantly reduced the rate of bradykinin release as well as HK cleavages detected by SDS-polyacrylamide gel electrophoresis either in the absence or presence of DxSO4, indicating that the exosite interaction facilitates bradykinin cleavage.	polyacrylamide	297-311	kininogen 1	Homo sapiens	81-83
8206938-10	1994	Blocking of the nonactive site, i.e. exosite, interaction between kallikrein and HK with excess prekallikrein or a synthetic peptide containing the region of HK that interacts with the kallikrein exosite significantly reduced the rate of bradykinin release as well as HK cleavages detected by SDS-polyacrylamide gel electrophoresis either in the absence or presence of DxSO4, indicating that the exosite interaction facilitates bradykinin cleavage.	polyacrylamide	297-311	kininogen 1	Homo sapiens	158-160
8206938-10	1994	Blocking of the nonactive site, i.e. exosite, interaction between kallikrein and HK with excess prekallikrein or a synthetic peptide containing the region of HK that interacts with the kallikrein exosite significantly reduced the rate of bradykinin release as well as HK cleavages detected by SDS-polyacrylamide gel electrophoresis either in the absence or presence of DxSO4, indicating that the exosite interaction facilitates bradykinin cleavage.	polyacrylamide	297-311	kininogen 1	Homo sapiens	158-160
8206938-10	1994	Blocking of the nonactive site, i.e. exosite, interaction between kallikrein and HK with excess prekallikrein or a synthetic peptide containing the region of HK that interacts with the kallikrein exosite significantly reduced the rate of bradykinin release as well as HK cleavages detected by SDS-polyacrylamide gel electrophoresis either in the absence or presence of DxSO4, indicating that the exosite interaction facilitates bradykinin cleavage.	dxso4	369-374	kininogen 1	Homo sapiens	81-83
8206938-10	1994	Blocking of the nonactive site, i.e. exosite, interaction between kallikrein and HK with excess prekallikrein or a synthetic peptide containing the region of HK that interacts with the kallikrein exosite significantly reduced the rate of bradykinin release as well as HK cleavages detected by SDS-polyacrylamide gel electrophoresis either in the absence or presence of DxSO4, indicating that the exosite interaction facilitates bradykinin cleavage.	dxso4	369-374	kininogen 1	Homo sapiens	158-160
8206938-10	1994	Blocking of the nonactive site, i.e. exosite, interaction between kallikrein and HK with excess prekallikrein or a synthetic peptide containing the region of HK that interacts with the kallikrein exosite significantly reduced the rate of bradykinin release as well as HK cleavages detected by SDS-polyacrylamide gel electrophoresis either in the absence or presence of DxSO4, indicating that the exosite interaction facilitates bradykinin cleavage.	dxso4	369-374	kininogen 1	Homo sapiens	158-160
8054469-0	1994	A CD and an NMR study of multiple bradykinin conformations in aqueous trifluoroethanol solutions.	Trifluoroethanol	70-86	kininogen 1	Homo sapiens	34-44
8054469-1	1994	CD and nmr studies have been carried out on aqueous trifluoroethanol (TFE) solutions of bradykinin (BK) and a bradykinin antagonist.	Trifluoroethanol	52-68	kininogen 1	Homo sapiens	88-98
8054469-1	1994	CD and nmr studies have been carried out on aqueous trifluoroethanol (TFE) solutions of bradykinin (BK) and a bradykinin antagonist.	Trifluoroethanol	52-68	kininogen 1	Homo sapiens	100-102
8054469-1	1994	CD and nmr studies have been carried out on aqueous trifluoroethanol (TFE) solutions of bradykinin (BK) and a bradykinin antagonist.	Trifluoroethanol	70-73	kininogen 1	Homo sapiens	88-98
8054469-1	1994	CD and nmr studies have been carried out on aqueous trifluoroethanol (TFE) solutions of bradykinin (BK) and a bradykinin antagonist.	Trifluoroethanol	70-73	kininogen 1	Homo sapiens	100-102
8054469-3	1994	The effect of increasing concentration of TFE in water on the difference ellipticity at 222 nm was examined and showed that BK may be a mixture of at least two different conformers, one of which largely forms when the TFE concentration is increased beyond 80%.	Trifluoroethanol	42-45	kininogen 1	Homo sapiens	124-126
8054469-3	1994	The effect of increasing concentration of TFE in water on the difference ellipticity at 222 nm was examined and showed that BK may be a mixture of at least two different conformers, one of which largely forms when the TFE concentration is increased beyond 80%.	Water	49-54	kininogen 1	Homo sapiens	124-126
8054469-3	1994	The effect of increasing concentration of TFE in water on the difference ellipticity at 222 nm was examined and showed that BK may be a mixture of at least two different conformers, one of which largely forms when the TFE concentration is increased beyond 80%.	Trifluoroethanol	218-221	kininogen 1	Homo sapiens	124-126
8054469-4	1994	The linear extrapolation of 100% of the difference ellipticity of BK at low TFE concentrations yields a value in agreement with that shown by the BK antagonist, indicating that the conformation of BK at the lower TFE concentrations is similar to that of the BK antagonist.	Trifluoroethanol	76-79	kininogen 1	Homo sapiens	66-68
8054469-6	1994	The total correlation spectroscopy (TOCSY) spectrum of BK in a 60/40% (v/v) TFE/H2O solution at 10 degrees C and a nuclear Overhauser effect spectroscopy (NOESY) spectrum that shows only sequential H alpha (i)-NH(i + 1) or the H alpha (i)-H delta delta" (i + 1) NOEs indicate that the majority of the molecules adopt an all-trans extended conformation.	Trifluoroethanol	76-79	kininogen 1	Homo sapiens	55-57
7517646-5	1994	The nitric oxide (NO) synthase inhibitors N omega-nitro-L-arginine benzyl ester and N omega-nitro-L-arginine reduced vasodilator responses to BK in a selective manner, indicating that responses to BK are mediated in part by the release of NO.	Nitric Oxide	4-16	kininogen 1	Homo sapiens	142-144
7517646-5	1994	The nitric oxide (NO) synthase inhibitors N omega-nitro-L-arginine benzyl ester and N omega-nitro-L-arginine reduced vasodilator responses to BK in a selective manner, indicating that responses to BK are mediated in part by the release of NO.	Nitric Oxide	4-16	kininogen 1	Homo sapiens	197-199
7517646-5	1994	The nitric oxide (NO) synthase inhibitors N omega-nitro-L-arginine benzyl ester and N omega-nitro-L-arginine reduced vasodilator responses to BK in a selective manner, indicating that responses to BK are mediated in part by the release of NO.	N(w)-nitroarginine benzyl ester	42-79	kininogen 1	Homo sapiens	142-144
7517646-5	1994	The nitric oxide (NO) synthase inhibitors N omega-nitro-L-arginine benzyl ester and N omega-nitro-L-arginine reduced vasodilator responses to BK in a selective manner, indicating that responses to BK are mediated in part by the release of NO.	N(w)-nitroarginine benzyl ester	42-79	kininogen 1	Homo sapiens	197-199
7517646-5	1994	The nitric oxide (NO) synthase inhibitors N omega-nitro-L-arginine benzyl ester and N omega-nitro-L-arginine reduced vasodilator responses to BK in a selective manner, indicating that responses to BK are mediated in part by the release of NO.	Nitroarginine	42-66	kininogen 1	Homo sapiens	142-144
7517646-5	1994	The nitric oxide (NO) synthase inhibitors N omega-nitro-L-arginine benzyl ester and N omega-nitro-L-arginine reduced vasodilator responses to BK in a selective manner, indicating that responses to BK are mediated in part by the release of NO.	Nitroarginine	42-66	kininogen 1	Homo sapiens	197-199
7517646-6	1994	Methylene blue, an inhibitor of the activation of soluble guanylate cyclase, increased lobar arterial pressure and decreased responses to BK.	Methylene Blue	0-14	kininogen 1	Homo sapiens	138-140
7517646-8	1994	The duration of the response to BK was enhanced by the guanosine 3",5"-cyclic monophosphate (cGMP) phosphodiesterase inhibitor Zaprinast, suggesting that responses to BK involve increases in cGMP levels.	Cyclic GMP	55-91	kininogen 1	Homo sapiens	32-34
7517646-8	1994	The duration of the response to BK was enhanced by the guanosine 3",5"-cyclic monophosphate (cGMP) phosphodiesterase inhibitor Zaprinast, suggesting that responses to BK involve increases in cGMP levels.	Cyclic GMP	55-91	kininogen 1	Homo sapiens	167-169
7517646-8	1994	The duration of the response to BK was enhanced by the guanosine 3",5"-cyclic monophosphate (cGMP) phosphodiesterase inhibitor Zaprinast, suggesting that responses to BK involve increases in cGMP levels.	Cyclic GMP	93-97	kininogen 1	Homo sapiens	32-34
7517646-8	1994	The duration of the response to BK was enhanced by the guanosine 3",5"-cyclic monophosphate (cGMP) phosphodiesterase inhibitor Zaprinast, suggesting that responses to BK involve increases in cGMP levels.	Cyclic GMP	93-97	kininogen 1	Homo sapiens	167-169
7517646-8	1994	The duration of the response to BK was enhanced by the guanosine 3",5"-cyclic monophosphate (cGMP) phosphodiesterase inhibitor Zaprinast, suggesting that responses to BK involve increases in cGMP levels.	zaprinast	127-136	kininogen 1	Homo sapiens	32-34
7517646-8	1994	The duration of the response to BK was enhanced by the guanosine 3",5"-cyclic monophosphate (cGMP) phosphodiesterase inhibitor Zaprinast, suggesting that responses to BK involve increases in cGMP levels.	zaprinast	127-136	kininogen 1	Homo sapiens	167-169
7517646-8	1994	The duration of the response to BK was enhanced by the guanosine 3",5"-cyclic monophosphate (cGMP) phosphodiesterase inhibitor Zaprinast, suggesting that responses to BK involve increases in cGMP levels.	Cyclic GMP	191-195	kininogen 1	Homo sapiens	32-34
7517646-8	1994	The duration of the response to BK was enhanced by the guanosine 3",5"-cyclic monophosphate (cGMP) phosphodiesterase inhibitor Zaprinast, suggesting that responses to BK involve increases in cGMP levels.	Cyclic GMP	191-195	kininogen 1	Homo sapiens	167-169
7517646-9	1994	Responses to BK were enhanced by captopril, indicating that BK is rapidly inactivated by kininase II in the lung.	Captopril	33-42	kininogen 1	Homo sapiens	13-15
7517646-9	1994	Responses to BK were enhanced by captopril, indicating that BK is rapidly inactivated by kininase II in the lung.	Captopril	33-42	kininogen 1	Homo sapiens	60-62
7514511-1	1994	The transient increase in [Ca2+]i in endothelial cells after stimulation with bradykinin can account for the initiation but not the sustained production of nitric oxide (NO).	Nitric Oxide	156-168	kininogen 1	Homo sapiens	78-88
8206638-3	1994	Thus when contracted with KCl, bradykinin-induced relaxation of PCA rings is mediated solely by nitric oxide (NO), whereas when contracted with the thromboxane mimetic U46619, a small component of the relaxation is attributable to NO and a large component is attributable to a non-NO mechanism that is independent of cyclooxygenase activity.	Potassium Chloride	26-29	kininogen 1	Homo sapiens	31-41
8206638-3	1994	Thus when contracted with KCl, bradykinin-induced relaxation of PCA rings is mediated solely by nitric oxide (NO), whereas when contracted with the thromboxane mimetic U46619, a small component of the relaxation is attributable to NO and a large component is attributable to a non-NO mechanism that is independent of cyclooxygenase activity.	Nitric Oxide	96-108	kininogen 1	Homo sapiens	31-41
8206638-3	1994	Thus when contracted with KCl, bradykinin-induced relaxation of PCA rings is mediated solely by nitric oxide (NO), whereas when contracted with the thromboxane mimetic U46619, a small component of the relaxation is attributable to NO and a large component is attributable to a non-NO mechanism that is independent of cyclooxygenase activity.	Thromboxanes	148-159	kininogen 1	Homo sapiens	31-41
8206638-5	1994	Bradykinin-induced relaxations of PCA rings precontracted with U46619 in the presence of indomethacin (10 mumol/L) were moderately attenuated by the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 100 mumol/L), whereas when precontracted with KCl, L-NAME abolished the relaxations.	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	63-69	kininogen 1	Homo sapiens	0-10
8206638-5	1994	Bradykinin-induced relaxations of PCA rings precontracted with U46619 in the presence of indomethacin (10 mumol/L) were moderately attenuated by the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 100 mumol/L), whereas when precontracted with KCl, L-NAME abolished the relaxations.	Indomethacin	89-101	kininogen 1	Homo sapiens	0-10
8206638-5	1994	Bradykinin-induced relaxations of PCA rings precontracted with U46619 in the presence of indomethacin (10 mumol/L) were moderately attenuated by the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 100 mumol/L), whereas when precontracted with KCl, L-NAME abolished the relaxations.	NG-Nitroarginine Methyl Ester	171-208	kininogen 1	Homo sapiens	0-10
8206638-5	1994	Bradykinin-induced relaxations of PCA rings precontracted with U46619 in the presence of indomethacin (10 mumol/L) were moderately attenuated by the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 100 mumol/L), whereas when precontracted with KCl, L-NAME abolished the relaxations.	NG-Nitroarginine Methyl Ester	210-216	kininogen 1	Homo sapiens	0-10
8206638-5	1994	Bradykinin-induced relaxations of PCA rings precontracted with U46619 in the presence of indomethacin (10 mumol/L) were moderately attenuated by the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 100 mumol/L), whereas when precontracted with KCl, L-NAME abolished the relaxations.	Potassium Chloride	264-267	kininogen 1	Homo sapiens	0-10
8206638-5	1994	Bradykinin-induced relaxations of PCA rings precontracted with U46619 in the presence of indomethacin (10 mumol/L) were moderately attenuated by the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 100 mumol/L), whereas when precontracted with KCl, L-NAME abolished the relaxations.	NG-Nitroarginine Methyl Ester	269-275	kininogen 1	Homo sapiens	0-10
8200990-0	1994	Cyclic AMP selectively enhances bradykinin receptor synthesis and expression in cultured arterial smooth muscle.	Cyclic AMP	0-10	kininogen 1	Homo sapiens	32-42
8200990-3	1994	The present study examined the effect of cyclic nucleotides on bradykinin-stimulated responses in cultured arterial smooth muscle cells.	Nucleotides, Cyclic	41-59	kininogen 1	Homo sapiens	63-73
8200990-4	1994	Short term stimulation (1 min) with cyclic AMP produced a variable inhibition of bradykinin-stimulated calcium mobilization which was lost in later passaged cells.	Cyclic AMP	36-46	kininogen 1	Homo sapiens	81-91
8200990-4	1994	Short term stimulation (1 min) with cyclic AMP produced a variable inhibition of bradykinin-stimulated calcium mobilization which was lost in later passaged cells.	Calcium	103-110	kininogen 1	Homo sapiens	81-91
8200990-5	1994	However, long-term stimulation (24 h) produced a consistent increase in bradykinin-stimulated calcium mobilization in both early and late passaged cells.	Calcium	94-101	kininogen 1	Homo sapiens	72-82
8200990-6	1994	Further analysis demonstrated that chronic exposure to cAMP produced a twofold increase in both the number of cell surface bradykinin receptors and in bradykinin-stimulated phosphoinositide hydrolysis.	Cyclic AMP	55-59	kininogen 1	Homo sapiens	123-133
8200990-6	1994	Further analysis demonstrated that chronic exposure to cAMP produced a twofold increase in both the number of cell surface bradykinin receptors and in bradykinin-stimulated phosphoinositide hydrolysis.	Cyclic AMP	55-59	kininogen 1	Homo sapiens	151-161
8200990-7	1994	The increase in bradykinin receptors was time dependent (&gt; 7 h) and blocked by protein synthesis inhibitors, suggesting that cAMP enhanced the synthesis of new bradykinin receptors.	Cyclic AMP	128-132	kininogen 1	Homo sapiens	16-26
8200990-7	1994	The increase in bradykinin receptors was time dependent (&gt; 7 h) and blocked by protein synthesis inhibitors, suggesting that cAMP enhanced the synthesis of new bradykinin receptors.	Cyclic AMP	128-132	kininogen 1	Homo sapiens	163-173
8200990-8	1994	The increase in bradykinin receptor binding and calcium mobilization was also stimulated by cholera toxin, forskolin, and isobutylmethylxanthine, but not isoproterenol or prostaglandin E2.	Colforsin	107-116	kininogen 1	Homo sapiens	16-26
8200990-8	1994	The increase in bradykinin receptor binding and calcium mobilization was also stimulated by cholera toxin, forskolin, and isobutylmethylxanthine, but not isoproterenol or prostaglandin E2.	1-Methyl-3-isobutylxanthine	122-144	kininogen 1	Homo sapiens	16-26
8200990-8	1994	The increase in bradykinin receptor binding and calcium mobilization was also stimulated by cholera toxin, forskolin, and isobutylmethylxanthine, but not isoproterenol or prostaglandin E2.	Isoproterenol	154-167	kininogen 1	Homo sapiens	16-26
8200990-10	1994	In summary, prolonged treatment with cAMP selectively stimulates the synthesis and expression of bradykinin receptors on arterial smooth muscle while decreasing the responsiveness to vasoconstrictor agonists such as angiotensin II and vasopressin.	Cyclic AMP	37-41	kininogen 1	Homo sapiens	97-107
8197121-1	1994	We report the synthesis and in vitro biological activity of the nonpeptide bradykinin receptor antagonist WIN 64338, [[4-[[2-[[bis(cyclohexylamino)methylene]amino]-3-(2- naphthyl)-1-oxopropyl]amino]phenyl]methyl]tributylphosphonium chloride monohydrochloride.	WIN 64338	106-115	kininogen 1	Homo sapiens	75-85
8197121-2	1994	WIN 64338 inhibits [3H]-bradykinin binding to the bradykinin B2 receptor on human IMR-90 cells with a binding inhibition constant (Ki) of 64 +/- 8 nM and demonstrates competitive inhibition of bradykinin-stimulated 45Ca2+ efflux from IMR-90 cells (pA2 = 7.1).	WIN 64338	0-9	kininogen 1	Homo sapiens	24-34
8197121-2	1994	WIN 64338 inhibits [3H]-bradykinin binding to the bradykinin B2 receptor on human IMR-90 cells with a binding inhibition constant (Ki) of 64 +/- 8 nM and demonstrates competitive inhibition of bradykinin-stimulated 45Ca2+ efflux from IMR-90 cells (pA2 = 7.1).	WIN 64338	0-9	kininogen 1	Homo sapiens	50-60
8197121-2	1994	WIN 64338 inhibits [3H]-bradykinin binding to the bradykinin B2 receptor on human IMR-90 cells with a binding inhibition constant (Ki) of 64 +/- 8 nM and demonstrates competitive inhibition of bradykinin-stimulated 45Ca2+ efflux from IMR-90 cells (pA2 = 7.1).	Tritium	20-22	kininogen 1	Homo sapiens	24-34
8197121-2	1994	WIN 64338 inhibits [3H]-bradykinin binding to the bradykinin B2 receptor on human IMR-90 cells with a binding inhibition constant (Ki) of 64 +/- 8 nM and demonstrates competitive inhibition of bradykinin-stimulated 45Ca2+ efflux from IMR-90 cells (pA2 = 7.1).	Tritium	20-22	kininogen 1	Homo sapiens	50-60
8197121-6	1994	Synthesis of WIN 64338 has provided a nonpeptide competitive bradykinin B2 antagonist active in both bradykinin radioligand binding and functional assays.	WIN 64338	13-22	kininogen 1	Homo sapiens	61-71
8197121-6	1994	Synthesis of WIN 64338 has provided a nonpeptide competitive bradykinin B2 antagonist active in both bradykinin radioligand binding and functional assays.	WIN 64338	13-22	kininogen 1	Homo sapiens	101-111
8003621-1	1994	The linear nonapeptide hormone bradykinin (Arg1-Pro2-Pro3-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9) is involved, either directly or indirectly, in a wide variety of physiological processes, particularly pain and hyperanalgesia.	ser6-pro7	68-77	kininogen 1	Homo sapiens	31-41
8003621-4	1994	The beta-turn forming potential of bradykinin in three vastly different local chemical environments, DMSO, 9:1 dioxane/water, and in the presence of 7.4 mM lyso phosphatidylcholine micelles, was investigated using two-dimensional homonuclear nmr experiments coupled with simulated annealing calculations.	Dimethyl Sulfoxide	101-105	kininogen 1	Homo sapiens	35-45
8003621-4	1994	The beta-turn forming potential of bradykinin in three vastly different local chemical environments, DMSO, 9:1 dioxane/water, and in the presence of 7.4 mM lyso phosphatidylcholine micelles, was investigated using two-dimensional homonuclear nmr experiments coupled with simulated annealing calculations.	1,4-dioxane	111-118	kininogen 1	Homo sapiens	35-45
8003621-4	1994	The beta-turn forming potential of bradykinin in three vastly different local chemical environments, DMSO, 9:1 dioxane/water, and in the presence of 7.4 mM lyso phosphatidylcholine micelles, was investigated using two-dimensional homonuclear nmr experiments coupled with simulated annealing calculations.	Water	119-124	kininogen 1	Homo sapiens	35-45
8003621-4	1994	The beta-turn forming potential of bradykinin in three vastly different local chemical environments, DMSO, 9:1 dioxane/water, and in the presence of 7.4 mM lyso phosphatidylcholine micelles, was investigated using two-dimensional homonuclear nmr experiments coupled with simulated annealing calculations.	Lysophosphatidylcholines	156-180	kininogen 1	Homo sapiens	35-45
7926636-0	1994	Generation of [Ala1,Thr6]bradykinin in the plasma of a snake, the reticulated python.	[ala1,thr6	14-24	kininogen 1	Homo sapiens	25-35
7926636-2	1994	The primary structure of python bradykinin was established as Ala-Pro-Pro-Gly-Phe-Thr-Pro-Phe-Arg.	Ala-Pro-Pro-Gly-Phe-Thr-Pro-Phe-Arg	62-97	kininogen 1	Homo sapiens	32-42
7926636-3	1994	This amino acid sequence contains two substitutions (Arg1--&gt;Ala and Ser6--&gt;Thr) compared with mammalian bradykinin.	Threonine	81-84	kininogen 1	Homo sapiens	110-120
8016771-0	1994	Effect of inhaled frusemide on responses of airways to bradykinin and adenosine 5"-monophosphate in asthma.	Furosemide	18-27	kininogen 1	Homo sapiens	55-65
8016771-3	1994	The effect of inhaled frusemide on bronchoconstriction induced by inhaled bradykinin, which is thought to cause bronchoconstriction via neural mechanisms, was studied and compared with the effects of adenosine 5"-monophosphate (AMP) which probably produces its airway effects by augmenting mast cell mediator release and interfering with neural pathways.	Furosemide	22-31	kininogen 1	Homo sapiens	74-84
8016771-8	1994	There was a significant correlation between baseline AMP and bradykinin PC20 values.	Adenosine Monophosphate	53-56	kininogen 1	Homo sapiens	61-71
8016771-10	1994	For bradykinin the geometric mean PC20 values following pretreatment with inhaled frusemide and matched placebo were 13.22 (2.53- &gt; 16.0) and 2.52 (0.45-5.61) mg/ml respectively (95% CI 0.43 to 1.01).	Furosemide	82-91	kininogen 1	Homo sapiens	4-14
8016771-11	1994	Frusemide afforded 5.45 and 5.24 fold protection against AMP and bradykinin-induced bronchoconstriction respectively.	Furosemide	0-9	kininogen 1	Homo sapiens	65-75
8032609-4	1994	The binding of [3H]-bradykinin to healthy lung membrane is time-dependent and saturable with a KD value of 1.08 +/- 08 nM and a Bmax value of 46.1 +/- 3.1 fmol mg-1 protein (n = 10).	Tritium	16-18	kininogen 1	Homo sapiens	20-30
8032609-8	1994	In both healthy and squamous-carcinoma preparations, bradykinin analogues displace [3H]-bradykinin binding with the following relative order of potency: Hoe 140 &gt; bradykinin &gt; kallidin &gt; D-Arg0[Hyp3,D-Phe7]bradykinin &gt;&gt;&gt; des-Arg9-bradykinin.	Tritium	84-86	kininogen 1	Homo sapiens	53-63
8032609-8	1994	In both healthy and squamous-carcinoma preparations, bradykinin analogues displace [3H]-bradykinin binding with the following relative order of potency: Hoe 140 &gt; bradykinin &gt; kallidin &gt; D-Arg0[Hyp3,D-Phe7]bradykinin &gt;&gt;&gt; des-Arg9-bradykinin.	Tritium	84-86	kininogen 1	Homo sapiens	88-98
8032609-8	1994	In both healthy and squamous-carcinoma preparations, bradykinin analogues displace [3H]-bradykinin binding with the following relative order of potency: Hoe 140 &gt; bradykinin &gt; kallidin &gt; D-Arg0[Hyp3,D-Phe7]bradykinin &gt;&gt;&gt; des-Arg9-bradykinin.	Tritium	84-86	kininogen 1	Homo sapiens	88-98
8032609-8	1994	In both healthy and squamous-carcinoma preparations, bradykinin analogues displace [3H]-bradykinin binding with the following relative order of potency: Hoe 140 &gt; bradykinin &gt; kallidin &gt; D-Arg0[Hyp3,D-Phe7]bradykinin &gt;&gt;&gt; des-Arg9-bradykinin.	Tritium	84-86	kininogen 1	Homo sapiens	88-98
8032609-8	1994	In both healthy and squamous-carcinoma preparations, bradykinin analogues displace [3H]-bradykinin binding with the following relative order of potency: Hoe 140 &gt; bradykinin &gt; kallidin &gt; D-Arg0[Hyp3,D-Phe7]bradykinin &gt;&gt;&gt; des-Arg9-bradykinin.	Tritium	84-86	kininogen 1	Homo sapiens	88-98
8032609-8	1994	In both healthy and squamous-carcinoma preparations, bradykinin analogues displace [3H]-bradykinin binding with the following relative order of potency: Hoe 140 &gt; bradykinin &gt; kallidin &gt; D-Arg0[Hyp3,D-Phe7]bradykinin &gt;&gt;&gt; des-Arg9-bradykinin.	d-arg0	196-202	kininogen 1	Homo sapiens	53-63
8032609-8	1994	In both healthy and squamous-carcinoma preparations, bradykinin analogues displace [3H]-bradykinin binding with the following relative order of potency: Hoe 140 &gt; bradykinin &gt; kallidin &gt; D-Arg0[Hyp3,D-Phe7]bradykinin &gt;&gt;&gt; des-Arg9-bradykinin.	-phe7	209-214	kininogen 1	Homo sapiens	53-63
8032609-9	1994	Of the analogues used, bradykinin and D-Arg0[Hyp3,D-Phe7]bradykinin appear to be able to differentiate the bradykinin receptors present in both preparations.	d-arg0	38-44	kininogen 1	Homo sapiens	57-67
8032609-9	1994	Of the analogues used, bradykinin and D-Arg0[Hyp3,D-Phe7]bradykinin appear to be able to differentiate the bradykinin receptors present in both preparations.	d-arg0	38-44	kininogen 1	Homo sapiens	57-67
8032622-2	1994	The B2 kinin receptor antagonist, [D-Arg0,Hyp3,Thi5,D-Tic7,Oic8]-bradykinin (Hoe 140), 200 micrograms administered by intranasal aerosol 2 min prior to challenge with HDM, 500 u significantly reduced nasal blockage induced by the antigen challenge.	thi5	47-51	kininogen 1	Homo sapiens	65-75
8144509-4	1994	Proteolytic cleavage in domain 4 to release bradykinin causes a conformational change, exposing a surface-binding region (domain 5) on the disulfide-linked light chain.	Disulfides	139-148	kininogen 1	Homo sapiens	44-54
8130263-0	1994	Differential role of extra- and intracellular calcium in bradykinin and interleukin 1 alpha stimulation of arachidonic acid release from A549 cells.	Calcium	46-53	kininogen 1	Homo sapiens	57-67
8130263-1	1994	The release of arachidonic acid in A549 cells was stimulated in a time- and dose-dependent manner by the Ca2+ ionophore ionomycin (t1/2 = 4 min), thapsigargin (t1/2 = 8 min), bradykinin (t1/2 = 12 min, EC50 = 3 nM), and interleukin 1 alpha (t1/2 = 28 min, EC50 = 0.3 ng/ml).	Arachidonic Acid	15-31	kininogen 1	Homo sapiens	175-185
8130263-1	1994	The release of arachidonic acid in A549 cells was stimulated in a time- and dose-dependent manner by the Ca2+ ionophore ionomycin (t1/2 = 4 min), thapsigargin (t1/2 = 8 min), bradykinin (t1/2 = 12 min, EC50 = 3 nM), and interleukin 1 alpha (t1/2 = 28 min, EC50 = 0.3 ng/ml).	Ionomycin	120-129	kininogen 1	Homo sapiens	175-185
8130263-1	1994	The release of arachidonic acid in A549 cells was stimulated in a time- and dose-dependent manner by the Ca2+ ionophore ionomycin (t1/2 = 4 min), thapsigargin (t1/2 = 8 min), bradykinin (t1/2 = 12 min, EC50 = 3 nM), and interleukin 1 alpha (t1/2 = 28 min, EC50 = 0.3 ng/ml).	Thapsigargin	146-158	kininogen 1	Homo sapiens	175-185
8130263-2	1994	Bradykinin (10 nM) and interleukin 1 alpha (1 ng/ml) stimulation was blocked by the bradykinin B2 receptor antagonist, D-Arg,[Hyp3,Thi5,8, D-Phe7]bradykinin and interleukin 1 receptor antagonist (IC50 = 30 mM and 20 ng/ml, respectively), suggesting receptor mediation.	D-Arginine	119-124	kininogen 1	Homo sapiens	0-10
8130263-2	1994	Bradykinin (10 nM) and interleukin 1 alpha (1 ng/ml) stimulation was blocked by the bradykinin B2 receptor antagonist, D-Arg,[Hyp3,Thi5,8, D-Phe7]bradykinin and interleukin 1 receptor antagonist (IC50 = 30 mM and 20 ng/ml, respectively), suggesting receptor mediation.	D-Arginine	119-124	kininogen 1	Homo sapiens	84-94
8130263-2	1994	Bradykinin (10 nM) and interleukin 1 alpha (1 ng/ml) stimulation was blocked by the bradykinin B2 receptor antagonist, D-Arg,[Hyp3,Thi5,8, D-Phe7]bradykinin and interleukin 1 receptor antagonist (IC50 = 30 mM and 20 ng/ml, respectively), suggesting receptor mediation.	D-Arginine	119-124	kininogen 1	Homo sapiens	146-156
8130263-2	1994	Bradykinin (10 nM) and interleukin 1 alpha (1 ng/ml) stimulation was blocked by the bradykinin B2 receptor antagonist, D-Arg,[Hyp3,Thi5,8, D-Phe7]bradykinin and interleukin 1 receptor antagonist (IC50 = 30 mM and 20 ng/ml, respectively), suggesting receptor mediation.	thi5	131-135	kininogen 1	Homo sapiens	0-10
8130263-2	1994	Bradykinin (10 nM) and interleukin 1 alpha (1 ng/ml) stimulation was blocked by the bradykinin B2 receptor antagonist, D-Arg,[Hyp3,Thi5,8, D-Phe7]bradykinin and interleukin 1 receptor antagonist (IC50 = 30 mM and 20 ng/ml, respectively), suggesting receptor mediation.	thi5	131-135	kininogen 1	Homo sapiens	84-94
8130263-6	1994	However, the presence of EGTA completely abolished bradykinin stimulation and partially blocked the effect of interleukin 1 alpha (43% inhibition).	Egtazic Acid	25-29	kininogen 1	Homo sapiens	51-61
8130263-7	1994	In the presence of extracellular Ca2+, ionomycin (3 mM), thapsigargin (0.3 mM), bradykinin (10 nM), and interleukin 1 alpha (1 ng/ml) stimulation of arachidonic acid release was blocked by the Ca2+ influx blocker LaCl3 (29, 44, 35, and 41% inhibition, respectively).	Arachidonic Acid	149-165	kininogen 1	Homo sapiens	80-90
8132619-1	1994	Neuropeptide Y (NPY) attenuated angiotensin II (AII)-or bradykinin (BK)-induced Ca2+ release from intracellular stores and inhibited forskolin-stimulated cAMP accumulation and omega-conotoxin-sensitive high K(+)-induced Ca2+ influx in the human neuroblastoma cell line SMS-KAN. All three NPY actions were mediated via Y2 receptors.	Cyclic AMP	154-158	kininogen 1	Homo sapiens	56-66
8132619-5	1994	NPY attenuated AII- or BK-induced inositol 1,4,5-trisphosphate production, and herbimycin A reversed this NPY effect.	Inositol 1,4,5-Trisphosphate	34-62	kininogen 1	Homo sapiens	23-25
8132619-6	1994	These results provide the first evidence that Y2 receptors negatively couple to AII- or BK-induced phosphoinositide turnover leading to Ca2+ mobilization through pertussis toxin-sensitive GTP-binding protein(s).	Phosphatidylinositols	99-115	kininogen 1	Homo sapiens	88-90
7516884-8	1994	The similarity in the inhibitory effects of N omega-nitro-L-arginine methyl ester and N omega-nitro-L-arginine on responses to acetylcholine, bradykinin, and substance P suggest that the L-arginine analog, N omega-nitro-L-arginine, as well as the methyl ester of N omega-nitro-L-arginine, are useful probes for studying endothelium-dependent vasodilator responses in the mesenteric vascular bed of the cat.	NG-Nitroarginine Methyl Ester	44-81	kininogen 1	Homo sapiens	142-152
7516884-8	1994	The similarity in the inhibitory effects of N omega-nitro-L-arginine methyl ester and N omega-nitro-L-arginine on responses to acetylcholine, bradykinin, and substance P suggest that the L-arginine analog, N omega-nitro-L-arginine, as well as the methyl ester of N omega-nitro-L-arginine, are useful probes for studying endothelium-dependent vasodilator responses in the mesenteric vascular bed of the cat.	Nitroarginine	44-68	kininogen 1	Homo sapiens	142-152
7516884-8	1994	The similarity in the inhibitory effects of N omega-nitro-L-arginine methyl ester and N omega-nitro-L-arginine on responses to acetylcholine, bradykinin, and substance P suggest that the L-arginine analog, N omega-nitro-L-arginine, as well as the methyl ester of N omega-nitro-L-arginine, are useful probes for studying endothelium-dependent vasodilator responses in the mesenteric vascular bed of the cat.	Arginine	58-68	kininogen 1	Homo sapiens	142-152
7516884-8	1994	The similarity in the inhibitory effects of N omega-nitro-L-arginine methyl ester and N omega-nitro-L-arginine on responses to acetylcholine, bradykinin, and substance P suggest that the L-arginine analog, N omega-nitro-L-arginine, as well as the methyl ester of N omega-nitro-L-arginine, are useful probes for studying endothelium-dependent vasodilator responses in the mesenteric vascular bed of the cat.	Nitroarginine	86-110	kininogen 1	Homo sapiens	142-152
7516884-8	1994	The similarity in the inhibitory effects of N omega-nitro-L-arginine methyl ester and N omega-nitro-L-arginine on responses to acetylcholine, bradykinin, and substance P suggest that the L-arginine analog, N omega-nitro-L-arginine, as well as the methyl ester of N omega-nitro-L-arginine, are useful probes for studying endothelium-dependent vasodilator responses in the mesenteric vascular bed of the cat.	Nitroarginine	86-110	kininogen 1	Homo sapiens	142-152
8117696-0	1994	Synthesis, characterization, and conformational analysis of the D/L-Tic7 stereoisomers of the bradykinin receptor antagonist D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin.	d-arg0	125-131	kininogen 1	Homo sapiens	94-104
8117696-0	1994	Synthesis, characterization, and conformational analysis of the D/L-Tic7 stereoisomers of the bradykinin receptor antagonist D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin.	d-arg0	125-131	kininogen 1	Homo sapiens	154-164
8117696-0	1994	Synthesis, characterization, and conformational analysis of the D/L-Tic7 stereoisomers of the bradykinin receptor antagonist D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin.	thi5	137-141	kininogen 1	Homo sapiens	94-104
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	d-arg0	0-6	kininogen 1	Homo sapiens	29-39
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	d-arg0	0-6	kininogen 1	Homo sapiens	94-104
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	d-arg0	0-6	kininogen 1	Homo sapiens	94-104
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	thi5	12-16	kininogen 1	Homo sapiens	29-39
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	thi5	12-16	kininogen 1	Homo sapiens	94-104
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	thi5	12-16	kininogen 1	Homo sapiens	94-104
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	oic8	24-28	kininogen 1	Homo sapiens	29-39
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	oic8	24-28	kininogen 1	Homo sapiens	94-104
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	oic8	24-28	kininogen 1	Homo sapiens	94-104
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	Tritium	91-93	kininogen 1	Homo sapiens	29-39
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	Tritium	91-93	kininogen 1	Homo sapiens	94-104
8117696-1	1994	D-Arg0[Hyp3,Thi5,D-Tic7,Oic8]bradykinin (HOE-140) is a potent (Ki = 0.11 nM) inhibitor of [3H]bradykinin binding to bradykinin B2 receptors found on human IMR-90 fetal lung fibroblasts.	Tritium	91-93	kininogen 1	Homo sapiens	94-104
8117696-5	1994	This is the first documentation of bradykinin binding and functional antagonist activity by a bradykinin peptide analogue with an L amino acid replacing Pro7.	Amino Acids	130-142	kininogen 1	Homo sapiens	35-45
8062861-0	1994	Bradykinin and thrombin stimulate release of arachidonic acid and formation of prostanoids in human periodontal ligament cells.	Arachidonic Acid	45-61	kininogen 1	Homo sapiens	0-10
8062861-0	1994	Bradykinin and thrombin stimulate release of arachidonic acid and formation of prostanoids in human periodontal ligament cells.	Prostaglandins	79-90	kininogen 1	Homo sapiens	0-10
8062861-3	1994	In the present study, the effect of bradykinin (BK) and thrombin, two inflammatory mediators, on prostanoid biosynthesis in human PDL-cells was investigated.	Prostaglandins	97-107	kininogen 1	Homo sapiens	36-46
8062861-3	1994	In the present study, the effect of bradykinin (BK) and thrombin, two inflammatory mediators, on prostanoid biosynthesis in human PDL-cells was investigated.	Prostaglandins	97-107	kininogen 1	Homo sapiens	48-50
8062861-4	1994	BK and thrombin caused a time-dependent burst of prostaglandin E2 (PGE2) formation (maximal effect after 2-5 min).	Dinoprostone	49-65	kininogen 1	Homo sapiens	0-2
8062861-4	1994	BK and thrombin caused a time-dependent burst of prostaglandin E2 (PGE2) formation (maximal effect after 2-5 min).	Dinoprostone	67-71	kininogen 1	Homo sapiens	0-2
8062861-5	1994	The stimulatory actions of BK and thrombin on PGE2 biosynthesis were dose-dependent; seen in PDL-cells isolated from four different patients and abolished by the non-steroidal anti-inflammatory drug indomethacin.	Dinoprostone	46-50	kininogen 1	Homo sapiens	27-29
8062861-5	1994	The stimulatory actions of BK and thrombin on PGE2 biosynthesis were dose-dependent; seen in PDL-cells isolated from four different patients and abolished by the non-steroidal anti-inflammatory drug indomethacin.	Indomethacin	199-211	kininogen 1	Homo sapiens	27-29
8062861-6	1994	BK and thrombin also dose-dependently stimulated the biosynthesis of PGI2.	Epoprostenol	69-73	kininogen 1	Homo sapiens	0-2
8062861-7	1994	BK agonists, with affinity to the B2 subtype of BK receptors, caused a significant increase of PGE2 biosynthesis in human PDL-cells.	Dinoprostone	95-99	kininogen 1	Homo sapiens	0-2
8062861-9	1994	BK and BK-B2 receptor agonists as well as thrombin, but not BK-B1 receptor agonists, also significantly increased [3H] release in human PDL-cells prelabelled with [3H]-arachidonic acid, indicating that BK and thrombin stimulate prostanoid biosynthesis, at least partly, due to activation of phospholipase A2.	Tritium	115-117	kininogen 1	Homo sapiens	0-2
8062861-9	1994	BK and BK-B2 receptor agonists as well as thrombin, but not BK-B1 receptor agonists, also significantly increased [3H] release in human PDL-cells prelabelled with [3H]-arachidonic acid, indicating that BK and thrombin stimulate prostanoid biosynthesis, at least partly, due to activation of phospholipase A2.	Tritium	115-117	kininogen 1	Homo sapiens	7-9
8062861-9	1994	BK and BK-B2 receptor agonists as well as thrombin, but not BK-B1 receptor agonists, also significantly increased [3H] release in human PDL-cells prelabelled with [3H]-arachidonic acid, indicating that BK and thrombin stimulate prostanoid biosynthesis, at least partly, due to activation of phospholipase A2.	Tritium	164-166	kininogen 1	Homo sapiens	0-2
8062861-9	1994	BK and BK-B2 receptor agonists as well as thrombin, but not BK-B1 receptor agonists, also significantly increased [3H] release in human PDL-cells prelabelled with [3H]-arachidonic acid, indicating that BK and thrombin stimulate prostanoid biosynthesis, at least partly, due to activation of phospholipase A2.	Tritium	164-166	kininogen 1	Homo sapiens	7-9
8062861-9	1994	BK and BK-B2 receptor agonists as well as thrombin, but not BK-B1 receptor agonists, also significantly increased [3H] release in human PDL-cells prelabelled with [3H]-arachidonic acid, indicating that BK and thrombin stimulate prostanoid biosynthesis, at least partly, due to activation of phospholipase A2.	Arachidonic Acid	168-184	kininogen 1	Homo sapiens	0-2
8062861-9	1994	BK and BK-B2 receptor agonists as well as thrombin, but not BK-B1 receptor agonists, also significantly increased [3H] release in human PDL-cells prelabelled with [3H]-arachidonic acid, indicating that BK and thrombin stimulate prostanoid biosynthesis, at least partly, due to activation of phospholipase A2.	Arachidonic Acid	168-184	kininogen 1	Homo sapiens	7-9
8062861-9	1994	BK and BK-B2 receptor agonists as well as thrombin, but not BK-B1 receptor agonists, also significantly increased [3H] release in human PDL-cells prelabelled with [3H]-arachidonic acid, indicating that BK and thrombin stimulate prostanoid biosynthesis, at least partly, due to activation of phospholipase A2.	Prostaglandins	228-238	kininogen 1	Homo sapiens	0-2
8062861-9	1994	BK and BK-B2 receptor agonists as well as thrombin, but not BK-B1 receptor agonists, also significantly increased [3H] release in human PDL-cells prelabelled with [3H]-arachidonic acid, indicating that BK and thrombin stimulate prostanoid biosynthesis, at least partly, due to activation of phospholipase A2.	Prostaglandins	228-238	kininogen 1	Homo sapiens	7-9
8176221-0	1994	IL-1 beta amplifies bradykinin-induced prostaglandin E2 production via a phospholipase D-linked mechanism.	Dinoprostone	39-55	kininogen 1	Homo sapiens	20-30
8176221-3	1994	Stimulation of synoviocytes with only BK elicited a rapid increase in inositol phosphates and a concomitant accumulation of diacylglycerol (DAG), monoacylglycerol, and free arachidonic acid (AA).	Inositol Phosphates	70-89	kininogen 1	Homo sapiens	38-40
8176221-3	1994	Stimulation of synoviocytes with only BK elicited a rapid increase in inositol phosphates and a concomitant accumulation of diacylglycerol (DAG), monoacylglycerol, and free arachidonic acid (AA).	Diglycerides	124-138	kininogen 1	Homo sapiens	38-40
8176221-3	1994	Stimulation of synoviocytes with only BK elicited a rapid increase in inositol phosphates and a concomitant accumulation of diacylglycerol (DAG), monoacylglycerol, and free arachidonic acid (AA).	Diglycerides	140-143	kininogen 1	Homo sapiens	38-40
8176221-3	1994	Stimulation of synoviocytes with only BK elicited a rapid increase in inositol phosphates and a concomitant accumulation of diacylglycerol (DAG), monoacylglycerol, and free arachidonic acid (AA).	Monoglycerides	146-162	kininogen 1	Homo sapiens	38-40
8176221-3	1994	Stimulation of synoviocytes with only BK elicited a rapid increase in inositol phosphates and a concomitant accumulation of diacylglycerol (DAG), monoacylglycerol, and free arachidonic acid (AA).	Arachidonic Acid	173-189	kininogen 1	Homo sapiens	38-40
8176221-5	1994	Thus, BK can induce AA release via the hydrolysis of phosphatidylinositols by a phospholipase C (PLC).	Phosphatidylinositols	53-74	kininogen 1	Homo sapiens	6-8
8176221-6	1994	BK also activated a phospholipase D (PLD) to cleave phosphatidylcholine (PC), because it caused an increase in phosphatidic acid (PA) content and a sustained DAG formation, which both were inhibited by ethanol in [3H]myristic acid-labeled cells.	Phosphatidylcholines	52-71	kininogen 1	Homo sapiens	0-2
8176221-6	1994	BK also activated a phospholipase D (PLD) to cleave phosphatidylcholine (PC), because it caused an increase in phosphatidic acid (PA) content and a sustained DAG formation, which both were inhibited by ethanol in [3H]myristic acid-labeled cells.	Phosphatidylcholines	73-75	kininogen 1	Homo sapiens	0-2
8176221-6	1994	BK also activated a phospholipase D (PLD) to cleave phosphatidylcholine (PC), because it caused an increase in phosphatidic acid (PA) content and a sustained DAG formation, which both were inhibited by ethanol in [3H]myristic acid-labeled cells.	Phosphatidic Acids	111-128	kininogen 1	Homo sapiens	0-2
8176221-6	1994	BK also activated a phospholipase D (PLD) to cleave phosphatidylcholine (PC), because it caused an increase in phosphatidic acid (PA) content and a sustained DAG formation, which both were inhibited by ethanol in [3H]myristic acid-labeled cells.	Phosphatidic Acids	130-132	kininogen 1	Homo sapiens	0-2
8176221-6	1994	BK also activated a phospholipase D (PLD) to cleave phosphatidylcholine (PC), because it caused an increase in phosphatidic acid (PA) content and a sustained DAG formation, which both were inhibited by ethanol in [3H]myristic acid-labeled cells.	Diglycerides	158-161	kininogen 1	Homo sapiens	0-2
8176221-6	1994	BK also activated a phospholipase D (PLD) to cleave phosphatidylcholine (PC), because it caused an increase in phosphatidic acid (PA) content and a sustained DAG formation, which both were inhibited by ethanol in [3H]myristic acid-labeled cells.	Ethanol	202-209	kininogen 1	Homo sapiens	0-2
8176221-6	1994	BK also activated a phospholipase D (PLD) to cleave phosphatidylcholine (PC), because it caused an increase in phosphatidic acid (PA) content and a sustained DAG formation, which both were inhibited by ethanol in [3H]myristic acid-labeled cells.	Tritium	214-216	kininogen 1	Homo sapiens	0-2
8176221-6	1994	BK also activated a phospholipase D (PLD) to cleave phosphatidylcholine (PC), because it caused an increase in phosphatidic acid (PA) content and a sustained DAG formation, which both were inhibited by ethanol in [3H]myristic acid-labeled cells.	Myristic Acid	217-230	kininogen 1	Homo sapiens	0-2
8176221-8	1994	Priming of synovial cells with rIL-1 beta 24 h before exposure to BK in the presence of ethanol further enhanced the BK-induced formation of PEt.	Ethanol	88-95	kininogen 1	Homo sapiens	66-68
8176221-8	1994	Priming of synovial cells with rIL-1 beta 24 h before exposure to BK in the presence of ethanol further enhanced the BK-induced formation of PEt.	Ethanol	88-95	kininogen 1	Homo sapiens	117-119
8176221-10	1994	Finally, we demonstrated that the IL-1-mediated amplification of PGE2 release in response to BK was reduced by the presence of ethanol in the culture medium, suggesting that part of the synergistic action of IL-1 and BK on prostanoid production was dependent on the activation of the PC-specific PLD pathway.	Dinoprostone	65-69	kininogen 1	Homo sapiens	93-95
8176221-10	1994	Finally, we demonstrated that the IL-1-mediated amplification of PGE2 release in response to BK was reduced by the presence of ethanol in the culture medium, suggesting that part of the synergistic action of IL-1 and BK on prostanoid production was dependent on the activation of the PC-specific PLD pathway.	Ethanol	127-134	kininogen 1	Homo sapiens	93-95
8176221-10	1994	Finally, we demonstrated that the IL-1-mediated amplification of PGE2 release in response to BK was reduced by the presence of ethanol in the culture medium, suggesting that part of the synergistic action of IL-1 and BK on prostanoid production was dependent on the activation of the PC-specific PLD pathway.	Prostaglandins	223-233	kininogen 1	Homo sapiens	93-95
8073865-4	1994	The nasal and oropharyngeal challenges were separated by 1 week and 1 mg of bradykinin dissolved in 10% ethanol in 0.9% saline was administered as a spray to both nasal passages or to the posterior oropharyngeal wall and tonsillar fauces.	Sodium Chloride	120-126	kininogen 1	Homo sapiens	76-86
7919134-4	1994	When Bk was added to cocultures in the presence of meclofenamate (10(-5) M), Isc decreased from 62 +/- 12 to 44.5 +/- 7 muA/cm2, not significantly different from that in the absence of meclofenamate.	Meclofenamic Acid	51-64	kininogen 1	Homo sapiens	5-7
7919134-4	1994	When Bk was added to cocultures in the presence of meclofenamate (10(-5) M), Isc decreased from 62 +/- 12 to 44.5 +/- 7 muA/cm2, not significantly different from that in the absence of meclofenamate.	Meclofenamic Acid	185-198	kininogen 1	Homo sapiens	5-7
8016771-12	1994	Furthermore, there was a significant correlation between protection afforded to the airways against AMP and bradykinin.	Adenosine Monophosphate	100-103	kininogen 1	Homo sapiens	108-118
8016771-13	1994	CONCLUSIONS: These data suggest that inhaled frusemide affords protection against bradykinin-induced bronchoconstriction which is comparable to that against AMP, supporting a common mechanism of action for frusemide.	Furosemide	45-54	kininogen 1	Homo sapiens	82-92
8167144-0	1994	Bradykinin stimulates fructose 2,6-bisphosphate metabolism in human fibroblasts.	Fructose	22-30	kininogen 1	Homo sapiens	0-10
8167144-0	1994	Bradykinin stimulates fructose 2,6-bisphosphate metabolism in human fibroblasts.	2,6-bisphosphate	31-47	kininogen 1	Homo sapiens	0-10
8167144-1	1994	Bradykinin (BK), a peptide released during inflammatory response, has been investigated for its ability to regulate glucose metabolism in human fibroblasts.	Glucose	116-123	kininogen 1	Homo sapiens	0-10
8167144-1	1994	Bradykinin (BK), a peptide released during inflammatory response, has been investigated for its ability to regulate glucose metabolism in human fibroblasts.	Glucose	116-123	kininogen 1	Homo sapiens	12-14
8167144-3	1994	The strict relationship between the glycolytic rate and the levels of fructose 2,6-bisphosphate (Fru-2,6-P2) strongly suggests that the metabolite plays a key role in the regulation of glucose metabolism by bradykinin.	fructose 2,6-diphosphate	70-95	kininogen 1	Homo sapiens	207-217
8167144-3	1994	The strict relationship between the glycolytic rate and the levels of fructose 2,6-bisphosphate (Fru-2,6-P2) strongly suggests that the metabolite plays a key role in the regulation of glucose metabolism by bradykinin.	fru-2,6-p2	97-107	kininogen 1	Homo sapiens	207-217
8167144-3	1994	The strict relationship between the glycolytic rate and the levels of fructose 2,6-bisphosphate (Fru-2,6-P2) strongly suggests that the metabolite plays a key role in the regulation of glucose metabolism by bradykinin.	Glucose	185-192	kininogen 1	Homo sapiens	207-217
8167144-4	1994	The mechanism by which bradykinin increases Fru-2,6-P2 content involves the activation of 6-phosphofructo-2-kinase (PFK-2), the enzyme responsible for the synthesis of the metabolite.	fru-2,6-p2	44-54	kininogen 1	Homo sapiens	23-33
8117696-5	1994	This is the first documentation of bradykinin binding and functional antagonist activity by a bradykinin peptide analogue with an L amino acid replacing Pro7.	Amino Acids	130-142	kininogen 1	Homo sapiens	94-104
8174845-4	1994	In comparison, intravenous administration of an active metabolite of delapril (3.0 mmol.kg-1) and oral administration of either delapril or enalapril (5.0 mmol.kg-1) showed slight, but not significant increases in insulin sensitivity indices and plasma bradykinin concentrations.	delapril	69-77	kininogen 1	Homo sapiens	253-263
8185716-1	1994	By the mediation of receptors in the endothelium, bradykinin, histamine, and thrombin--besides platelet-derived substances such as adenosine diphosphate and triphosphate (ADP, ATP) and serotonin--play an essential physiological role in the activation of the protective metabolic process in the endothelium, which is so important to vessel dilatation.	Adenosine Diphosphate	131-152	kininogen 1	Homo sapiens	50-60
8185716-1	1994	By the mediation of receptors in the endothelium, bradykinin, histamine, and thrombin--besides platelet-derived substances such as adenosine diphosphate and triphosphate (ADP, ATP) and serotonin--play an essential physiological role in the activation of the protective metabolic process in the endothelium, which is so important to vessel dilatation.	triphosphoric acid	157-169	kininogen 1	Homo sapiens	50-60
8185716-1	1994	By the mediation of receptors in the endothelium, bradykinin, histamine, and thrombin--besides platelet-derived substances such as adenosine diphosphate and triphosphate (ADP, ATP) and serotonin--play an essential physiological role in the activation of the protective metabolic process in the endothelium, which is so important to vessel dilatation.	Adenosine Triphosphate	176-179	kininogen 1	Homo sapiens	50-60
8185716-1	1994	By the mediation of receptors in the endothelium, bradykinin, histamine, and thrombin--besides platelet-derived substances such as adenosine diphosphate and triphosphate (ADP, ATP) and serotonin--play an essential physiological role in the activation of the protective metabolic process in the endothelium, which is so important to vessel dilatation.	Serotonin	185-194	kininogen 1	Homo sapiens	50-60
8174845-4	1994	In comparison, intravenous administration of an active metabolite of delapril (3.0 mmol.kg-1) and oral administration of either delapril or enalapril (5.0 mmol.kg-1) showed slight, but not significant increases in insulin sensitivity indices and plasma bradykinin concentrations.	Enalapril	140-149	kininogen 1	Homo sapiens	253-263
8174845-5	1994	Infusion of a bradykinin antagonist (N-alpha-adamantane-acetyl-D-Arg-[Hyp3,Thi5,8,D-Phe7]-b bradykinin) (0.5 nmol.kg-1 x min-1) abolished the effect of captopril on insulin sensitivity.	n-alpha-adamantane-acetyl-d-arg	37-68	kininogen 1	Homo sapiens	14-24
8174845-5	1994	Infusion of a bradykinin antagonist (N-alpha-adamantane-acetyl-D-Arg-[Hyp3,Thi5,8,D-Phe7]-b bradykinin) (0.5 nmol.kg-1 x min-1) abolished the effect of captopril on insulin sensitivity.	n-alpha-adamantane-acetyl-d-arg	37-68	kininogen 1	Homo sapiens	92-102
8174845-5	1994	Infusion of a bradykinin antagonist (N-alpha-adamantane-acetyl-D-Arg-[Hyp3,Thi5,8,D-Phe7]-b bradykinin) (0.5 nmol.kg-1 x min-1) abolished the effect of captopril on insulin sensitivity.	thi5	75-79	kininogen 1	Homo sapiens	14-24
8174845-5	1994	Infusion of a bradykinin antagonist (N-alpha-adamantane-acetyl-D-Arg-[Hyp3,Thi5,8,D-Phe7]-b bradykinin) (0.5 nmol.kg-1 x min-1) abolished the effect of captopril on insulin sensitivity.	,d-phe7	81-88	kininogen 1	Homo sapiens	14-24
8174845-5	1994	Infusion of a bradykinin antagonist (N-alpha-adamantane-acetyl-D-Arg-[Hyp3,Thi5,8,D-Phe7]-b bradykinin) (0.5 nmol.kg-1 x min-1) abolished the effect of captopril on insulin sensitivity.	,d-phe7	81-88	kininogen 1	Homo sapiens	92-102
8174845-8	1994	In these four groups, oral administration of captopril (2.0 mmol.kg-1) significantly increased insulin sensitivity indices, and a concomitant increase in plasma bradykinin concentrations was observed.	Captopril	45-54	kininogen 1	Homo sapiens	161-171
7515129-6	1994	L-NMMA and ADMA inhibited endothelium-dependent relaxations (EC50 = 4.7 +/- 1.1 microM and 17.9 +/- 4.9 microM, respectively); methylguanidine caused endothelium-independent contractions and reversed the relaxations to bradykinin and sodium nitroprusside (EC50 &gt; 100 microM); aminoguanidine was without effect.	omega-N-Methylarginine	0-6	kininogen 1	Homo sapiens	219-229
8175303-3	1994	METHODS: Behavioral pain responses and histologic alterations of the arteries were determined after intrafemoral injection of bradykinin to saline- or CM-pretreated rats.	Sodium Chloride	140-146	kininogen 1	Homo sapiens	126-136
8175303-5	1994	RESULTS: Contrast media enhanced bradykinin-induced pain was dose dependent with the following potency order: iopamidol &gt; iopromide &gt; ZK 139129 &gt; ZK 119095.	Iopamidol	110-119	kininogen 1	Homo sapiens	33-43
8175303-5	1994	RESULTS: Contrast media enhanced bradykinin-induced pain was dose dependent with the following potency order: iopamidol &gt; iopromide &gt; ZK 139129 &gt; ZK 119095.	iopromide	125-134	kininogen 1	Homo sapiens	33-43
7515129-6	1994	L-NMMA and ADMA inhibited endothelium-dependent relaxations (EC50 = 4.7 +/- 1.1 microM and 17.9 +/- 4.9 microM, respectively); methylguanidine caused endothelium-independent contractions and reversed the relaxations to bradykinin and sodium nitroprusside (EC50 &gt; 100 microM); aminoguanidine was without effect.	N,N-dimethylarginine	11-15	kininogen 1	Homo sapiens	219-229
7515129-6	1994	L-NMMA and ADMA inhibited endothelium-dependent relaxations (EC50 = 4.7 +/- 1.1 microM and 17.9 +/- 4.9 microM, respectively); methylguanidine caused endothelium-independent contractions and reversed the relaxations to bradykinin and sodium nitroprusside (EC50 &gt; 100 microM); aminoguanidine was without effect.	Methylguanidine	127-142	kininogen 1	Homo sapiens	219-229
8167373-8	1994	In mixtures of BSA with a 9-10 molar excess of biologically active peptides, such as growth hormone releasing factor (GRF), glucagon, bradykinin or insulin in ammonium acetate at pH 7.5, complexes with a ratio of 1:1, 1:2 and in some cases 1:3 were detected.	ammonium acetate	159-175	kininogen 1	Homo sapiens	134-144
8206319-4	1994	On the contrary, pretreatment with IGF-II for 10 min enhanced the cAMP production stimulated by bradykinin (10 nM, 3 min) by 2.5-fold whereas no additive effects of IGF-II on the increased ligand binding to the mannose 6-phosphate/IGF-II receptor in response to bradykinin were observed.	Cyclic AMP	66-70	kininogen 1	Homo sapiens	96-106
8206319-4	1994	On the contrary, pretreatment with IGF-II for 10 min enhanced the cAMP production stimulated by bradykinin (10 nM, 3 min) by 2.5-fold whereas no additive effects of IGF-II on the increased ligand binding to the mannose 6-phosphate/IGF-II receptor in response to bradykinin were observed.	mannose-6-phosphate	211-230	kininogen 1	Homo sapiens	96-106
8177372-0	1994	Reduced Na+/K+ ATPase transport activity, resting membrane potential, and bradykinin-stimulated phosphatidylinositol synthesis by polyol accumulation in cultured neuroblastoma cells.	Phosphatidylinositols	96-116	kininogen 1	Homo sapiens	74-84
8177372-5	1994	Chronic exposure of neuroblastoma cells to media containing 30 mM glucose, galactose, or mannose caused a significant decrease in Na+/K+ ATPase transport activity, resting membrane potential, and bradykinin-stimulated 32P incorporation into phosphatidylinositol compared to cells cultured in medium containing 30 mM fructose.	Glucose	66-73	kininogen 1	Homo sapiens	196-206
8177372-5	1994	Chronic exposure of neuroblastoma cells to media containing 30 mM glucose, galactose, or mannose caused a significant decrease in Na+/K+ ATPase transport activity, resting membrane potential, and bradykinin-stimulated 32P incorporation into phosphatidylinositol compared to cells cultured in medium containing 30 mM fructose.	Galactose	75-84	kininogen 1	Homo sapiens	196-206
8177372-5	1994	Chronic exposure of neuroblastoma cells to media containing 30 mM glucose, galactose, or mannose caused a significant decrease in Na+/K+ ATPase transport activity, resting membrane potential, and bradykinin-stimulated 32P incorporation into phosphatidylinositol compared to cells cultured in medium containing 30 mM fructose.	Mannose	89-96	kininogen 1	Homo sapiens	196-206
8177372-5	1994	Chronic exposure of neuroblastoma cells to media containing 30 mM glucose, galactose, or mannose caused a significant decrease in Na+/K+ ATPase transport activity, resting membrane potential, and bradykinin-stimulated 32P incorporation into phosphatidylinositol compared to cells cultured in medium containing 30 mM fructose.	Phosphorus-32	218-221	kininogen 1	Homo sapiens	196-206
8177372-5	1994	Chronic exposure of neuroblastoma cells to media containing 30 mM glucose, galactose, or mannose caused a significant decrease in Na+/K+ ATPase transport activity, resting membrane potential, and bradykinin-stimulated 32P incorporation into phosphatidylinositol compared to cells cultured in medium containing 30 mM fructose.	Phosphatidylinositols	241-261	kininogen 1	Homo sapiens	196-206
8177372-5	1994	Chronic exposure of neuroblastoma cells to media containing 30 mM glucose, galactose, or mannose caused a significant decrease in Na+/K+ ATPase transport activity, resting membrane potential, and bradykinin-stimulated 32P incorporation into phosphatidylinositol compared to cells cultured in medium containing 30 mM fructose.	Fructose	316-324	kininogen 1	Homo sapiens	196-206
8177372-6	1994	In contrast, basal incorporation of 32P into phosphatidylinositol or basal and bradykinin-stimulated 32P incorporation into phosphatidylinositol 4,5-bisphosphate were not effected.	Phosphorus-32	101-104	kininogen 1	Homo sapiens	79-89
8177372-6	1994	In contrast, basal incorporation of 32P into phosphatidylinositol or basal and bradykinin-stimulated 32P incorporation into phosphatidylinositol 4,5-bisphosphate were not effected.	Phosphatidylinositol 4,5-Diphosphate	124-161	kininogen 1	Homo sapiens	79-89
8177372-8	1994	myo-Inositol metabolism and content and bradykinin-stimulated phosphatidylinositol synthesis were also maintained when media containing 30 mM glucose, galactose, or mannose was supplemented with 250 microM myo-inositol.	Phosphatidylinositols	62-82	kininogen 1	Homo sapiens	40-50
8177372-8	1994	myo-Inositol metabolism and content and bradykinin-stimulated phosphatidylinositol synthesis were also maintained when media containing 30 mM glucose, galactose, or mannose was supplemented with 250 microM myo-inositol.	Glucose	142-149	kininogen 1	Homo sapiens	40-50
8177372-8	1994	myo-Inositol metabolism and content and bradykinin-stimulated phosphatidylinositol synthesis were also maintained when media containing 30 mM glucose, galactose, or mannose was supplemented with 250 microM myo-inositol.	Inositol	206-218	kininogen 1	Homo sapiens	40-50
7515323-0	1994	Enhancement of cytosolic calcium, prostacyclin and nitric oxide by bradykinin and the ACE inhibitor ramiprilat in porcine brain capillary endothelial cells.	Calcium	25-32	kininogen 1	Homo sapiens	67-77
7515323-0	1994	Enhancement of cytosolic calcium, prostacyclin and nitric oxide by bradykinin and the ACE inhibitor ramiprilat in porcine brain capillary endothelial cells.	Nitric Oxide	51-63	kininogen 1	Homo sapiens	67-77
7515323-1	1994	We studied whether primary cultured porcine brain capillary endothelial cells (PBCEC) respond to bradykinin with an enhanced intracellular cytosolic calcium concentration [Ca2+]i with subsequent formation of nitric oxide (NO) and prostacyclin (PGI2).	Calcium	149-156	kininogen 1	Homo sapiens	97-107
7515323-1	1994	We studied whether primary cultured porcine brain capillary endothelial cells (PBCEC) respond to bradykinin with an enhanced intracellular cytosolic calcium concentration [Ca2+]i with subsequent formation of nitric oxide (NO) and prostacyclin (PGI2).	Nitric Oxide	208-220	kininogen 1	Homo sapiens	97-107
7515323-1	1994	We studied whether primary cultured porcine brain capillary endothelial cells (PBCEC) respond to bradykinin with an enhanced intracellular cytosolic calcium concentration [Ca2+]i with subsequent formation of nitric oxide (NO) and prostacyclin (PGI2).	Epoprostenol	244-248	kininogen 1	Homo sapiens	97-107
7515323-4	1994	Bradykinin and the ACE inhibitor ramiprilat concentration-dependently increased the formation of cyclic GMP which was completely prevented by the stereospecific inhibitor of NO synthase, NG-nitro-L-arginine.	Nitroarginine	187-206	kininogen 1	Homo sapiens	0-10
8307969-5	1994	Stimulation of fibroblasts with bradykinin or endothelin and Jurkat cells with anti-CD3 resulted in DG kinase-mediated formation of PA, but its level was unaffected by PLC pretreatment.	Phosphatidic Acids	132-134	kininogen 1	Homo sapiens	32-42
8307969-6	1994	Likewise, in streptolysin O-permeabilized fibroblasts, where bradykinin stimulation in the presence of [gamma-32P]ATP and guanosine 5"-O-(thiotriphosphate) generates [32P]PA exclusively via DG kinase, PLC pretreatment did not affect the amount of [32P]PA formed.	[gamma-32p]atp	103-117	kininogen 1	Homo sapiens	61-71
8307969-6	1994	Likewise, in streptolysin O-permeabilized fibroblasts, where bradykinin stimulation in the presence of [gamma-32P]ATP and guanosine 5"-O-(thiotriphosphate) generates [32P]PA exclusively via DG kinase, PLC pretreatment did not affect the amount of [32P]PA formed.	guanosine 5"-o-	122-137	kininogen 1	Homo sapiens	61-71
8307969-6	1994	Likewise, in streptolysin O-permeabilized fibroblasts, where bradykinin stimulation in the presence of [gamma-32P]ATP and guanosine 5"-O-(thiotriphosphate) generates [32P]PA exclusively via DG kinase, PLC pretreatment did not affect the amount of [32P]PA formed.	thiotriphosphate	138-154	kininogen 1	Homo sapiens	61-71
8307969-6	1994	Likewise, in streptolysin O-permeabilized fibroblasts, where bradykinin stimulation in the presence of [gamma-32P]ATP and guanosine 5"-O-(thiotriphosphate) generates [32P]PA exclusively via DG kinase, PLC pretreatment did not affect the amount of [32P]PA formed.	Phosphorus-32	110-113	kininogen 1	Homo sapiens	61-71
8307969-6	1994	Likewise, in streptolysin O-permeabilized fibroblasts, where bradykinin stimulation in the presence of [gamma-32P]ATP and guanosine 5"-O-(thiotriphosphate) generates [32P]PA exclusively via DG kinase, PLC pretreatment did not affect the amount of [32P]PA formed.	Phosphatidic Acids	171-173	kininogen 1	Homo sapiens	61-71
8307969-6	1994	Likewise, in streptolysin O-permeabilized fibroblasts, where bradykinin stimulation in the presence of [gamma-32P]ATP and guanosine 5"-O-(thiotriphosphate) generates [32P]PA exclusively via DG kinase, PLC pretreatment did not affect the amount of [32P]PA formed.	Phosphorus-32	167-170	kininogen 1	Homo sapiens	61-71
8307969-6	1994	Likewise, in streptolysin O-permeabilized fibroblasts, where bradykinin stimulation in the presence of [gamma-32P]ATP and guanosine 5"-O-(thiotriphosphate) generates [32P]PA exclusively via DG kinase, PLC pretreatment did not affect the amount of [32P]PA formed.	Phosphatidic Acids	252-254	kininogen 1	Homo sapiens	61-71
7994606-4	1994	In these cells, pharmacological agents such as thapsigargin or ionomycin, and the physiological activator bradykinin, only induced transient increases in cytoplasmic calcium level, due to the emptying of internal stores, while in control cells, this initial step is followed by an additional and sustained transmembrane calcium influx.	Calcium	166-173	kininogen 1	Homo sapiens	106-116
8017900-2	1994	The column has excellent capabilities to quantitatively remove carboxy-terminal basic amino acids from peptides, as is demonstrated using the synthetic peptide substrate hippuryl-L-arginine and the nonapeptide bradykinin, and remains stable for several months.	Amino Acids, Basic	80-97	kininogen 1	Homo sapiens	210-220
8017900-2	1994	The column has excellent capabilities to quantitatively remove carboxy-terminal basic amino acids from peptides, as is demonstrated using the synthetic peptide substrate hippuryl-L-arginine and the nonapeptide bradykinin, and remains stable for several months.	Peptides	103-111	kininogen 1	Homo sapiens	210-220
7994606-4	1994	In these cells, pharmacological agents such as thapsigargin or ionomycin, and the physiological activator bradykinin, only induced transient increases in cytoplasmic calcium level, due to the emptying of internal stores, while in control cells, this initial step is followed by an additional and sustained transmembrane calcium influx.	Calcium	320-327	kininogen 1	Homo sapiens	106-116
7515369-3	1994	We characterized the potency, efficacy and time course of NG-monomethyl-l-arginine (l-NMMA) as an inhibitor of bradykinin-mediated, endothelium-dependent dilation using the human hand-vein compliance technique.	omega-N-Methylarginine	58-82	kininogen 1	Homo sapiens	111-121
7515369-3	1994	We characterized the potency, efficacy and time course of NG-monomethyl-l-arginine (l-NMMA) as an inhibitor of bradykinin-mediated, endothelium-dependent dilation using the human hand-vein compliance technique.	omega-N-Methylarginine	84-90	kininogen 1	Homo sapiens	111-121
7515369-4	1994	We also compared the efficacy of l-NMMA with methylene blue, an inhibitor of guanylate cyclase, in blocking bradykinin-mediated vasodilation.	omega-N-Methylarginine	33-39	kininogen 1	Homo sapiens	108-118
7515369-4	1994	We also compared the efficacy of l-NMMA with methylene blue, an inhibitor of guanylate cyclase, in blocking bradykinin-mediated vasodilation.	Methylene Blue	45-59	kininogen 1	Homo sapiens	108-118
7515369-5	1994	l-NMMA potently inhibited bradykinin-induced venodilation with a log ED50 of 3.74 +/- 0.52 (geometric mean of 5.5 micrograms/min).	omega-N-Methylarginine	0-6	kininogen 1	Homo sapiens	26-36
7515369-7	1994	l-NMMA (25 micrograms/min) decreased bradykinin"s maximal venodilatory response from 90 +/- 22% to 39 +/- 15% (p &lt; 0.05).	omega-N-Methylarginine	0-6	kininogen 1	Homo sapiens	37-47
7515369-8	1994	Complete recovery of bradykinin venodilation was obtained within 155 minutes after stopping l-NMMA infusion, indicating that its effects were reversible.	omega-N-Methylarginine	92-98	kininogen 1	Homo sapiens	21-31
7515369-9	1994	In another set of experiments we compared the efficacy of methylene blue to l-NMMA; methylene blue decreased bradykinin-mediated venodilatory response to 53 +/- 17%; when l-NMMA was added, the response was further decreased to 32 +/- 9% (p &lt; 0.002).	omega-N-Methylarginine	76-82	kininogen 1	Homo sapiens	109-119
7515369-9	1994	In another set of experiments we compared the efficacy of methylene blue to l-NMMA; methylene blue decreased bradykinin-mediated venodilatory response to 53 +/- 17%; when l-NMMA was added, the response was further decreased to 32 +/- 9% (p &lt; 0.002).	Methylene Blue	84-98	kininogen 1	Homo sapiens	109-119
7507342-7	1994	The cells also increase chloride transport in response to bradykinin or calcium ionophore.	Chlorides	24-32	kininogen 1	Homo sapiens	58-68
8290560-9	1994	These and previous observations suggest that the differences in bombesin and bradykinin responses in fibroblasts and perhaps other cell types are likely to be due to alteration of inositol trisphosphate-mediated release of intracellular Ca2+.	inositol 1,2,3-trisphosphate	180-202	kininogen 1	Homo sapiens	77-87
8130263-8	1994	Nifedipine also blocked ionomycin and thapsigargin stimulation but only partially blocked bradykinin and interleukin 1 alpha stimulation.	Nifedipine	0-10	kininogen 1	Homo sapiens	90-100
8173526-4	1994	Detection limits of 1.2 fmol for fluorescamine-derivatized bradykinin and 90 attomol for O-phthaldialdehyde-derivatized bradykinin were achieved.	Fluorescamine	33-46	kininogen 1	Homo sapiens	59-69
7509245-5	1994	Indomethacin 10(-6) M abolished Bk-induced contraction, suggesting that cyclooxygenase products are involved in Bk action.	Indomethacin	0-12	kininogen 1	Homo sapiens	32-34
7509245-5	1994	Indomethacin 10(-6) M abolished Bk-induced contraction, suggesting that cyclooxygenase products are involved in Bk action.	Indomethacin	0-12	kininogen 1	Homo sapiens	112-114
7509245-6	1994	Capsaicin 10(-5) M, which selectively depletes C fibers from airway mediators through the ruthenium red pathway, and ruthenium red 10(-5) M significantly inhibited the concentration-response curves to Bk.	Ruthenium Red	90-103	kininogen 1	Homo sapiens	201-203
7509245-6	1994	Capsaicin 10(-5) M, which selectively depletes C fibers from airway mediators through the ruthenium red pathway, and ruthenium red 10(-5) M significantly inhibited the concentration-response curves to Bk.	Ruthenium Red	117-130	kininogen 1	Homo sapiens	201-203
8012902-1	1994	To determine whether the ductus arteriosus can form endothelium-derived relaxing factor--nitric oxide, we used isolated ductal strips from near-term fetal lamb and examined their response to bradykinin (a nitric oxide stimulator), L-arginine (a nitric oxide precursor), and agents interfering with the synthesis (N omega-nitro-L-arginine) and action (methylene blue) of nitric oxide.	Nitric Oxide	205-217	kininogen 1	Homo sapiens	191-201
8173526-4	1994	Detection limits of 1.2 fmol for fluorescamine-derivatized bradykinin and 90 attomol for O-phthaldialdehyde-derivatized bradykinin were achieved.	o-Phthalaldehyde	89-107	kininogen 1	Homo sapiens	120-130
8012902-1	1994	To determine whether the ductus arteriosus can form endothelium-derived relaxing factor--nitric oxide, we used isolated ductal strips from near-term fetal lamb and examined their response to bradykinin (a nitric oxide stimulator), L-arginine (a nitric oxide precursor), and agents interfering with the synthesis (N omega-nitro-L-arginine) and action (methylene blue) of nitric oxide.	Nitric Oxide	205-217	kininogen 1	Homo sapiens	191-201
8012902-1	1994	To determine whether the ductus arteriosus can form endothelium-derived relaxing factor--nitric oxide, we used isolated ductal strips from near-term fetal lamb and examined their response to bradykinin (a nitric oxide stimulator), L-arginine (a nitric oxide precursor), and agents interfering with the synthesis (N omega-nitro-L-arginine) and action (methylene blue) of nitric oxide.	Nitric Oxide	205-217	kininogen 1	Homo sapiens	191-201
8012902-2	1994	Bradykinin relaxed the indomethacin-contracted ductus dose dependently from a threshold of about 10(-10) M, and peak relaxation was greater at high (176-210 mmHg; 1 mmHg = 133.3 Pa) than low (15-25 mmHg) PO2.	Indomethacin	23-35	kininogen 1	Homo sapiens	0-10
8012902-2	1994	Bradykinin relaxed the indomethacin-contracted ductus dose dependently from a threshold of about 10(-10) M, and peak relaxation was greater at high (176-210 mmHg; 1 mmHg = 133.3 Pa) than low (15-25 mmHg) PO2.	PO-2	204-207	kininogen 1	Homo sapiens	0-10
8012902-4	1994	Pretreatment with nitric oxide inhibitors also prevented, in part (methylene blue, 1 microM) or in full (N omega-nitro-L-arginine, 100 microM), the relaxant effect of bradykinin.	Nitric Oxide	18-30	kininogen 1	Homo sapiens	167-177
8012902-4	1994	Pretreatment with nitric oxide inhibitors also prevented, in part (methylene blue, 1 microM) or in full (N omega-nitro-L-arginine, 100 microM), the relaxant effect of bradykinin.	Methylene Blue	67-81	kininogen 1	Homo sapiens	167-177
8012902-4	1994	Pretreatment with nitric oxide inhibitors also prevented, in part (methylene blue, 1 microM) or in full (N omega-nitro-L-arginine, 100 microM), the relaxant effect of bradykinin.	Nitroarginine	105-129	kininogen 1	Homo sapiens	167-177
8012902-5	1994	Paradoxically, L-arginine (10 microM) had an inhibiting rather than an enhancing effect on the bradykinin relaxation.	Arginine	15-25	kininogen 1	Homo sapiens	95-105
8287604-5	1994	Similarly, the vasopermeability-enhancing activity from ethanol-fractionated or boiled HAE plasma, collected during either attack or remission, co-eluted with bradykinin on reverse-phase high performance liquid chromatography (HPLC).	Ethanol	56-63	kininogen 1	Homo sapiens	159-169
8261589-4	1994	However, after an initial bradykinin exposure in RAECs, ryanodine markedly blunted the rapid increase in Ca2+ on a second exposure to bradykinin.	Ryanodine	56-65	kininogen 1	Homo sapiens	134-144
8026713-0	1994	Reduced endothelium-dependent vasodilation by acetylcholine and bradykinin in isolated nitroglycerin-tolerant blood vessels.	Nitroglycerin	87-100	kininogen 1	Homo sapiens	64-74
8156826-11	1994	Muscarinic agonists, histamine and bradykinin, but not adrenergic, serotonergic agonists or prostaglandins, increased phosphoinositide turnover.	Phosphatidylinositols	118-134	kininogen 1	Homo sapiens	35-45
8263514-0	1994	Decreased myo-inositol uptake is associated with reduced bradykinin-stimulated phosphatidylinositol synthesis and diacylglycerol content in cultured neuroblastoma cells exposed to L-fucose.	Inositol	10-22	kininogen 1	Homo sapiens	57-67
8130654-2	1994	The trypsin-generated active form can not only cleave a small synthetic substrate, hippuryl-L-arginine, but can remove terminal arginine from bradykinin.	hippuryl-L-arginine	83-102	kininogen 1	Homo sapiens	142-152
8130654-2	1994	The trypsin-generated active form can not only cleave a small synthetic substrate, hippuryl-L-arginine, but can remove terminal arginine from bradykinin.	Arginine	94-102	kininogen 1	Homo sapiens	142-152
8263514-0	1994	Decreased myo-inositol uptake is associated with reduced bradykinin-stimulated phosphatidylinositol synthesis and diacylglycerol content in cultured neuroblastoma cells exposed to L-fucose.	Phosphatidylinositols	79-99	kininogen 1	Homo sapiens	57-67
8263514-0	1994	Decreased myo-inositol uptake is associated with reduced bradykinin-stimulated phosphatidylinositol synthesis and diacylglycerol content in cultured neuroblastoma cells exposed to L-fucose.	Fucose	180-188	kininogen 1	Homo sapiens	57-67
8263514-3	1994	In these studies, L-fucose supplementation of culture medium was used to assess the effect of decreased myo-inositol metabolism and content on bradykinin-stimulated phosphatidylinositol synthesis and diacylglycerol production.	Fucose	18-26	kininogen 1	Homo sapiens	143-153
8263514-3	1994	In these studies, L-fucose supplementation of culture medium was used to assess the effect of decreased myo-inositol metabolism and content on bradykinin-stimulated phosphatidylinositol synthesis and diacylglycerol production.	Inositol	104-116	kininogen 1	Homo sapiens	143-153
8263514-3	1994	In these studies, L-fucose supplementation of culture medium was used to assess the effect of decreased myo-inositol metabolism and content on bradykinin-stimulated phosphatidylinositol synthesis and diacylglycerol production.	Phosphatidylinositols	165-185	kininogen 1	Homo sapiens	143-153
8263514-3	1994	In these studies, L-fucose supplementation of culture medium was used to assess the effect of decreased myo-inositol metabolism and content on bradykinin-stimulated phosphatidylinositol synthesis and diacylglycerol production.	Diglycerides	200-214	kininogen 1	Homo sapiens	143-153
8263514-4	1994	Chronic exposure of cells to 30 mM L-fucose caused a sustained decrease in bradykinin-stimulated, but not basal, 3H-inositol phosphate release and 32P incorporation into phosphatidylinositol in cells incubated in serum-free, unsupplemented medium.	Fucose	35-43	kininogen 1	Homo sapiens	75-85
8263514-4	1994	Chronic exposure of cells to 30 mM L-fucose caused a sustained decrease in bradykinin-stimulated, but not basal, 3H-inositol phosphate release and 32P incorporation into phosphatidylinositol in cells incubated in serum-free, unsupplemented medium.	3h-inositol phosphate	113-134	kininogen 1	Homo sapiens	75-85
8263514-8	1994	Bradykinin stimulated diacylglycerol production in neuroblastoma cells by increasing the hydrolysis of both phosphoinositides and phosphatidylcholine.	Diglycerides	22-36	kininogen 1	Homo sapiens	0-10
8263514-8	1994	Bradykinin stimulated diacylglycerol production in neuroblastoma cells by increasing the hydrolysis of both phosphoinositides and phosphatidylcholine.	Phosphatidylinositols	108-125	kininogen 1	Homo sapiens	0-10
8263514-8	1994	Bradykinin stimulated diacylglycerol production in neuroblastoma cells by increasing the hydrolysis of both phosphoinositides and phosphatidylcholine.	Phosphatidylcholines	130-149	kininogen 1	Homo sapiens	0-10
8263514-9	1994	Bradykinin-stimulated production of total diacylglycerol was similar for control and L-fucose-conditioned cells.	Diglycerides	42-56	kininogen 1	Homo sapiens	0-10
8263514-10	1994	However, there was a decrease in the bradykinin-induced generation of the 1-stearoyl-2-arachidonoyl diacylglycerol molecular species in the cells chronically exposed to 30 mM L-fucose.	1-stearoyl-2-arachidonoyl diacylglycerol	74-114	kininogen 1	Homo sapiens	37-47
8263514-10	1994	However, there was a decrease in the bradykinin-induced generation of the 1-stearoyl-2-arachidonoyl diacylglycerol molecular species in the cells chronically exposed to 30 mM L-fucose.	Fucose	175-183	kininogen 1	Homo sapiens	37-47
7515508-7	1994	Bradykinin and tachykinin cause indirect airway narrowing, probably by liberation of leukotrienes.	Leukotrienes	85-97	kininogen 1	Homo sapiens	0-10
8139697-3	1994	The integrity of endothelium was assessed by the bradykinin-induced relaxation of PGF2 alpha (3 mumol/l)-precontracted vessels which was absent after mechanical removal of endothelium.	Dinoprost	82-92	kininogen 1	Homo sapiens	49-59
8258520-5	1993	The endothelium-dependent vasodilator bradykinin evoked increases in ophthalmic flow (maximal increase, 26% +/- 2%; P &lt; 0.05 versus control) prevented by L-NAME.	NG-Nitroarginine Methyl Ester	157-163	kininogen 1	Homo sapiens	38-48
8149238-0	1993	Involvement of EP3 subtype of prostaglandin E receptors in PGE2-induced enhancement of the bradykinin response of nociceptors.	Dinoprostone	59-63	kininogen 1	Homo sapiens	91-101
8149238-1	1993	Prostaglandin E2 augments bradykinin-induced discharges of polymodal receptors as studied in vitro preparations.	Dinoprostone	0-16	kininogen 1	Homo sapiens	26-36
8279522-0	1993	Effects of ATP and bradykinin on endothelial cell Ca2+ homeostasis and formation of cGMP and prostacyclin.	Cyclic GMP	84-88	kininogen 1	Homo sapiens	19-29
8279522-0	1993	Effects of ATP and bradykinin on endothelial cell Ca2+ homeostasis and formation of cGMP and prostacyclin.	Epoprostenol	93-105	kininogen 1	Homo sapiens	19-29
8279522-2	1993	In adrenal medulla endothelial cells, we found that ATP and bradykinin could activate Ca2+ influx, although Ca2+ influx did not appear to be due to depletion of intracellular Ca2+ pools per se, since depletion of intracellular Ca2+ pools with thapsigargin reduced rather than enhanced both unidirectional and steady-state 45Ca2+ uptake.	Thapsigargin	243-255	kininogen 1	Homo sapiens	60-70
8279522-5	1993	Bradykinin-induced cGMP and PGI2 formation and ATP-induced PGI2 formation each required Ca2+ release from intracellular Ca2+ pools, since depletion of these pools with thapsigargin inhibited their formation.	Cyclic GMP	19-23	kininogen 1	Homo sapiens	0-10
8279522-5	1993	Bradykinin-induced cGMP and PGI2 formation and ATP-induced PGI2 formation each required Ca2+ release from intracellular Ca2+ pools, since depletion of these pools with thapsigargin inhibited their formation.	Epoprostenol	28-32	kininogen 1	Homo sapiens	0-10
8279522-5	1993	Bradykinin-induced cGMP and PGI2 formation and ATP-induced PGI2 formation each required Ca2+ release from intracellular Ca2+ pools, since depletion of these pools with thapsigargin inhibited their formation.	Thapsigargin	168-180	kininogen 1	Homo sapiens	0-10
8087627-0	1993	Tumor necrosis factor alpha potentiates the increase in cytosolic free calcium induced by bradykinin in guinea-pig tracheal smooth muscle cells.	Calcium	71-78	kininogen 1	Homo sapiens	90-100
8252688-6	1993	Hypercholesterolemic subjects were more sensitive to bradykinin, with an ED50 of 4.2 ng/min versus 10.9 ng/min in controls (P = .05); a similarly increased sensitivity was found in the presence of indomethacin.	Indomethacin	197-209	kininogen 1	Homo sapiens	53-63
8252688-8	1993	In five hypercholesterolemic subjects, treated with lovastatin to normalize serum cholesterol concentrations, maximal responsiveness to bradykinin decreased from 103 +/- 52% to 80 +/- 28%.	Lovastatin	52-62	kininogen 1	Homo sapiens	136-146
8252688-8	1993	In five hypercholesterolemic subjects, treated with lovastatin to normalize serum cholesterol concentrations, maximal responsiveness to bradykinin decreased from 103 +/- 52% to 80 +/- 28%.	Cholesterol	13-24	kininogen 1	Homo sapiens	136-146
8254041-4	1993	In the presence of both indomethacin and NLA, bradykinin evoked transient and concentration-dependent hyperpolarizations only in tissues with endothelium, which were augmented by perindoprilat and mimicked by the calcium ionophore A23187.	Indomethacin	24-36	kininogen 1	Homo sapiens	46-56
8254041-4	1993	In the presence of both indomethacin and NLA, bradykinin evoked transient and concentration-dependent hyperpolarizations only in tissues with endothelium, which were augmented by perindoprilat and mimicked by the calcium ionophore A23187.	perindoprilat	179-192	kininogen 1	Homo sapiens	46-56
8254041-4	1993	In the presence of both indomethacin and NLA, bradykinin evoked transient and concentration-dependent hyperpolarizations only in tissues with endothelium, which were augmented by perindoprilat and mimicked by the calcium ionophore A23187.	Calcium	213-220	kininogen 1	Homo sapiens	46-56
8254041-4	1993	In the presence of both indomethacin and NLA, bradykinin evoked transient and concentration-dependent hyperpolarizations only in tissues with endothelium, which were augmented by perindoprilat and mimicked by the calcium ionophore A23187.	Calcimycin	231-237	kininogen 1	Homo sapiens	46-56
8254041-6	1993	In rings contracted with prostaglandin F2 alpha, the cumulative addition of bradykinin caused a concentration-dependent relaxation during contractions evoked by prostaglandin F2 alpha, which was not abolished by NLA and indomethacin.	Dinoprost	25-41	kininogen 1	Homo sapiens	76-86
8254041-6	1993	In rings contracted with prostaglandin F2 alpha, the cumulative addition of bradykinin caused a concentration-dependent relaxation during contractions evoked by prostaglandin F2 alpha, which was not abolished by NLA and indomethacin.	Dinoprost	25-47	kininogen 1	Homo sapiens	76-86
8254041-6	1993	In rings contracted with prostaglandin F2 alpha, the cumulative addition of bradykinin caused a concentration-dependent relaxation during contractions evoked by prostaglandin F2 alpha, which was not abolished by NLA and indomethacin.	Nitroarginine	212-215	kininogen 1	Homo sapiens	76-86
8254041-6	1993	In rings contracted with prostaglandin F2 alpha, the cumulative addition of bradykinin caused a concentration-dependent relaxation during contractions evoked by prostaglandin F2 alpha, which was not abolished by NLA and indomethacin.	Indomethacin	220-232	kininogen 1	Homo sapiens	76-86
8258520-12	1993	CONCLUSIONS: Endothelium-derived nitric oxide released under basal conditions or stimulated by bradykinin significantly regulated flow to the porcine ophthalmic microcirculation.	Nitric Oxide	33-45	kininogen 1	Homo sapiens	95-105
8239805-7	1993	In contrast, the endothelium-dependent relaxations in response to acetylcholine, substance P, and bradykinin were significantly greater in the inferior epigastric than in the internal mammary arteries (maximal relaxations expressed as percent of prostaglandin F2 alpha-induced precontraction: acetylcholine, 94% +/- 5% versus 77% +/- 5%; substance P, 85% +/- 4% versus 24% +/- 5%; bradykinin, 77% +/- 5% versus 26% +/- 3%).	Dinoprost	246-262	kininogen 1	Homo sapiens	98-108
8123881-6	1993	BK interacts with multiple endogenous mesenteric vasodilator mediators, such as nitric oxide, prostacyclin, and neuropeptides.	Nitric Oxide	80-92	kininogen 1	Homo sapiens	0-2
8123881-6	1993	BK interacts with multiple endogenous mesenteric vasodilator mediators, such as nitric oxide, prostacyclin, and neuropeptides.	Epoprostenol	94-106	kininogen 1	Homo sapiens	0-2
7504289-0	1993	Human bradykinin B2 receptors isolated by receptor-specific monoclonal antibodies are tyrosine phosphorylated.	Tyrosine	86-94	kininogen 1	Homo sapiens	6-16
7504289-1	1993	We report the immunoaffinity isolation of bradykinin B2 receptors in a tyrosine-phosphorylated state from WI-38 human lung fibroblasts.	Tyrosine	71-79	kininogen 1	Homo sapiens	42-52
7504289-9	1993	Genistein completely inhibits bradykinin-mediated prostaglandin E2 production with an IC50 of 8 microM, indicating that tyrosine kinase activity is critical for the signal transduction leading to arachidonic acid release.	Genistein	0-9	kininogen 1	Homo sapiens	30-40
7504289-9	1993	Genistein completely inhibits bradykinin-mediated prostaglandin E2 production with an IC50 of 8 microM, indicating that tyrosine kinase activity is critical for the signal transduction leading to arachidonic acid release.	Dinoprostone	50-66	kininogen 1	Homo sapiens	30-40
7504289-9	1993	Genistein completely inhibits bradykinin-mediated prostaglandin E2 production with an IC50 of 8 microM, indicating that tyrosine kinase activity is critical for the signal transduction leading to arachidonic acid release.	Arachidonic Acid	196-212	kininogen 1	Homo sapiens	30-40
8250885-3	1993	Following stimulation with bradykinin or calcium ionophore A23187 NO and intracellular dinitrosyl iron complexes were detected by ESR spectroscopic analysis of frozen cells.	dinitrosyl iron	87-102	kininogen 1	Homo sapiens	27-37
8250885-5	1993	In transferrin and iron-free medium stimulation of endothelial cells by bradykinin or thimerosal resulted in a loss of non-heme iron.	Iron	19-23	kininogen 1	Homo sapiens	72-82
8250885-5	1993	In transferrin and iron-free medium stimulation of endothelial cells by bradykinin or thimerosal resulted in a loss of non-heme iron.	Iron	128-132	kininogen 1	Homo sapiens	72-82
8131993-0	1993	Bradykinin-evoked release of [3H]noradrenaline from the human neuroblastoma SH-SY5Y.	[3h]noradrenaline	29-46	kininogen 1	Homo sapiens	0-10
7510651-0	1993	A nitric oxide synthase inhibitor reduces desensitisation of bradykinin-induced activation of phospholipase C in sensory neurones.	Nitric Oxide	2-14	kininogen 1	Homo sapiens	61-71
8239805-7	1993	In contrast, the endothelium-dependent relaxations in response to acetylcholine, substance P, and bradykinin were significantly greater in the inferior epigastric than in the internal mammary arteries (maximal relaxations expressed as percent of prostaglandin F2 alpha-induced precontraction: acetylcholine, 94% +/- 5% versus 77% +/- 5%; substance P, 85% +/- 4% versus 24% +/- 5%; bradykinin, 77% +/- 5% versus 26% +/- 3%).	Acetylcholine	293-306	kininogen 1	Homo sapiens	98-108
8307852-0	1993	Interactive effect of inhaled bradykinin with histamine and PGD2 in bronchial asthma.	Histamine	46-55	kininogen 1	Homo sapiens	30-40
7719512-5	1993	The basal and bradykinin (10 microM) stimulated PGI2 release of these valves in the medium were measured during consecutive incubation lasting 15 minutes at 37 degrees C, using a radioimmunoassay for 6-oxo-PGF1 alpha.	Epoprostenol	48-52	kininogen 1	Homo sapiens	14-24
8293770-6	1993	Whereas Ang I exerted no facilitating action on noradrenaline, bradykinin stimulated noradrenaline release dose-dependently, almost during converting enzyme inhibition.	Norepinephrine	85-98	kininogen 1	Homo sapiens	63-73
8292848-1	1993	A series of peptide analogs and fragments of bradykinin were designed and synthesized on solid supports using Boc and Fmoc strategies, and on polyethylene pins using Fmoc strategy.	Polyethylene	142-154	kininogen 1	Homo sapiens	45-55
8292848-8	1993	The best inhibitor found in this study, Ala2,6-des-Pro3-bradykinin, has an apparent Ki of 30.2 nM, compared to an apparent Ki of 94 nM for des-Pro3-bradykinin, which was reported to be a better inhibitor of angiotensin-converting enzyme than captopril.	Captopril	242-251	kininogen 1	Homo sapiens	56-66
8292848-8	1993	The best inhibitor found in this study, Ala2,6-des-Pro3-bradykinin, has an apparent Ki of 30.2 nM, compared to an apparent Ki of 94 nM for des-Pro3-bradykinin, which was reported to be a better inhibitor of angiotensin-converting enzyme than captopril.	Captopril	242-251	kininogen 1	Homo sapiens	148-158
7505360-5	1993	Enalapril (10 mg) inhibited AI similarly to losartan 100 mg without significantly influencing responses to angiotensin II, and augmented vasodilator responses to bradykinin (p &lt; 0.0001).	Enalapril	0-9	kininogen 1	Homo sapiens	162-172
8240234-9	1993	Both the bradykinin-induced change in [Ca2+]i and the stimulation of 45Ca2+ efflux was completely blocked by loading the cells with the Ca2+ chelator BAPTA.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	150-155	kininogen 1	Homo sapiens	9-19
8242287-8	1993	Relaxation in response to the bradykinin stimulus was abolished in the presence of L-nitroarginine methyl ester, a specific inhibitor of the synthesis of endothelium-derived relaxing factor (EDRF).	NG-Nitroarginine Methyl Ester	83-111	kininogen 1	Homo sapiens	30-40
7505360-6	1993	In human forearm vasculature, oral losartan (20-100 mg) inhibits vasoconstriction to ANG I and ANG II without significantly influencing bradykinin-induced vasodilation, whereas enalapril selectively inhibits ANG I-induced vasoconstriction while potentiating the vasodilator effect of bradykinin.	Losartan	35-43	kininogen 1	Homo sapiens	284-294
8408228-2	1993	The reduction in EGF binding by bradykinin, ATP, and TPA was similarly reversed by concomitant incubation with staurosporine, a protein kinase C inhibitor, implying that the phosphorylation of EGF receptors was catalyzed probably by a protein kinase C of the same or similar type in each case.	Staurosporine	111-124	kininogen 1	Homo sapiens	32-42
8408228-3	1993	This possibility was confirmed by the fact that the major phosphorylation site of EGF receptors by the stimulation with either bradykinin, ATP, or TPA was the same (Thr-654).	Threonine	165-168	kininogen 1	Homo sapiens	127-137
8408228-4	1993	Different from the stimulations with ATP and TPA, the effect of bradykinin of decreasing the high-affinity EGF binding was transient (a minimum binding at 2.5 min); the reduced EGF binding was, however, sustained for up to 30 min in the presence of calyculin A, a phosphoprotein phosphatase inhibitor.	Adenosine Triphosphate	37-40	kininogen 1	Homo sapiens	64-74
8408228-4	1993	Different from the stimulations with ATP and TPA, the effect of bradykinin of decreasing the high-affinity EGF binding was transient (a minimum binding at 2.5 min); the reduced EGF binding was, however, sustained for up to 30 min in the presence of calyculin A, a phosphoprotein phosphatase inhibitor.	Tetradecanoylphorbol Acetate	45-48	kininogen 1	Homo sapiens	64-74
8408228-4	1993	Different from the stimulations with ATP and TPA, the effect of bradykinin of decreasing the high-affinity EGF binding was transient (a minimum binding at 2.5 min); the reduced EGF binding was, however, sustained for up to 30 min in the presence of calyculin A, a phosphoprotein phosphatase inhibitor.	calyculin A	249-260	kininogen 1	Homo sapiens	64-74
8409525-0	1993	Phorbol ester TPA- and bradykinin-induced arachidonic acid release from keratinocytes is catalyzed by a cytosolic phospholipase A2 (cPLA2).	Phorbol Esters	0-13	kininogen 1	Homo sapiens	23-33
8409525-0	1993	Phorbol ester TPA- and bradykinin-induced arachidonic acid release from keratinocytes is catalyzed by a cytosolic phospholipase A2 (cPLA2).	Arachidonic Acid	42-58	kininogen 1	Homo sapiens	23-33
8409525-1	1993	In a previous paper, we have shown that bradykinin (Bk) and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulate arachidonic acid release from HEL-30 keratinocytes along a Bk-B2 receptor G-protein-coupled pathway or a protein kinase C-dependent mechanism, respectively.	Arachidonic Acid	131-147	kininogen 1	Homo sapiens	40-50
8409525-1	1993	In a previous paper, we have shown that bradykinin (Bk) and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulate arachidonic acid release from HEL-30 keratinocytes along a Bk-B2 receptor G-protein-coupled pathway or a protein kinase C-dependent mechanism, respectively.	Arachidonic Acid	131-147	kininogen 1	Homo sapiens	52-54
8214034-10	1993	Neomycin, which inhibits IP3 production, completely abolished the [Ca2+]i response to bradykinin stimulation but did not affect the second phase of the histamine response.	Neomycin	0-8	kininogen 1	Homo sapiens	86-96
7689642-1	1993	Bradykinin- and substance P (SP)-stimulated second messenger studies in isolated subsets of neuroglia showed bradykinin-stimulated synthesis of phosphoinositides (PI) in type-1 astrocytes and oligodendrocytes.	Phosphatidylinositols	144-161	kininogen 1	Homo sapiens	0-10
7689642-1	1993	Bradykinin- and substance P (SP)-stimulated second messenger studies in isolated subsets of neuroglia showed bradykinin-stimulated synthesis of phosphoinositides (PI) in type-1 astrocytes and oligodendrocytes.	Phosphatidylinositols	144-161	kininogen 1	Homo sapiens	109-119
8339418-8	1993	Intravenous bradykinin increased PGI2 biosynthesis 5.1 +/- 1.6-fold (n = 4) before aspirin treatment.	Epoprostenol	33-37	kininogen 1	Homo sapiens	12-22
8339418-9	1993	Oral aspirin 75 mg/d for 14 days abolished bradykinin-induced PGI2 formation, whereas dermal aspirin 750 mg/d had no effect despite similar inhibition of TXA2 biosynthesis.	Aspirin	5-12	kininogen 1	Homo sapiens	43-53
8339418-9	1993	Oral aspirin 75 mg/d for 14 days abolished bradykinin-induced PGI2 formation, whereas dermal aspirin 750 mg/d had no effect despite similar inhibition of TXA2 biosynthesis.	Epoprostenol	62-66	kininogen 1	Homo sapiens	43-53
8344795-5	1993	However, all local anesthetics (10(-5)M) and bupivacaine (10(-5)-10(-6)M) reduced endothelium-dependent relaxations to bradykinin (10(-9)-10(-6)M), whereas the endothelium-independent relaxations to the nitric oxide-donor 3-morpholino-sydnonimine (SIN-1; 10(-9)-10(-5)M) were unaffected by local anesthetics.	Bupivacaine	45-56	kininogen 1	Homo sapiens	119-129
8344795-5	1993	However, all local anesthetics (10(-5)M) and bupivacaine (10(-5)-10(-6)M) reduced endothelium-dependent relaxations to bradykinin (10(-9)-10(-6)M), whereas the endothelium-independent relaxations to the nitric oxide-donor 3-morpholino-sydnonimine (SIN-1; 10(-9)-10(-5)M) were unaffected by local anesthetics.	Nitric Oxide	203-215	kininogen 1	Homo sapiens	119-129
8344795-5	1993	However, all local anesthetics (10(-5)M) and bupivacaine (10(-5)-10(-6)M) reduced endothelium-dependent relaxations to bradykinin (10(-9)-10(-6)M), whereas the endothelium-independent relaxations to the nitric oxide-donor 3-morpholino-sydnonimine (SIN-1; 10(-9)-10(-5)M) were unaffected by local anesthetics.	-morpholino-sydnonimine	223-246	kininogen 1	Homo sapiens	119-129
8344795-7	1993	CONCLUSION: These findings demonstrate that in porcine ciliary arteries, local anesthetics impair endothelial formation of nitric oxide from L-arginine after stimulation with bradykinin, which may contribute importantly to the reduction in blood flow to the eye during retrobulbar anesthesia.	Nitric Oxide	123-135	kininogen 1	Homo sapiens	175-185
8344795-7	1993	CONCLUSION: These findings demonstrate that in porcine ciliary arteries, local anesthetics impair endothelial formation of nitric oxide from L-arginine after stimulation with bradykinin, which may contribute importantly to the reduction in blood flow to the eye during retrobulbar anesthesia.	Arginine	141-151	kininogen 1	Homo sapiens	175-185
8397092-2	1993	Histamine (EC50 6.5 microM), bradykinin (EC50 9.7 nM), carbachol (EC50 10 microM), substance P and NaF all produced concentration dependent [3H]inositol phosphate formation in these cells.	Tritium	141-143	kininogen 1	Homo sapiens	29-39
8397092-2	1993	Histamine (EC50 6.5 microM), bradykinin (EC50 9.7 nM), carbachol (EC50 10 microM), substance P and NaF all produced concentration dependent [3H]inositol phosphate formation in these cells.	Inositol Phosphates	144-162	kininogen 1	Homo sapiens	29-39
8247227-0	1993	Serum- and bradykinin-induced calcium transients in familial Alzheimer"s fibroblasts.	Calcium	30-37	kininogen 1	Homo sapiens	11-21
8247227-1	1993	The calcium-sensitive photoprotein, aequorin, was used to examine serum- and bradykinin-induced transient increases in free cytosolic calcium ions in skin fibroblasts from 10 individuals with early onset familial AD (FAD), including four who were biopsied before their clinical symptoms would allow a diagnosis of AD, 2 individuals with late onset FAD, 8 at-risk but nonsymptomatic individuals, and 13 controls.	Calcium	4-11	kininogen 1	Homo sapiens	77-87
8247227-1	1993	The calcium-sensitive photoprotein, aequorin, was used to examine serum- and bradykinin-induced transient increases in free cytosolic calcium ions in skin fibroblasts from 10 individuals with early onset familial AD (FAD), including four who were biopsied before their clinical symptoms would allow a diagnosis of AD, 2 individuals with late onset FAD, 8 at-risk but nonsymptomatic individuals, and 13 controls.	Calcium	134-141	kininogen 1	Homo sapiens	77-87
8247227-2	1993	The data show that (a) among controls, the peaks of the calcium transients increase in height as a function of donor age; (b) transients induced by 10% serum, 10 nM bradykinin (BK) or 100 nM BK were generally lower in FAD fibroblasts, including those from donors in the early stages of the disease, than in age-matched control cells; (c) such transients are reduced in cells from a proportion of the nonsymptomatic, at-risk individuals.	Calcium	56-63	kininogen 1	Homo sapiens	191-193
8247227-3	1993	Thus, serum- and BK-induced calcium transients are reduced in fibroblasts from both early and more advanced stage FAD donors and perhaps even from donors who are presymptomatic carriers of the defective gene.	Calcium	28-35	kininogen 1	Homo sapiens	17-19
8210518-2	1993	More recently, both functional and neurochemical evidence have been accumulated that BK evokes release of neuropeptides, including calcitonin gene-related peptide and the tachykinins substance P and neurokinin A, from peripheral terminals of capsaicin-sensitive primary afferents.	Capsaicin	242-251	kininogen 1	Homo sapiens	85-87
8344943-2	1993	Prolylcarboxypeptidase, a lysosomal serine carboxypeptidase, cleaves COOH-terminal amino acids linked to proline, as in angiotensin II and III and [des-Arg9] bradykinin.	Carbonic Acid	69-73	kininogen 1	Homo sapiens	158-168
8344943-2	1993	Prolylcarboxypeptidase, a lysosomal serine carboxypeptidase, cleaves COOH-terminal amino acids linked to proline, as in angiotensin II and III and [des-Arg9] bradykinin.	Proline	105-112	kininogen 1	Homo sapiens	158-168
8344943-2	1993	Prolylcarboxypeptidase, a lysosomal serine carboxypeptidase, cleaves COOH-terminal amino acids linked to proline, as in angiotensin II and III and [des-Arg9] bradykinin.	des-arg9	148-156	kininogen 1	Homo sapiens	158-168
8396328-5	1993	Bradykinin-stimulated prostaglandin E2 (PGE2) release was potentiated by EGF, and, in the presence of indomethacin, the inhibition of the EGF-induced DNA synthesis by bradykinin was minimized.	Dinoprostone	22-38	kininogen 1	Homo sapiens	0-10
8396328-5	1993	Bradykinin-stimulated prostaglandin E2 (PGE2) release was potentiated by EGF, and, in the presence of indomethacin, the inhibition of the EGF-induced DNA synthesis by bradykinin was minimized.	Dinoprostone	40-44	kininogen 1	Homo sapiens	0-10
8396328-5	1993	Bradykinin-stimulated prostaglandin E2 (PGE2) release was potentiated by EGF, and, in the presence of indomethacin, the inhibition of the EGF-induced DNA synthesis by bradykinin was minimized.	Indomethacin	102-114	kininogen 1	Homo sapiens	0-10
8396328-5	1993	Bradykinin-stimulated prostaglandin E2 (PGE2) release was potentiated by EGF, and, in the presence of indomethacin, the inhibition of the EGF-induced DNA synthesis by bradykinin was minimized.	Indomethacin	102-114	kininogen 1	Homo sapiens	167-177
8396328-6	1993	The results presented demonstrate that bradykinin can inhibit EGF- and PDGF-induced DNA synthesis and suggest that PGE2 synthesis is responsible for the observed bradykinin inhibition of EGF-induced DNA synthesis.	Dinoprostone	115-119	kininogen 1	Homo sapiens	162-172
8373725-0	1993	Interleukin-1 selectively potentiates bradykinin-stimulated arachidonic acid release from human synovial fibroblasts.	Arachidonic Acid	60-76	kininogen 1	Homo sapiens	38-48
8396347-0	1993	Calcium entry, mobilization, and extrusion in postcapillary venular endothelium exposed to bradykinin.	Calcium	0-7	kininogen 1	Homo sapiens	91-101
8396347-1	1993	The effect of bradykinin (BK) on cytosolic calcium in coronary venular endothelial cells (CVEC) was studied using the intracellular calcium indicator indo 1.	Calcium	43-50	kininogen 1	Homo sapiens	14-24
8396347-1	1993	The effect of bradykinin (BK) on cytosolic calcium in coronary venular endothelial cells (CVEC) was studied using the intracellular calcium indicator indo 1.	Calcium	43-50	kininogen 1	Homo sapiens	26-28
8396347-3	1993	In calcium-free medium, poststimulation cytosolic calcium concentration returned to levels below prestimulation values, implying that BK modulates calcium extrusion mechanisms that are normally masked by calcium influx into the cell.	Calcium	3-10	kininogen 1	Homo sapiens	134-136
8396347-3	1993	In calcium-free medium, poststimulation cytosolic calcium concentration returned to levels below prestimulation values, implying that BK modulates calcium extrusion mechanisms that are normally masked by calcium influx into the cell.	Calcium	50-57	kininogen 1	Homo sapiens	134-136
8396347-3	1993	In calcium-free medium, poststimulation cytosolic calcium concentration returned to levels below prestimulation values, implying that BK modulates calcium extrusion mechanisms that are normally masked by calcium influx into the cell.	Calcium	50-57	kininogen 1	Homo sapiens	134-136
8396347-3	1993	In calcium-free medium, poststimulation cytosolic calcium concentration returned to levels below prestimulation values, implying that BK modulates calcium extrusion mechanisms that are normally masked by calcium influx into the cell.	Calcium	50-57	kininogen 1	Homo sapiens	134-136
8396347-6	1993	Under these conditions, the final dose of BK caused a fall, rather than rise, in cytosolic calcium.	Calcium	91-98	kininogen 1	Homo sapiens	42-44
8396347-8	1993	Subsequent exposure of these cells to BK also led to a fall in cytosolic calcium.	Calcium	73-80	kininogen 1	Homo sapiens	38-40
8396347-9	1993	The preconditioning and thapsigargin studies are consistent with a modulation of calcium extrusion processes by BK in CVEC.	Thapsigargin	24-36	kininogen 1	Homo sapiens	112-114
8396347-9	1993	The preconditioning and thapsigargin studies are consistent with a modulation of calcium extrusion processes by BK in CVEC.	Calcium	81-88	kininogen 1	Homo sapiens	112-114
7686736-0	1993	Bradykinin receptors and signal transduction pathways in human fibroblasts: integral role for extracellular calcium.	Calcium	108-115	kininogen 1	Homo sapiens	0-10
7686736-1	1993	Bradykinin receptors have been identified in human gingival fibroblasts; the primary signal transduction pathways and their dependence on calcium have been characterized.	Calcium	138-145	kininogen 1	Homo sapiens	0-10
7686736-2	1993	Binding data revealed a calcium-independent binding of bradykinin to the cell membrane with a receptor density of 25,000 receptors per cell and a Kd of 1.6 nM.	Calcium	24-31	kininogen 1	Homo sapiens	55-65
7686736-3	1993	The bradykinin receptor-mediated activation of phospholipase C (PLC) resulted in an extensive and rapid stimulation of phosphoinositide metabolism.	Phosphatidylinositols	119-135	kininogen 1	Homo sapiens	4-14
7686736-13	1993	Together these results demonstrate the presence of bradykinin receptors in human gingival fibroblasts; these receptors are coupled to signal transduction mechanisms involving the PLC, PLA2, and tyrosine kinase effector systems, all of which require extracellular calcium to achieve maximal activation.	Calcium	263-270	kininogen 1	Homo sapiens	51-61
8268545-3	1993	When using heparin as the anticoagulant, large increases in bradykinin levels in plasma were observed after its passage through the column during the procedure.	Heparin	11-18	kininogen 1	Homo sapiens	60-70
8373725-1	1993	Exposure of human synovial fibroblasts prelabelled with [3H]arachidonic acid to bradykinin causes a rapid and sustained increase in arachidonic acid release, a transient increase in cytosolic calcium and an increase in radiolabelled diacylglycerol.	[3h]arachidonic acid	56-76	kininogen 1	Homo sapiens	80-90
8392931-5	1993	We found in bradykinin-stimulated human fibroblasts that PLD mediates transphosphatidylation from PC (donor) to the endogenous "alcohol" DG (acceptor), yielding bis(1,2-diacylglycero)-3-sn-phosphate (bisphosphatidic acid; bisPA).	Phosphatidylcholines	98-100	kininogen 1	Homo sapiens	12-22
8373725-1	1993	Exposure of human synovial fibroblasts prelabelled with [3H]arachidonic acid to bradykinin causes a rapid and sustained increase in arachidonic acid release, a transient increase in cytosolic calcium and an increase in radiolabelled diacylglycerol.	Arachidonic Acid	60-76	kininogen 1	Homo sapiens	80-90
8373725-1	1993	Exposure of human synovial fibroblasts prelabelled with [3H]arachidonic acid to bradykinin causes a rapid and sustained increase in arachidonic acid release, a transient increase in cytosolic calcium and an increase in radiolabelled diacylglycerol.	Calcium	192-199	kininogen 1	Homo sapiens	80-90
8392931-5	1993	We found in bradykinin-stimulated human fibroblasts that PLD mediates transphosphatidylation from PC (donor) to the endogenous "alcohol" DG (acceptor), yielding bis(1,2-diacylglycero)-3-sn-phosphate (bisphosphatidic acid; bisPA).	alcohol" dg	128-139	kininogen 1	Homo sapiens	12-22
8392931-5	1993	We found in bradykinin-stimulated human fibroblasts that PLD mediates transphosphatidylation from PC (donor) to the endogenous "alcohol" DG (acceptor), yielding bis(1,2-diacylglycero)-3-sn-phosphate (bisphosphatidic acid; bisPA).	bis(1,2-diacylglycero)-3-sn-phosphate	161-198	kininogen 1	Homo sapiens	12-22
8373725-1	1993	Exposure of human synovial fibroblasts prelabelled with [3H]arachidonic acid to bradykinin causes a rapid and sustained increase in arachidonic acid release, a transient increase in cytosolic calcium and an increase in radiolabelled diacylglycerol.	Diglycerides	233-247	kininogen 1	Homo sapiens	80-90
8392931-5	1993	We found in bradykinin-stimulated human fibroblasts that PLD mediates transphosphatidylation from PC (donor) to the endogenous "alcohol" DG (acceptor), yielding bis(1,2-diacylglycero)-3-sn-phosphate (bisphosphatidic acid; bisPA).	bisphosphatidic acid	200-220	kininogen 1	Homo sapiens	12-22
8373725-2	1993	Activation of arachidonic acid release by bradykinin was potentiated by interleukin-1 added either simultaneously with bradykinin or to cultures 24 h before addition of bradykinin.	Arachidonic Acid	14-30	kininogen 1	Homo sapiens	42-52
8373725-2	1993	Activation of arachidonic acid release by bradykinin was potentiated by interleukin-1 added either simultaneously with bradykinin or to cultures 24 h before addition of bradykinin.	Arachidonic Acid	14-30	kininogen 1	Homo sapiens	119-129
8392931-5	1993	We found in bradykinin-stimulated human fibroblasts that PLD mediates transphosphatidylation from PC (donor) to the endogenous "alcohol" DG (acceptor), yielding bis(1,2-diacylglycero)-3-sn-phosphate (bisphosphatidic acid; bisPA).	bispa	222-227	kininogen 1	Homo sapiens	12-22
8373725-2	1993	Activation of arachidonic acid release by bradykinin was potentiated by interleukin-1 added either simultaneously with bradykinin or to cultures 24 h before addition of bradykinin.	Arachidonic Acid	14-30	kininogen 1	Homo sapiens	119-129
8392931-7	1993	Long-term phorbol ester treatment blocks bradykinin-induced activation of PLD and consequent bisPA formation, thereby unveiling rapid formation of DG.	Phorbol Esters	10-23	kininogen 1	Homo sapiens	41-51
8373725-4	1993	The stimulation of arachidonic acid release in response to bradykinin, in the absence or presence of interleukin-1, was not affected by RHC-80267, an inhibitor of diacylglycerol kinase, suggesting that deacylation of diacylglycerol was not an important pathway of arachidonic acid production in cultures exposed to bradykinin.	Arachidonic Acid	19-35	kininogen 1	Homo sapiens	59-69
8392931-7	1993	Long-term phorbol ester treatment blocks bradykinin-induced activation of PLD and consequent bisPA formation, thereby unveiling rapid formation of DG.	bispa	93-98	kininogen 1	Homo sapiens	41-51
8373725-4	1993	The stimulation of arachidonic acid release in response to bradykinin, in the absence or presence of interleukin-1, was not affected by RHC-80267, an inhibitor of diacylglycerol kinase, suggesting that deacylation of diacylglycerol was not an important pathway of arachidonic acid production in cultures exposed to bradykinin.	Arachidonic Acid	19-35	kininogen 1	Homo sapiens	315-325
8373725-4	1993	The stimulation of arachidonic acid release in response to bradykinin, in the absence or presence of interleukin-1, was not affected by RHC-80267, an inhibitor of diacylglycerol kinase, suggesting that deacylation of diacylglycerol was not an important pathway of arachidonic acid production in cultures exposed to bradykinin.	Diglycerides	163-177	kininogen 1	Homo sapiens	59-69
8373725-4	1993	The stimulation of arachidonic acid release in response to bradykinin, in the absence or presence of interleukin-1, was not affected by RHC-80267, an inhibitor of diacylglycerol kinase, suggesting that deacylation of diacylglycerol was not an important pathway of arachidonic acid production in cultures exposed to bradykinin.	Arachidonic Acid	264-280	kininogen 1	Homo sapiens	59-69
8373725-6	1993	Bradykinin-stimulated release of arachidonic acid was prevented by down-regulating protein kinase C by pretreatment with phorbol 12-myristate 13-acetate and was unaffected by inhibitors of protein synthesis actinomycin D or cycloheximide.	Arachidonic Acid	33-49	kininogen 1	Homo sapiens	0-10
8373725-6	1993	Bradykinin-stimulated release of arachidonic acid was prevented by down-regulating protein kinase C by pretreatment with phorbol 12-myristate 13-acetate and was unaffected by inhibitors of protein synthesis actinomycin D or cycloheximide.	Tetradecanoylphorbol Acetate	121-152	kininogen 1	Homo sapiens	0-10
8373725-6	1993	Bradykinin-stimulated release of arachidonic acid was prevented by down-regulating protein kinase C by pretreatment with phorbol 12-myristate 13-acetate and was unaffected by inhibitors of protein synthesis actinomycin D or cycloheximide.	Dactinomycin	207-220	kininogen 1	Homo sapiens	0-10
8373725-6	1993	Bradykinin-stimulated release of arachidonic acid was prevented by down-regulating protein kinase C by pretreatment with phorbol 12-myristate 13-acetate and was unaffected by inhibitors of protein synthesis actinomycin D or cycloheximide.	Cycloheximide	224-237	kininogen 1	Homo sapiens	0-10
8373725-7	1993	On the other hand, interleukin-1 amplification of bradykinin-stimulated release of arachidonic acid was blocked by actinomycin D and cycloheximide.	Arachidonic Acid	83-99	kininogen 1	Homo sapiens	50-60
8373725-7	1993	On the other hand, interleukin-1 amplification of bradykinin-stimulated release of arachidonic acid was blocked by actinomycin D and cycloheximide.	Dactinomycin	115-128	kininogen 1	Homo sapiens	50-60
8373725-7	1993	On the other hand, interleukin-1 amplification of bradykinin-stimulated release of arachidonic acid was blocked by actinomycin D and cycloheximide.	Cycloheximide	133-146	kininogen 1	Homo sapiens	50-60
8373725-8	1993	The results from this study point to activation of phospholipase A2 as the source of arachidonic acid in response to bradykinin.	Arachidonic Acid	85-101	kininogen 1	Homo sapiens	117-127
8393025-6	1993	Nedocromil sodium was able to inhibit the bronchoconstriction induced in patients with asthma by exposure to bradykinin, sulfur dioxide, metabisulfite, and ultrasonically nebulized water.	Nedocromil	0-17	kininogen 1	Homo sapiens	109-119
8504157-6	1993	PMA and bradykinin elicited a rapid and sustained response with the peaks of PA-labeling attained at 5 and &lt; 1 min after stimulation, respectively.	Phosphatidic Acids	77-79	kininogen 1	Homo sapiens	8-18
7686400-0	1993	Increase of bradykinin-stimulated arachidonic acid release in a delta F508 cystic fibrosis epithelial cell line.	Arachidonic Acid	34-50	kininogen 1	Homo sapiens	12-22
7686400-1	1993	Modification of chloride conductance by bradykinin in epithelial cells has been attributed to an activation of protein kinase A resulting from adenylcyclase stimulation by arachidonic acid cyclooxygenase products.	Chlorides	16-24	kininogen 1	Homo sapiens	40-50
7686400-4	1993	Bradykinin stimulated the release of arachidonic acid and the synthesis of cyclooxygenase derivatives (mainly PGE2).	Arachidonic Acid	37-53	kininogen 1	Homo sapiens	0-10
7686400-4	1993	Bradykinin stimulated the release of arachidonic acid and the synthesis of cyclooxygenase derivatives (mainly PGE2).	Dinoprostone	110-114	kininogen 1	Homo sapiens	0-10
7686400-5	1993	The cell line from the cystic fibrosis patient bearing a phenylalanine 508 deletion, which is the major form of the disease, showed a higher bradykinin-induced arachidonic acid release than either control cells or cells from a patient presenting a minor form of the disease.	Phenylalanine	57-70	kininogen 1	Homo sapiens	141-151
7686400-5	1993	The cell line from the cystic fibrosis patient bearing a phenylalanine 508 deletion, which is the major form of the disease, showed a higher bradykinin-induced arachidonic acid release than either control cells or cells from a patient presenting a minor form of the disease.	Arachidonic Acid	160-176	kininogen 1	Homo sapiens	141-151
8499491-0	1993	Effect of bradykinin on cytosolic calcium in neuroblastoma cells using the fluorescent indicator fluo-3.	Calcium	34-41	kininogen 1	Homo sapiens	10-20
8358540-15	1993	Bradykinin stimulated IPn, accumulation in HeLa cells, and the ECm in control cells of 1.9 +/- 0.2 nM was not significantly different from the EC50 value from histamine-pretreated cells of 1.6 +/- 0.9 nM.	isoamyl nitrite	22-25	kininogen 1	Homo sapiens	0-10
8358540-16	1993	The bradykinin response at 1 microM was 194 +/- 48% over basal IPn accumulation in control cells and this value was significantly different (P &lt;0.04) from the 1 microM bradykinin-induced IPn accumulation in histamine pretreated HeLa cells of 143 +/- 38% over basal.6.	isoamyl nitrite	63-66	kininogen 1	Homo sapiens	4-14
8358540-16	1993	The bradykinin response at 1 microM was 194 +/- 48% over basal IPn accumulation in control cells and this value was significantly different (P &lt;0.04) from the 1 microM bradykinin-induced IPn accumulation in histamine pretreated HeLa cells of 143 +/- 38% over basal.6.	isoamyl nitrite	190-193	kininogen 1	Homo sapiens	171-181
8358540-16	1993	The bradykinin response at 1 microM was 194 +/- 48% over basal IPn accumulation in control cells and this value was significantly different (P &lt;0.04) from the 1 microM bradykinin-induced IPn accumulation in histamine pretreated HeLa cells of 143 +/- 38% over basal.6.	Histamine	210-219	kininogen 1	Homo sapiens	4-14
8358540-16	1993	The bradykinin response at 1 microM was 194 +/- 48% over basal IPn accumulation in control cells and this value was significantly different (P &lt;0.04) from the 1 microM bradykinin-induced IPn accumulation in histamine pretreated HeLa cells of 143 +/- 38% over basal.6.	Histamine	210-219	kininogen 1	Homo sapiens	171-181
8388750-9	1993	The protein kinase C inhibitors (PKC), sphingosine and H7, completely block the induction of HK receptors by BK.	Sphingosine	39-50	kininogen 1	Homo sapiens	109-111
8388750-9	1993	The protein kinase C inhibitors (PKC), sphingosine and H7, completely block the induction of HK receptors by BK.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	55-57	kininogen 1	Homo sapiens	109-111
8507648-2	1993	Presence of a bradykinin B2 receptor antagonist [D-Arg0,Hyp3,Thi5,8,D-Phe7]-bradykinin (200 nM) in the circulation prevented shock caused by an intrajugular injection of pseudomonal elastase (0.8 mg/kg body weight).	d-arg0	49-55	kininogen 1	Homo sapiens	14-24
8507648-2	1993	Presence of a bradykinin B2 receptor antagonist [D-Arg0,Hyp3,Thi5,8,D-Phe7]-bradykinin (200 nM) in the circulation prevented shock caused by an intrajugular injection of pseudomonal elastase (0.8 mg/kg body weight).	thi5,	61-66	kininogen 1	Homo sapiens	14-24
8322908-1	1993	This study documents the discrete solute permeability mechanisms associated with physiologically high concentrations of human alpha-thrombin and bradykinin stimulation of bovine pulmonary artery endothelial cell (BPAEC) monolayers using fluorescein isothiocyanate-hydroxyethyl starch macromolecules.	Fluorescein-5-isothiocyanate	237-263	kininogen 1	Homo sapiens	145-155
8322908-1	1993	This study documents the discrete solute permeability mechanisms associated with physiologically high concentrations of human alpha-thrombin and bradykinin stimulation of bovine pulmonary artery endothelial cell (BPAEC) monolayers using fluorescein isothiocyanate-hydroxyethyl starch macromolecules.	Starch	277-283	kininogen 1	Homo sapiens	145-155
8499491-0	1993	Effect of bradykinin on cytosolic calcium in neuroblastoma cells using the fluorescent indicator fluo-3.	Fluo-3	97-103	kininogen 1	Homo sapiens	10-20
8499491-1	1993	Neuroblastoma cells were used to examine the effect of chronic exposure to increased concentrations of glucose, galactose, or L-fucose on bradykinin-stimulated intracellular calcium release using the calcium indicator fluo-3.	Glucose	103-110	kininogen 1	Homo sapiens	138-148
8499491-1	1993	Neuroblastoma cells were used to examine the effect of chronic exposure to increased concentrations of glucose, galactose, or L-fucose on bradykinin-stimulated intracellular calcium release using the calcium indicator fluo-3.	Galactose	112-121	kininogen 1	Homo sapiens	138-148
8499491-1	1993	Neuroblastoma cells were used to examine the effect of chronic exposure to increased concentrations of glucose, galactose, or L-fucose on bradykinin-stimulated intracellular calcium release using the calcium indicator fluo-3.	Fucose	126-134	kininogen 1	Homo sapiens	138-148
8499491-1	1993	Neuroblastoma cells were used to examine the effect of chronic exposure to increased concentrations of glucose, galactose, or L-fucose on bradykinin-stimulated intracellular calcium release using the calcium indicator fluo-3.	Calcium	174-181	kininogen 1	Homo sapiens	138-148
8499491-1	1993	Neuroblastoma cells were used to examine the effect of chronic exposure to increased concentrations of glucose, galactose, or L-fucose on bradykinin-stimulated intracellular calcium release using the calcium indicator fluo-3.	Calcium	200-207	kininogen 1	Homo sapiens	138-148
8499491-1	1993	Neuroblastoma cells were used to examine the effect of chronic exposure to increased concentrations of glucose, galactose, or L-fucose on bradykinin-stimulated intracellular calcium release using the calcium indicator fluo-3.	Fluo-3	218-224	kininogen 1	Homo sapiens	138-148
8103727-5	1993	The carbohydrate-free and the two mono-glycosylated analogues are about equally active with bradykinin.	Carbohydrates	4-16	kininogen 1	Homo sapiens	92-102
8499491-2	1993	Bradykinin caused a concentration dependent increase in the intracellular calcium concentration and phosphoinositide hydrolysis in neuroblastoma cells.	Calcium	74-81	kininogen 1	Homo sapiens	0-10
8499491-4	1993	Treatment of the cells with 10(-6) M bradykinin exhausts calcium release such that the successive treatment of the cells with norepinephrine, carbachol, or serotonin results in no secondary response.	Calcium	57-64	kininogen 1	Homo sapiens	37-47
8499491-4	1993	Treatment of the cells with 10(-6) M bradykinin exhausts calcium release such that the successive treatment of the cells with norepinephrine, carbachol, or serotonin results in no secondary response.	Norepinephrine	126-140	kininogen 1	Homo sapiens	37-47
8499491-4	1993	Treatment of the cells with 10(-6) M bradykinin exhausts calcium release such that the successive treatment of the cells with norepinephrine, carbachol, or serotonin results in no secondary response.	Carbachol	142-151	kininogen 1	Homo sapiens	37-47
8499491-4	1993	Treatment of the cells with 10(-6) M bradykinin exhausts calcium release such that the successive treatment of the cells with norepinephrine, carbachol, or serotonin results in no secondary response.	Serotonin	156-165	kininogen 1	Homo sapiens	37-47
8499491-5	1993	In contrast, bradykinin treatment of the cells following exposure to norepinephrine, carbachol, or serotonin caused a secondary increase in calcium release.	Norepinephrine	69-83	kininogen 1	Homo sapiens	13-23
8499491-5	1993	In contrast, bradykinin treatment of the cells following exposure to norepinephrine, carbachol, or serotonin caused a secondary increase in calcium release.	Carbachol	85-94	kininogen 1	Homo sapiens	13-23
8499491-5	1993	In contrast, bradykinin treatment of the cells following exposure to norepinephrine, carbachol, or serotonin caused a secondary increase in calcium release.	Serotonin	99-108	kininogen 1	Homo sapiens	13-23
8499491-5	1993	In contrast, bradykinin treatment of the cells following exposure to norepinephrine, carbachol, or serotonin caused a secondary increase in calcium release.	Calcium	140-147	kininogen 1	Homo sapiens	13-23
8499491-7	1993	Bradykinin-stimulated calcium release is not effected by chronic exposure of the cells to increased concentrations of glucose, galactose, or L-fucose.	Calcium	22-29	kininogen 1	Homo sapiens	0-10
8389325-0	1993	Captopril inhibits endothelin-1 secretion from endothelial cells through bradykinin.	Captopril	0-9	kininogen 1	Homo sapiens	73-83
8389325-4	1993	Moreover, in the presence of 10(-6) M D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin, a bradykinin B2 receptor antagonist, captopril did not inhibit but rather stimulated endothelin-1 secretion, whereas bradykinin inhibited endothelin-1 secretion, and this inhibition by bradykinin was reversed by coincubation with NG-nitro-L-arginine.	D-Arginine	38-43	kininogen 1	Homo sapiens	65-75
8389325-4	1993	Moreover, in the presence of 10(-6) M D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin, a bradykinin B2 receptor antagonist, captopril did not inhibit but rather stimulated endothelin-1 secretion, whereas bradykinin inhibited endothelin-1 secretion, and this inhibition by bradykinin was reversed by coincubation with NG-nitro-L-arginine.	thi5	50-54	kininogen 1	Homo sapiens	65-75
8389325-4	1993	Moreover, in the presence of 10(-6) M D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin, a bradykinin B2 receptor antagonist, captopril did not inhibit but rather stimulated endothelin-1 secretion, whereas bradykinin inhibited endothelin-1 secretion, and this inhibition by bradykinin was reversed by coincubation with NG-nitro-L-arginine.	,d-phe7	56-63	kininogen 1	Homo sapiens	65-75
8389325-5	1993	In addition, enhancement of nitric oxide production induced by either captopril or bradykinin was inhibited by D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin.	Nitric Oxide	28-40	kininogen 1	Homo sapiens	83-93
8389325-5	1993	In addition, enhancement of nitric oxide production induced by either captopril or bradykinin was inhibited by D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin.	Nitric Oxide	28-40	kininogen 1	Homo sapiens	138-148
8389325-5	1993	In addition, enhancement of nitric oxide production induced by either captopril or bradykinin was inhibited by D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin.	Captopril	70-79	kininogen 1	Homo sapiens	138-148
8389325-5	1993	In addition, enhancement of nitric oxide production induced by either captopril or bradykinin was inhibited by D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin.	D-Arginine	111-116	kininogen 1	Homo sapiens	83-93
8389325-5	1993	In addition, enhancement of nitric oxide production induced by either captopril or bradykinin was inhibited by D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin.	thi5	123-127	kininogen 1	Homo sapiens	83-93
8389325-5	1993	In addition, enhancement of nitric oxide production induced by either captopril or bradykinin was inhibited by D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin.	thi5	123-127	kininogen 1	Homo sapiens	138-148
8389325-5	1993	In addition, enhancement of nitric oxide production induced by either captopril or bradykinin was inhibited by D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin.	,d-phe7	129-136	kininogen 1	Homo sapiens	83-93
8389325-5	1993	In addition, enhancement of nitric oxide production induced by either captopril or bradykinin was inhibited by D-Arg,[Hyp3,Thi5,8,D-Phe7]-bradykinin.	,d-phe7	129-136	kininogen 1	Homo sapiens	138-148
8390257-2	1993	The degradation of BK in semen was completely abolished by the metalloprotease inhibitors EDTA and o-phenanthroline.	Edetic Acid	90-94	kininogen 1	Homo sapiens	19-21
8390257-2	1993	The degradation of BK in semen was completely abolished by the metalloprotease inhibitors EDTA and o-phenanthroline.	1,10-phenanthroline	99-115	kininogen 1	Homo sapiens	19-21
8390257-5	1993	HPLC analysis demonstrated that exogenous BK in semen is cleaved at Gly4-Phe5, Phe5-Ser6 and Pro7-Phe8.	glycyl-glycyl-glycyl-glycine	68-72	kininogen 1	Homo sapiens	42-44
7683612-0	1993	The role of calcium in cell shrinkage and intracellular alkalinization by bradykinin in Ha-ras oncogene expressing cells.	Calcium	12-19	kininogen 1	Homo sapiens	74-84
7683612-7	1993	At 100 nmol/l ionomycin intracellular calcium is increased from 114 +/- 17 nmol/l to 342 +/- 24 nmol/l (n = 9), a value within the range of intracellular calcium concentrations following application of bradykinin.	Ionomycin	14-23	kininogen 1	Homo sapiens	202-212
7683612-8	1993	The calcium increase is paralleled by a decrease of cell volume by 12 +/- 2% (n = 5) and an increase of intracellular pH from 6.78 +/- 0.02 to 6.90 +/- 0.03 (n = 11), values similar to those following application of bradykinin.	Calcium	4-11	kininogen 1	Homo sapiens	216-226
7683612-11	1993	It is concluded that bradykinin leads to intracellular alkalinization mainly by increasing intracellular calcium concentration.	Calcium	105-112	kininogen 1	Homo sapiens	21-31
8319757-0	1993	Inhibitory effects of Hoe 140 on vasodilator responses to bradykinin in the mesenteric vascular bed of the cat.	4-hydroxy-2-octenal	22-25	kininogen 1	Homo sapiens	58-68
8319757-1	1993	The effect of Hoe 140, a bradykinin B2 receptor antagonist, on vasodilator responses to bradykinin was investigated in the mesenteric vascular bed of the cat under constant flow conditions.	4-hydroxy-2-octenal	14-17	kininogen 1	Homo sapiens	88-98
8319757-2	1993	Injections of bradykinin into the mesenteric vascular bed induced dose-related decreases in perfusion pressure which were reduced significantly following administration of Hoe 140 (D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin) (100 micrograms/kg i.v.).	4-hydroxy-2-octenal	172-175	kininogen 1	Homo sapiens	14-24
8319757-2	1993	Injections of bradykinin into the mesenteric vascular bed induced dose-related decreases in perfusion pressure which were reduced significantly following administration of Hoe 140 (D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin) (100 micrograms/kg i.v.).	4-hydroxy-2-octenal	172-175	kininogen 1	Homo sapiens	210-220
8319757-2	1993	Injections of bradykinin into the mesenteric vascular bed induced dose-related decreases in perfusion pressure which were reduced significantly following administration of Hoe 140 (D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin) (100 micrograms/kg i.v.).	D-Arginine	181-186	kininogen 1	Homo sapiens	14-24
8319757-2	1993	Injections of bradykinin into the mesenteric vascular bed induced dose-related decreases in perfusion pressure which were reduced significantly following administration of Hoe 140 (D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin) (100 micrograms/kg i.v.).	D-Arginine	181-186	kininogen 1	Homo sapiens	210-220
8319757-2	1993	Injections of bradykinin into the mesenteric vascular bed induced dose-related decreases in perfusion pressure which were reduced significantly following administration of Hoe 140 (D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin) (100 micrograms/kg i.v.).	thi5	193-197	kininogen 1	Homo sapiens	14-24
8319757-2	1993	Injections of bradykinin into the mesenteric vascular bed induced dose-related decreases in perfusion pressure which were reduced significantly following administration of Hoe 140 (D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin) (100 micrograms/kg i.v.).	d-tic7	198-204	kininogen 1	Homo sapiens	14-24
8319757-5	1993	These results suggest that Hoe 140 is a potent, highly selective, long-acting bradykinin B2 receptor antagonist with little agonistic activity in the mesenteric vascular bed of the cat.	4-hydroxy-2-octenal	27-30	kininogen 1	Homo sapiens	78-88
7683685-3	1993	Image analysis data from individual cells stimulated by BK in the presence of genistein and tyrphostin showed that these inhibitors block the plateau phase but not the rapid transient phase of the BK-induced calcium response.	Calcium	208-215	kininogen 1	Homo sapiens	197-199
7683685-4	1993	That the loss of the plateau phase was due to blockage of calcium entry rather than stimulation of calcium pump activity was confirmed by examining the influx of Ba2+ following BK stimulation.	N-methyl-valyl-amiclenomycin	162-166	kininogen 1	Homo sapiens	177-179
7683685-2	1993	Immunoblots with anti-phosphotyrosine antibodies following BK stimulation of human fibroblasts showed tyrosine phosphorylation of specific proteins that could be inhibited by the tyrosine kinase inhibitors genistein and tyrphostin.	Phosphotyrosine	22-37	kininogen 1	Homo sapiens	59-61
7683685-6	1993	The fact that three structurally distinct inhibitors of tyrosine kinase activity inhibited BK-stimulated calcium influx, while an inactive analogue of genistein (daidzein) did not, strongly suggests the involvement of tyrosine kinases in the regulation of a BK-induced calcium entry pathway.	Calcium	105-112	kininogen 1	Homo sapiens	91-93
7683685-2	1993	Immunoblots with anti-phosphotyrosine antibodies following BK stimulation of human fibroblasts showed tyrosine phosphorylation of specific proteins that could be inhibited by the tyrosine kinase inhibitors genistein and tyrphostin.	Tyrosine	29-37	kininogen 1	Homo sapiens	59-61
7683685-2	1993	Immunoblots with anti-phosphotyrosine antibodies following BK stimulation of human fibroblasts showed tyrosine phosphorylation of specific proteins that could be inhibited by the tyrosine kinase inhibitors genistein and tyrphostin.	Genistein	206-215	kininogen 1	Homo sapiens	59-61
7683685-6	1993	The fact that three structurally distinct inhibitors of tyrosine kinase activity inhibited BK-stimulated calcium influx, while an inactive analogue of genistein (daidzein) did not, strongly suggests the involvement of tyrosine kinases in the regulation of a BK-induced calcium entry pathway.	Calcium	269-276	kininogen 1	Homo sapiens	91-93
7683685-2	1993	Immunoblots with anti-phosphotyrosine antibodies following BK stimulation of human fibroblasts showed tyrosine phosphorylation of specific proteins that could be inhibited by the tyrosine kinase inhibitors genistein and tyrphostin.	Tyrphostins	220-230	kininogen 1	Homo sapiens	59-61
8388656-3	1993	Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisinopril, ramiprilat, and captopril.	Lisinopril	138-148	kininogen 1	Homo sapiens	12-22
8388656-3	1993	Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisinopril, ramiprilat, and captopril.	ramiprilat	150-160	kininogen 1	Homo sapiens	12-22
8388656-3	1993	Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisinopril, ramiprilat, and captopril.	Captopril	166-175	kininogen 1	Homo sapiens	12-22
8388656-6	1993	The functional consequence of bradykinin degradation was demonstrated by the potentiating effect of ramiprilat on the generation of endothelium-derived relaxing factors nitric oxide and prostacyclin from endothelial cells.	ramiprilat	100-110	kininogen 1	Homo sapiens	30-40
8388656-6	1993	The functional consequence of bradykinin degradation was demonstrated by the potentiating effect of ramiprilat on the generation of endothelium-derived relaxing factors nitric oxide and prostacyclin from endothelial cells.	Nitric Oxide	169-181	kininogen 1	Homo sapiens	30-40
8498571-3	1993	Thus we hypothesized that bradykinin would also increase transcapillary water flux.	Water	72-77	kininogen 1	Homo sapiens	26-36
8388656-6	1993	The functional consequence of bradykinin degradation was demonstrated by the potentiating effect of ramiprilat on the generation of endothelium-derived relaxing factors nitric oxide and prostacyclin from endothelial cells.	Epoprostenol	186-198	kininogen 1	Homo sapiens	30-40
8489507-0	1993	Effect of temperature on bradykinin-induced arachidonate release and calcium mobilization in vascular endothelial cells.	Arachidonic Acid	44-56	kininogen 1	Homo sapiens	25-35
8489507-6	1993	Ins(1,4,5)P3, mobilized sequestered Ca2+ to a similar degree at 37 degrees C and 22 degrees C, although Ca2+ release was prolonged at 22 degrees C. In intact cells, BK mobilized intracellular Ca2+ stores and activated Ca2+ entry.	Inositol 1,4,5-Trisphosphate	0-12	kininogen 1	Homo sapiens	165-167
8393713-1	1993	The conformation of two agonist-antagonist pairs of bradykinin (Arg1-Pro2-Pro2-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9) analogues were studied in CD3OH/H2O solution by 1H-nmr techniques.	pro2-gly4-phe5	74-88	kininogen 1	Homo sapiens	52-62
8489507-10	1993	As with BK, the peak [Ca2+]i reached after thapsigargin treatment was higher at 22 degrees C. This effect of lower temperature on [Ca2+]i was most probably due to decreased Ca2+ efflux after a decrease in activity of the Ca(2+)-ATPase on the plasma membrane.	Thapsigargin	43-55	kininogen 1	Homo sapiens	8-10
8393713-1	1993	The conformation of two agonist-antagonist pairs of bradykinin (Arg1-Pro2-Pro2-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9) analogues were studied in CD3OH/H2O solution by 1H-nmr techniques.	ser6-pro7	89-98	kininogen 1	Homo sapiens	52-62
8489507-11	1993	Both A23187 and BK were shown to stimulate phospholipase A2 and arachidonic acid release at 22 degrees C. In each case, the rate and extent of release were decreased compared with that at 37 degrees C. Among several effects, lowering the temperature decreases the activity of phospholipase C, Ca(2+)-ATPase(s), Ca(2+)-entry mechanisms and phospholipase A2.	Arachidonic Acid	64-80	kininogen 1	Homo sapiens	16-18
8489507-12	1993	Together, these effects lead to a higher and more prolonged elevation of [Ca2+]i, but a decrease in arachidonate release in response to BK.	Arachidonic Acid	100-112	kininogen 1	Homo sapiens	136-138
8393713-1	1993	The conformation of two agonist-antagonist pairs of bradykinin (Arg1-Pro2-Pro2-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9) analogues were studied in CD3OH/H2O solution by 1H-nmr techniques.	Methanol-d3	136-141	kininogen 1	Homo sapiens	52-62
8393713-1	1993	The conformation of two agonist-antagonist pairs of bradykinin (Arg1-Pro2-Pro2-Gly4-Phe5-Ser6-Pro7-Phe8-Arg9) analogues were studied in CD3OH/H2O solution by 1H-nmr techniques.	Water	142-145	kininogen 1	Homo sapiens	52-62
7688545-0	1993	Bradykinin inhibits cyclic AMP accumulation in D384-human astrocytoma cells via a calcium-dependent inhibition of adenylyl cyclase.	Cyclic AMP	20-30	kininogen 1	Homo sapiens	0-10
8393713-2	1993	The first agonist peptide studied, D-Arg0-Arg1-Pro2-Hyp3-Gly4-Thi5-Ser6-Pro7- Thi8-Arg9, differs from the bradykinin sequence by the addition of D-Arg0, the replacement of the Phe moieties in positions 5 and 8 by Thi (Thi = beta-(2-thienyl)-L-alanine), and Hyp3 (Hyp = L-4-hydroxy-L-proline) in position 3.	d-arg0	35-41	kininogen 1	Homo sapiens	106-116
7688545-0	1993	Bradykinin inhibits cyclic AMP accumulation in D384-human astrocytoma cells via a calcium-dependent inhibition of adenylyl cyclase.	Calcium	82-89	kininogen 1	Homo sapiens	0-10
7688545-1	1993	Bradykinin causes a concentration-dependent, transient rise in intracellular Ca2+ and a sustained inhibition of forskolin-, dopamine- and 5"-N-ethyl-carboxamidoadenosine (NECA)-stimulated cAMP accumulation in D384 astrocytoma cells.	Colforsin	112-121	kininogen 1	Homo sapiens	0-10
7688545-1	1993	Bradykinin causes a concentration-dependent, transient rise in intracellular Ca2+ and a sustained inhibition of forskolin-, dopamine- and 5"-N-ethyl-carboxamidoadenosine (NECA)-stimulated cAMP accumulation in D384 astrocytoma cells.	Dopamine	124-132	kininogen 1	Homo sapiens	0-10
7688545-1	1993	Bradykinin causes a concentration-dependent, transient rise in intracellular Ca2+ and a sustained inhibition of forskolin-, dopamine- and 5"-N-ethyl-carboxamidoadenosine (NECA)-stimulated cAMP accumulation in D384 astrocytoma cells.	Adenosine-5'-(N-ethylcarboxamide)	138-169	kininogen 1	Homo sapiens	0-10
7688545-1	1993	Bradykinin causes a concentration-dependent, transient rise in intracellular Ca2+ and a sustained inhibition of forskolin-, dopamine- and 5"-N-ethyl-carboxamidoadenosine (NECA)-stimulated cAMP accumulation in D384 astrocytoma cells.	Adenosine-5'-(N-ethylcarboxamide)	171-175	kininogen 1	Homo sapiens	0-10
7688545-1	1993	Bradykinin causes a concentration-dependent, transient rise in intracellular Ca2+ and a sustained inhibition of forskolin-, dopamine- and 5"-N-ethyl-carboxamidoadenosine (NECA)-stimulated cAMP accumulation in D384 astrocytoma cells.	Cyclic AMP	188-192	kininogen 1	Homo sapiens	0-10
7688545-2	1993	Chelation of intracellular calcium abolished bradykinin"s inhibitory effect on cAMP accumulation.	Calcium	27-34	kininogen 1	Homo sapiens	45-55
7688545-2	1993	Chelation of intracellular calcium abolished bradykinin"s inhibitory effect on cAMP accumulation.	Cyclic AMP	79-83	kininogen 1	Homo sapiens	45-55
8395230-5	1993	The inhibitor of neutral endopeptidase, phosphoramidon (10(-8) mol/l), decreased the degradation of bradykinin in the supernatant of endothelial cells; the half-life of bradykinin was then increased from 29 +/- 1 to 46 +/- 2 minutes.	phosphoramidon	40-54	kininogen 1	Homo sapiens	100-110
8395230-5	1993	The inhibitor of neutral endopeptidase, phosphoramidon (10(-8) mol/l), decreased the degradation of bradykinin in the supernatant of endothelial cells; the half-life of bradykinin was then increased from 29 +/- 1 to 46 +/- 2 minutes.	phosphoramidon	40-54	kininogen 1	Homo sapiens	169-179
8395230-6	1993	The angiotensin-converting enzyme inhibitor, lisinopril (10(-8) mol/l), increased the half-life of bradykinin to 244 +/- 20 minutes; the combination of both inhibitors increased the half-life of bradykinin to 381 +/- 51 minutes.	Lisinopril	45-55	kininogen 1	Homo sapiens	99-109
8395230-6	1993	The angiotensin-converting enzyme inhibitor, lisinopril (10(-8) mol/l), increased the half-life of bradykinin to 244 +/- 20 minutes; the combination of both inhibitors increased the half-life of bradykinin to 381 +/- 51 minutes.	Lisinopril	45-55	kininogen 1	Homo sapiens	195-205
8335573-3	1993	Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-NG-mono-methylarginine (L-NMMA; 300 microM).	bisphenol A	76-79	kininogen 1	Homo sapiens	21-31
8335573-3	1993	Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-NG-mono-methylarginine (L-NMMA; 300 microM).	bisphenol A	76-79	kininogen 1	Homo sapiens	33-35
8335573-3	1993	Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-NG-mono-methylarginine (L-NMMA; 300 microM).	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	129-136	kininogen 1	Homo sapiens	21-31
8335573-3	1993	Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-NG-mono-methylarginine (L-NMMA; 300 microM).	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	129-136	kininogen 1	Homo sapiens	33-35
8335573-3	1993	Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-NG-mono-methylarginine (L-NMMA; 300 microM).	omega-N-Methylarginine	220-244	kininogen 1	Homo sapiens	21-31
8335573-3	1993	Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-NG-mono-methylarginine (L-NMMA; 300 microM).	omega-N-Methylarginine	220-244	kininogen 1	Homo sapiens	33-35
8335573-3	1993	Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-NG-mono-methylarginine (L-NMMA; 300 microM).	omega-N-Methylarginine	246-252	kininogen 1	Homo sapiens	21-31
8335573-3	1993	Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-NG-mono-methylarginine (L-NMMA; 300 microM).	omega-N-Methylarginine	246-252	kininogen 1	Homo sapiens	33-35
8335573-4	1993	TNF-alpha (0.00417, 0.0417, 0.417, and 1.25 micrograms/ml) incubated with BPA for 60 min inhibited EDR of the BPA to ACh, BK, and histamine.	bisphenol A	74-77	kininogen 1	Homo sapiens	122-124
8242430-5	1993	Calcium mobilization triggered by cadmium or bradykinin was relatively insensitive to genistein.	Calcium	0-7	kininogen 1	Homo sapiens	45-55
7688545-9	1993	Bradykinin treatment, which attenuates cAMP accumulation in intact cells, did not do so in plasma membranes.	Cyclic AMP	39-43	kininogen 1	Homo sapiens	0-10
7688545-10	1993	These findings suggest that bradykinin-induced inhibition of cAMP formation in D384 cells requires mobilization of [Ca2+]i and subsequent entry of Ca2+ which directly interacts with a component of the adenylyl cyclase system.	Cyclic AMP	61-65	kininogen 1	Homo sapiens	28-38
8315520-7	1993	A local accumulation of bradykinin may lead to activation of pro-inflammatory peptides (e.g. substance P, neuropeptide Y) and a local release of histamine.	Histamine	145-154	kininogen 1	Homo sapiens	24-34
8100493-11	1993	BK and ATP also significantly increased formation of inositol phosphates in BCEC.	Inositol Phosphates	53-72	kininogen 1	Homo sapiens	0-2
8458876-4	1993	By microinjection of inhibitory antibodies specific to distinct G alpha subunits into living cells, we have determined that G alpha q transduces bradykinin- and thrombin-stimulated intracellular calcium transients which are likely to be mediated by PLC beta 1.	Calcium	195-202	kininogen 1	Homo sapiens	145-155
8458876-6	1993	These results indicate that both thrombin and bradykinin utilize Gq to couple to increases in intracellular calcium, and that Gq is a necessary component of the mitogenic action of these factors.	Calcium	108-115	kininogen 1	Homo sapiens	46-56
8458876-6	1993	These results indicate that both thrombin and bradykinin utilize Gq to couple to increases in intracellular calcium, and that Gq is a necessary component of the mitogenic action of these factors.	glycylglutamine	65-67	kininogen 1	Homo sapiens	46-56
8511729-2	1993	Like histamine, nasal challenge with bradykinin induces rhinorrhoea, nasal blockage, and plasma protein leakage.	Histamine	5-14	kininogen 1	Homo sapiens	37-47
8511729-13	1993	In contrast, although NAR was increased significantly more by histamine than by the vehicle, the effect of bradykinin on NAR was significantly greater than histamine and vehicle in both magnitude and duration of effect.	Histamine	156-165	kininogen 1	Homo sapiens	107-117
8456975-6	1993	In rings with endothelium contracted with prostaglandin F2 alpha, pertussis toxin (100 ng/ml) or LPC (10(-5) M) inhibited the endothelium-dependent relaxations evoked by UK-14,304, an alpha 2-adrenergic agonist, or by serotonin, but not those caused by bradykinin or ADP.	uk-14	170-175	kininogen 1	Homo sapiens	253-263
8443392-2	1993	Excision of the vasoactive peptide bradykinin by plasma kallikrein results in kinin-free HK that consists of a 65-Kd N-terminal heavy chain (HK-HC) linked to the C-terminal 45-Kd light chain (HK-LC) by a disulfide bridge.	Disulfides	204-213	kininogen 1	Homo sapiens	35-45
1467832-6	1992	Bradykinin induced comparable endothelium-dependent relaxations of proximal and distal rings of porcine coronary arteries contracted with prostaglandin F2 alpha in the presence of nitro-L-arginine.	Dinoprost	138-160	kininogen 1	Homo sapiens	0-10
8391072-2	1993	Since ACE inactivates bradykinin in addition to its action on angiotensin I we hypothesized that losartan and enalapril have different effects on the response to angiotensin and bradykinin.	Losartan	97-105	kininogen 1	Homo sapiens	22-32
8391072-2	1993	Since ACE inactivates bradykinin in addition to its action on angiotensin I we hypothesized that losartan and enalapril have different effects on the response to angiotensin and bradykinin.	Losartan	97-105	kininogen 1	Homo sapiens	178-188
8391072-2	1993	Since ACE inactivates bradykinin in addition to its action on angiotensin I we hypothesized that losartan and enalapril have different effects on the response to angiotensin and bradykinin.	Enalapril	110-119	kininogen 1	Homo sapiens	22-32
8391072-2	1993	Since ACE inactivates bradykinin in addition to its action on angiotensin I we hypothesized that losartan and enalapril have different effects on the response to angiotensin and bradykinin.	Enalapril	110-119	kininogen 1	Homo sapiens	178-188
8382669-6	1993	Bradykinin-coupled PPI turnover was linear up to 60 min and was blocked by &gt; 90% by the B2 antagonist [Thi5,8,D-Phe7]-bradykinin.	thi5,8,d-phe7	106-119	kininogen 1	Homo sapiens	0-10
8382669-6	1993	Bradykinin-coupled PPI turnover was linear up to 60 min and was blocked by &gt; 90% by the B2 antagonist [Thi5,8,D-Phe7]-bradykinin.	thi5,8,d-phe7	106-119	kininogen 1	Homo sapiens	121-131
8419539-5	1993	Experiments of [Ca2+]i measurement with the fura-2 technique showed that P2y agonists, as well as bradykinin, were able to increase [Ca2+]i, this effect being independent of the presence of extracellular Ca2+.	Fura-2	44-50	kininogen 1	Homo sapiens	98-108
8419539-6	1993	The peptide bradykinin, determined to be coupled to phosphatidylinositol hydrolysis and internal Ca2+ mobilization in chromaffin cells, exhibited a behavior similar to that of P2y agonists in adenosine transport inhibition (39%).	Phosphatidylinositols	52-72	kininogen 1	Homo sapiens	12-22
8419539-6	1993	The peptide bradykinin, determined to be coupled to phosphatidylinositol hydrolysis and internal Ca2+ mobilization in chromaffin cells, exhibited a behavior similar to that of P2y agonists in adenosine transport inhibition (39%).	chromaffin	118-128	kininogen 1	Homo sapiens	12-22
8419539-6	1993	The peptide bradykinin, determined to be coupled to phosphatidylinositol hydrolysis and internal Ca2+ mobilization in chromaffin cells, exhibited a behavior similar to that of P2y agonists in adenosine transport inhibition (39%).	Adenosine	192-201	kininogen 1	Homo sapiens	12-22
8426248-0	1993	Effect of flurbiprofen on tissue levels of immunoreactive bradykinin and acute postoperative pain.	Flurbiprofen	10-22	kininogen 1	Homo sapiens	58-68
8426248-1	1993	This study evaluates whether preoperative administration of flurbiprofen alters the levels of immunoreactive bradykinin (iBK) peripherally released into inflamed tissue.	Flurbiprofen	60-72	kininogen 1	Homo sapiens	109-119
8447970-3	1993	Acute exposure to ethanol resulted in an inhibition of bradykinin mediated [Ca2+]i mobilization with significant effects observed only at 400 mM ethanol.	Ethanol	18-25	kininogen 1	Homo sapiens	55-65
8503874-1	1993	Oxidant stress induced by t-butyl hydroperoxide (t-BuOOH) inhibits bradykinin-stimulated Ca2+ signalling in vascular endothelial cells.	tert-Butylhydroperoxide	26-47	kininogen 1	Homo sapiens	67-77
8503874-1	1993	Oxidant stress induced by t-butyl hydroperoxide (t-BuOOH) inhibits bradykinin-stimulated Ca2+ signalling in vascular endothelial cells.	di-tert-butyl peroxide	49-56	kininogen 1	Homo sapiens	67-77
8503874-4	1993	By contrast, incubation with t-BuOOH progressively decreased the response of [Ca2+]i to bradykinin and increased that to ionomycin, suggesting that the total (ionomycin-releasable) Ca2+ pool remains replete during oxidant stress.	di-tert-butyl peroxide	29-36	kininogen 1	Homo sapiens	88-98
8503874-11	1993	Together, these findings suggest that (1) the inhibitory effect of t-BuOOH on bradykinin-stimulated release of Ca2+ from internal stores is not related to depletion of these stores, and (2) inhibition of the store-dependent Ca(2+)-influx pathway occurs by a direct effect of the influx pathway or by inhibition of the mechanism which links the internal Ca2+ store to plasmalemmal Ca2+ influx.	di-tert-butyl peroxide	67-74	kininogen 1	Homo sapiens	78-88
7679681-3	1993	In arterial strips precontracted with PGF2 alpha, substance P and bradykinin both elicited relaxation that was almost completely abolished by removal of the endothelium.	Dinoprost	38-48	kininogen 1	Homo sapiens	66-76
8383737-5	1993	Bradykinin-induced prostaglandin E2 production seemed to be associated primarily with the lower affinity site.	Dinoprostone	19-35	kininogen 1	Homo sapiens	0-10
8383737-6	1993	All three B2 receptor antagonists displaced labeled bradykinin from both classes of binding sites and inhibited bradykinin-induced prostaglandin E2 production, but Hoe 140 was up to 40-fold more potent than NPC 567 and showed an affinity comparable to that of bradykinin for both binding sites.	Dinoprostone	131-147	kininogen 1	Homo sapiens	112-122
8383737-6	1993	All three B2 receptor antagonists displaced labeled bradykinin from both classes of binding sites and inhibited bradykinin-induced prostaglandin E2 production, but Hoe 140 was up to 40-fold more potent than NPC 567 and showed an affinity comparable to that of bradykinin for both binding sites.	Dinoprostone	131-147	kininogen 1	Homo sapiens	112-122
8383737-7	1993	This higher potency of Hoe 140, and its stability against peptidases, suggests that this compound will be useful in evaluating the role of bradykinin in inflammatory diseases of the airways.	4-hydroxy-2-octenal	23-26	kininogen 1	Homo sapiens	139-149
8385778-0	1993	Arachidonic acid release and inositol lipid metabolism in response to bradykinin and related peptides in human endometrial cells in vitro.	Arachidonic Acid	0-16	kininogen 1	Homo sapiens	70-80
8385778-0	1993	Arachidonic acid release and inositol lipid metabolism in response to bradykinin and related peptides in human endometrial cells in vitro.	inositol lipid	29-43	kininogen 1	Homo sapiens	70-80
8385778-2	1993	The aim of the present study was to investigate the action of the potent vasoactive peptide bradykinin and the structurally related peptide, kallidin, on endometrial function by examining their effect on phosphoinositide hydrolysis and arachidonic acid release from endometrial cells in vitro.	Arachidonic Acid	236-252	kininogen 1	Homo sapiens	92-102
8385778-4	1993	Bradykinin and kallidin stimulated a dose and time-dependent release of arachidonic acid from stromal cells which, with 100 nmol/L bradykinin, was 30-150% above basal release and maximal at 5 min.	Arachidonic Acid	72-88	kininogen 1	Homo sapiens	0-10
8385778-4	1993	Bradykinin and kallidin stimulated a dose and time-dependent release of arachidonic acid from stromal cells which, with 100 nmol/L bradykinin, was 30-150% above basal release and maximal at 5 min.	Arachidonic Acid	72-88	kininogen 1	Homo sapiens	131-141
8385778-6	1993	Bradykinin also stimulated a dose dependent increase in inositol monophosphate production.	Inositol Phosphates	56-78	kininogen 1	Homo sapiens	0-10
7680560-6	1993	NOS inhibitor-induced CBF slowing was also observed when cells were pre-stimulated with either bradykinin or substance P and was completely reversed by L-arginine or SNP but not by D-arginine.	Arginine	152-162	kininogen 1	Homo sapiens	95-105
8447370-3	1993	Bradykinin-stimulated release of [3H]arachidonic acid was increased 1.8-fold over release from control cultures by prior irradiation.	[3h]arachidonic acid	33-53	kininogen 1	Homo sapiens	0-10
8447370-4	1993	In unlabeled cultures, prior irradiation produced a threefold increase in bradykinin-stimulated prostaglandin (PG) E2 synthesis as measured by immunoassay.	Dinoprostone	96-117	kininogen 1	Homo sapiens	74-84
8447442-3	1993	The following three possibilities were examined, namely, 1) signaling events other than [Ca2+]i are different for BK and AVP; 2) BK, but not AVP, stimulates prostaglandins in VSMC, thus resulting in divergent effects on VSMC tone; and 3) AVP and BK exhibit qualitatively similar effects on VSMC signal transduction but divergent effects on VSMC tone are mediated by endothelial events.	Prostaglandins	157-171	kininogen 1	Homo sapiens	129-131
8447442-3	1993	The following three possibilities were examined, namely, 1) signaling events other than [Ca2+]i are different for BK and AVP; 2) BK, but not AVP, stimulates prostaglandins in VSMC, thus resulting in divergent effects on VSMC tone; and 3) AVP and BK exhibit qualitatively similar effects on VSMC signal transduction but divergent effects on VSMC tone are mediated by endothelial events.	Prostaglandins	157-171	kininogen 1	Homo sapiens	129-131
8447442-4	1993	The results demonstrated that BK stimulated a rise in inositol trisphosphate (IP3), [Ca2+]i, 45Ca2+ efflux, and Ca2+ influx and a biphasic change in intracellular pH when N-2-hydroxyethylpiperazine-N"-2-ethanesulfonic acid-buffered solution was used.	inositol 1,2,3-trisphosphate	54-76	kininogen 1	Homo sapiens	30-32
8447442-4	1993	The results demonstrated that BK stimulated a rise in inositol trisphosphate (IP3), [Ca2+]i, 45Ca2+ efflux, and Ca2+ influx and a biphasic change in intracellular pH when N-2-hydroxyethylpiperazine-N"-2-ethanesulfonic acid-buffered solution was used.	Inositol 1,4,5-Trisphosphate	78-81	kininogen 1	Homo sapiens	30-32
8447442-4	1993	The results demonstrated that BK stimulated a rise in inositol trisphosphate (IP3), [Ca2+]i, 45Ca2+ efflux, and Ca2+ influx and a biphasic change in intracellular pH when N-2-hydroxyethylpiperazine-N"-2-ethanesulfonic acid-buffered solution was used.	HEPES	171-222	kininogen 1	Homo sapiens	30-32
8447442-6	1993	The cyclooxygenase inhibitor, meclofenamate, enhanced the effect of both BK and AVP on VSMC tone, as assessed by shape change, by a comparable degree.	Meclofenamic Acid	30-43	kininogen 1	Homo sapiens	73-75
8447442-8	1993	Methylene blue, a blocker of cytosolic guanylate cyclase and therefore of the production of guanosine 3",5"-cyclic monophosphate (2nd messenger of endothelium-derived relaxing factor, EDRF), and nordihydroguaiaretic acid, an inhibitor of EDRF, both prevented this endothelium-dependent effect of BK.	Methylene Blue	0-14	kininogen 1	Homo sapiens	296-298
8447442-9	1993	These results therefore indicate that BK is a constrictor of VSMC, an effect that can be overridden by the hormone"s endothelial effect to stimulate the release of a vasodilator(s), which is most likely EDRF.	vsmc	61-65	kininogen 1	Homo sapiens	38-40
8447447-7	1993	Endothelin-1 (ET-1) and bradykinin (BK) elicited dilator responses that were significantly (P &lt; 0.05) reduced in the presence of L-NNA.	Nitroarginine	132-137	kininogen 1	Homo sapiens	24-34
8447447-7	1993	Endothelin-1 (ET-1) and bradykinin (BK) elicited dilator responses that were significantly (P &lt; 0.05) reduced in the presence of L-NNA.	Nitroarginine	132-137	kininogen 1	Homo sapiens	36-38
8292107-8	1993	Potential mechanisms of injury include idiopathic hypersensitivity and modulation of eicosanoid metabolism by inhibition of kininase II and subsequent increased hepatic bradykinin activity.	Eicosanoids	85-95	kininogen 1	Homo sapiens	169-179
8386065-7	1993	Bradykinin concentrations in the organ bath measured by a specific bradykinin radioimmunoassay remained stable during the addition of lisinopril.	Lisinopril	134-144	kininogen 1	Homo sapiens	0-10
8386065-11	1993	Endothelium dependent relaxation to lisinopril and captopril was also observed in human coronary arteries treated with bradykinin (&gt; or = 10(-7) M), but not in those treated with substance P (10(-8) M).	Lisinopril	36-46	kininogen 1	Homo sapiens	119-129
8386065-11	1993	Endothelium dependent relaxation to lisinopril and captopril was also observed in human coronary arteries treated with bradykinin (&gt; or = 10(-7) M), but not in those treated with substance P (10(-8) M).	Captopril	51-60	kininogen 1	Homo sapiens	119-129
8468119-3	1993	By contrast, berbamine was able to suppress microvascular leakage induced by platelet-activating factor and bradykinin, but not by leukotriene D4 or histamine.	berbamine	13-22	kininogen 1	Homo sapiens	108-118
7679158-3	1993	Utilizing the dorsal hand vein technique, dose-response curves to bradykinin (maximum dose = 513 ng/min) were constructed in veins preconstricted with the alpha-adrenergic agonist phenylephrine in healthy young volunteers.	Phenylephrine	180-193	kininogen 1	Homo sapiens	66-76
7679158-10	1993	Methylene blue partially antagonized the vasodilatory response to bradykinin, decreasing the EMAX by 50%.	Methylene Blue	0-14	kininogen 1	Homo sapiens	66-76
7679158-13	1993	The mechanism of bradykinin-induced vasodilation involves both EDRF and prostacyclin, and possibly another, as yet unidentified, mediator as well.	Epoprostenol	72-84	kininogen 1	Homo sapiens	17-27
7694438-8	1993	Extracranial pain and tenderness may, however, be induced experimentally by intramuscular injections of hypertonic saline and potassium chloride as well as of endogenous substances like bradykinin with 5-hydroxytryptamine and bradykinin with substance P.	Serotonin	202-221	kininogen 1	Homo sapiens	186-196
7683173-7	1993	Neither analog inhibited histamine release in response to bradykinin (BK), NT1-12, compound 48/80 (48/80), the calcium ionophore A23187, or anti-IgE stimulation of passively sensitized mast cells.	Histamine	25-34	kininogen 1	Homo sapiens	58-68
8447970-3	1993	Acute exposure to ethanol resulted in an inhibition of bradykinin mediated [Ca2+]i mobilization with significant effects observed only at 400 mM ethanol.	Ethanol	145-152	kininogen 1	Homo sapiens	55-65
8447970-6	1993	However, chronic exposure to ethanol significantly reduced the magnitude of bradykinin mediated [Ca2+]i mobilization both in the absence and presence of extracellular [Ca2+].	Ethanol	29-36	kininogen 1	Homo sapiens	76-86
8447970-9	1993	In addition, chronic ethanol exposure appears to have selective effects on receptor mediated [Ca2+]i mobilization because this response to bradykinin, but not neurotensin, was significantly reduced in cells exposed to ethanol.	Ethanol	21-28	kininogen 1	Homo sapiens	139-149
8447970-9	1993	In addition, chronic ethanol exposure appears to have selective effects on receptor mediated [Ca2+]i mobilization because this response to bradykinin, but not neurotensin, was significantly reduced in cells exposed to ethanol.	Ethanol	218-225	kininogen 1	Homo sapiens	139-149
8304779-0	1993	Inositol phosphate formation and release of intracellular free calcium by bradykinin in HaCaT keratinocytes.	Calcium	63-70	kininogen 1	Homo sapiens	74-84
8304779-4	1993	Activation of HaCaT keratinocytes with bradykinin resulted in a time- and dose-dependent release of inositol trisphosphate and intracellular calcium, with an EC50 value of 50 nM for bradykinin-induced inositol trisphosphate formation.	inositol 1,2,3-trisphosphate	100-122	kininogen 1	Homo sapiens	39-49
8304779-4	1993	Activation of HaCaT keratinocytes with bradykinin resulted in a time- and dose-dependent release of inositol trisphosphate and intracellular calcium, with an EC50 value of 50 nM for bradykinin-induced inositol trisphosphate formation.	inositol 1,2,3-trisphosphate	100-122	kininogen 1	Homo sapiens	182-192
8304779-4	1993	Activation of HaCaT keratinocytes with bradykinin resulted in a time- and dose-dependent release of inositol trisphosphate and intracellular calcium, with an EC50 value of 50 nM for bradykinin-induced inositol trisphosphate formation.	Calcium	141-148	kininogen 1	Homo sapiens	39-49
8304779-4	1993	Activation of HaCaT keratinocytes with bradykinin resulted in a time- and dose-dependent release of inositol trisphosphate and intracellular calcium, with an EC50 value of 50 nM for bradykinin-induced inositol trisphosphate formation.	Calcium	141-148	kininogen 1	Homo sapiens	182-192
8304779-4	1993	Activation of HaCaT keratinocytes with bradykinin resulted in a time- and dose-dependent release of inositol trisphosphate and intracellular calcium, with an EC50 value of 50 nM for bradykinin-induced inositol trisphosphate formation.	inositol 1,2,3-trisphosphate	201-223	kininogen 1	Homo sapiens	39-49
8304779-4	1993	Activation of HaCaT keratinocytes with bradykinin resulted in a time- and dose-dependent release of inositol trisphosphate and intracellular calcium, with an EC50 value of 50 nM for bradykinin-induced inositol trisphosphate formation.	inositol 1,2,3-trisphosphate	201-223	kininogen 1	Homo sapiens	182-192
8096380-5	1993	Prostaglandin E2 did not induce significant vascular leakage (maximum 5 microL) when injected alone, but when co-injected with histamine and bradykinin, the vascular leakage of both histamine and bradykinin was increased.	Dinoprostone	0-16	kininogen 1	Homo sapiens	141-151
8096380-5	1993	Prostaglandin E2 did not induce significant vascular leakage (maximum 5 microL) when injected alone, but when co-injected with histamine and bradykinin, the vascular leakage of both histamine and bradykinin was increased.	Dinoprostone	0-16	kininogen 1	Homo sapiens	196-206
8096380-5	1993	Prostaglandin E2 did not induce significant vascular leakage (maximum 5 microL) when injected alone, but when co-injected with histamine and bradykinin, the vascular leakage of both histamine and bradykinin was increased.	Histamine	127-136	kininogen 1	Homo sapiens	196-206
8096380-5	1993	Prostaglandin E2 did not induce significant vascular leakage (maximum 5 microL) when injected alone, but when co-injected with histamine and bradykinin, the vascular leakage of both histamine and bradykinin was increased.	Histamine	182-191	kininogen 1	Homo sapiens	141-151
8357330-5	1993	Bradykinin is a potent activator of the L-arginine nitric oxide system (endothelium-derived relaxing factor).	Arginine	40-50	kininogen 1	Homo sapiens	0-10
8357330-5	1993	Bradykinin is a potent activator of the L-arginine nitric oxide system (endothelium-derived relaxing factor).	Nitric Oxide	51-63	kininogen 1	Homo sapiens	0-10
8448072-0	1993	A comparison of the effects of captopril and enalapril on skin responses to intradermal bradykinin and skin blood flow in the human forearm.	Captopril	31-40	kininogen 1	Homo sapiens	88-98
8448072-0	1993	A comparison of the effects of captopril and enalapril on skin responses to intradermal bradykinin and skin blood flow in the human forearm.	Enalapril	45-54	kininogen 1	Homo sapiens	88-98
8448072-4	1993	Intradermal injections of 0, 1, 2.5 and 5 micrograms of bradykinin in 0.9% sodium chloride were made into the forearm of twelve healthy volunteers before and at 2, 6 and 24 h after single oral doses of 25 mg captopril, 10 mg enalapril or placebo.	Sodium Chloride	75-90	kininogen 1	Homo sapiens	56-66
8448072-8	1993	Compared with placebo, captopril significantly augmented the cutaneous vasodilator effects of bradykinin, measured by LDF and erythema area, at 2 h and the weal responses at 2 and 6 h. Enalapril enhanced the vasodilator responses to bradykinin at 2 and 6 h and the weal responses at 2, 6 and 24 h. Neither captopril nor enalapril significantly affected forearm skin blood flow.	Captopril	23-32	kininogen 1	Homo sapiens	94-104
8448072-8	1993	Compared with placebo, captopril significantly augmented the cutaneous vasodilator effects of bradykinin, measured by LDF and erythema area, at 2 h and the weal responses at 2 and 6 h. Enalapril enhanced the vasodilator responses to bradykinin at 2 and 6 h and the weal responses at 2, 6 and 24 h. Neither captopril nor enalapril significantly affected forearm skin blood flow.	Captopril	23-32	kininogen 1	Homo sapiens	233-243
8448072-8	1993	Compared with placebo, captopril significantly augmented the cutaneous vasodilator effects of bradykinin, measured by LDF and erythema area, at 2 h and the weal responses at 2 and 6 h. Enalapril enhanced the vasodilator responses to bradykinin at 2 and 6 h and the weal responses at 2, 6 and 24 h. Neither captopril nor enalapril significantly affected forearm skin blood flow.	Enalapril	185-194	kininogen 1	Homo sapiens	94-104
8448072-8	1993	Compared with placebo, captopril significantly augmented the cutaneous vasodilator effects of bradykinin, measured by LDF and erythema area, at 2 h and the weal responses at 2 and 6 h. Enalapril enhanced the vasodilator responses to bradykinin at 2 and 6 h and the weal responses at 2, 6 and 24 h. Neither captopril nor enalapril significantly affected forearm skin blood flow.	Enalapril	185-194	kininogen 1	Homo sapiens	233-243
8448072-8	1993	Compared with placebo, captopril significantly augmented the cutaneous vasodilator effects of bradykinin, measured by LDF and erythema area, at 2 h and the weal responses at 2 and 6 h. Enalapril enhanced the vasodilator responses to bradykinin at 2 and 6 h and the weal responses at 2, 6 and 24 h. Neither captopril nor enalapril significantly affected forearm skin blood flow.	Captopril	306-315	kininogen 1	Homo sapiens	94-104
8448072-8	1993	Compared with placebo, captopril significantly augmented the cutaneous vasodilator effects of bradykinin, measured by LDF and erythema area, at 2 h and the weal responses at 2 and 6 h. Enalapril enhanced the vasodilator responses to bradykinin at 2 and 6 h and the weal responses at 2, 6 and 24 h. Neither captopril nor enalapril significantly affected forearm skin blood flow.	Enalapril	320-329	kininogen 1	Homo sapiens	94-104
8448072-10	1993	This study showed that captopril and enalapril potentiated the effects of intradermal bradykinin both with respect to blood flow changes and weal formation in keeping with effective kininase II inhibition and the time course of these changes are consistent with enalapril being a longer acting drug than captopril.	Captopril	23-32	kininogen 1	Homo sapiens	86-96
8448072-10	1993	This study showed that captopril and enalapril potentiated the effects of intradermal bradykinin both with respect to blood flow changes and weal formation in keeping with effective kininase II inhibition and the time course of these changes are consistent with enalapril being a longer acting drug than captopril.	Enalapril	37-46	kininogen 1	Homo sapiens	86-96
8448072-10	1993	This study showed that captopril and enalapril potentiated the effects of intradermal bradykinin both with respect to blood flow changes and weal formation in keeping with effective kininase II inhibition and the time course of these changes are consistent with enalapril being a longer acting drug than captopril.	Enalapril	262-271	kininogen 1	Homo sapiens	86-96
8448072-10	1993	This study showed that captopril and enalapril potentiated the effects of intradermal bradykinin both with respect to blood flow changes and weal formation in keeping with effective kininase II inhibition and the time course of these changes are consistent with enalapril being a longer acting drug than captopril.	Captopril	304-313	kininogen 1	Homo sapiens	86-96
8220264-3	1993	It hydrolyzed bradykinin at the Phe5-Ser6 peptide bond at a rate of 1.090 mumol min-1 mg protein-1 at pH 8.0 and 37 degrees C. The molecular weight of this endopeptidase H2, estimated by SDS-polyacrylamide gel electrophoresis and by gel filtration, was 60 kDa, and its optimum pH for bradykinin hydrolysis was near 8.5.	Sodium Dodecyl Sulfate	187-190	kininogen 1	Homo sapiens	14-24
8220264-3	1993	It hydrolyzed bradykinin at the Phe5-Ser6 peptide bond at a rate of 1.090 mumol min-1 mg protein-1 at pH 8.0 and 37 degrees C. The molecular weight of this endopeptidase H2, estimated by SDS-polyacrylamide gel electrophoresis and by gel filtration, was 60 kDa, and its optimum pH for bradykinin hydrolysis was near 8.5.	polyacrylamide	191-205	kininogen 1	Homo sapiens	14-24
8220264-8	1993	Endopeptidase H2 hydrolyzes the Phe-Ser bond of peptides related to bradykinin and its activity appears to be limited to peptide chains of &lt; or = 18 amino acid residues since it does not hydrolyze BAM 22, peptide E or kininogen.	Phenylalanine	32-35	kininogen 1	Homo sapiens	68-78
8220264-8	1993	Endopeptidase H2 hydrolyzes the Phe-Ser bond of peptides related to bradykinin and its activity appears to be limited to peptide chains of &lt; or = 18 amino acid residues since it does not hydrolyze BAM 22, peptide E or kininogen.	Serine	36-39	kininogen 1	Homo sapiens	68-78
8518537-7	1993	This anti-trophic action may be partially due to the impairment of the angiotensin axis, but also due to enhancement of bradykinin availability, which results in an augmented release of endothelial anti-trophic signals such as EDRF/NO and prostacyclin.	Epoprostenol	239-251	kininogen 1	Homo sapiens	120-130
10148559-2	1993	Surfaces preincubated for short times in 10 mM or 100 mM H 2O 2 bound relatively large amounts of anti-high molecular weight kininogen (a-HMWK) after immersion in blood plasma.	Hydrogen Peroxide	57-63	kininogen 1	Homo sapiens	138-142
10148559-4	1993	Large amounts of a-HMWK and a-Fib were also deposited onto surfaces washed in trichloroethane, acetone and ethanol, whereas radiofrequency plasma-treated surfaces or surfaces incubated in deionized water bound preferentially a-HMWK after plasma immersion.	Ethanol	107-114	kininogen 1	Homo sapiens	19-23
7512465-6	1993	Bradykinin activates endothelial bradykinin (B2) receptors, which results in the formation of nitric oxide and prostacyclin.	Nitric Oxide	94-106	kininogen 1	Homo sapiens	0-10
7512465-6	1993	Bradykinin activates endothelial bradykinin (B2) receptors, which results in the formation of nitric oxide and prostacyclin.	Nitric Oxide	94-106	kininogen 1	Homo sapiens	33-43
7512465-6	1993	Bradykinin activates endothelial bradykinin (B2) receptors, which results in the formation of nitric oxide and prostacyclin.	Epoprostenol	111-123	kininogen 1	Homo sapiens	0-10
7512465-6	1993	Bradykinin activates endothelial bradykinin (B2) receptors, which results in the formation of nitric oxide and prostacyclin.	Epoprostenol	111-123	kininogen 1	Homo sapiens	33-43
7512465-7	1993	Hence, ACE inhibitors not only prevent the formation of angiotensin II, but also increase the local levels of bradykinin and in turn nitric oxide and prostacyclin.	Nitric Oxide	133-145	kininogen 1	Homo sapiens	110-120
7512465-7	1993	Hence, ACE inhibitors not only prevent the formation of angiotensin II, but also increase the local levels of bradykinin and in turn nitric oxide and prostacyclin.	Epoprostenol	150-162	kininogen 1	Homo sapiens	110-120
8436153-0	1993	Cutaneous blood flow changes and weal induced by intradermal bradykinin following pretreatment with indomethacin and captopril.	Indomethacin	100-112	kininogen 1	Homo sapiens	61-71
8436153-0	1993	Cutaneous blood flow changes and weal induced by intradermal bradykinin following pretreatment with indomethacin and captopril.	Captopril	117-126	kininogen 1	Homo sapiens	61-71
8436153-5	1993	Captopril 25 mg significantly potentiated the increase in local cutaneous blood flow measured by LDF, but not erythema area, and weal volume induced by bradykinin.	Captopril	0-9	kininogen 1	Homo sapiens	152-162
8436153-7	1993	The enhanced cutaneous effects of bradykinin following administration of captopril are in keeping with effective kininase II inhibition in the tissues.	Captopril	73-82	kininogen 1	Homo sapiens	34-44
7508046-3	1993	Bradykinin, which is rapidly degraded by ACE, stimulates the release of endothelium-derived vasodilator mediators, including nitric oxide, endothelium-derived hyperpolarizing factor, and prostacyclin.	Nitric Oxide	125-137	kininogen 1	Homo sapiens	0-10
7508046-3	1993	Bradykinin, which is rapidly degraded by ACE, stimulates the release of endothelium-derived vasodilator mediators, including nitric oxide, endothelium-derived hyperpolarizing factor, and prostacyclin.	endothelium-derived hyperpolarizing factor	139-181	kininogen 1	Homo sapiens	0-10
7508046-3	1993	Bradykinin, which is rapidly degraded by ACE, stimulates the release of endothelium-derived vasodilator mediators, including nitric oxide, endothelium-derived hyperpolarizing factor, and prostacyclin.	Epoprostenol	187-199	kininogen 1	Homo sapiens	0-10
7508047-2	1993	The angiotensin-converting enzyme (ACE) inhibitor enalaprilat (10(-7) M) markedly augmented endothelium-dependent relaxations to bradykinin in SV (concentration shift: 10-fold; n = 6; p &lt; 0.005), but not in IMA; in both blood vessels, it had no effect on endothelium-dependent relaxations to acetylcholine.	Enalaprilat	50-61	kininogen 1	Homo sapiens	129-139
7508049-8	1993	Like bradykinin (30 nM), moexiprilat (0.3 microM) elicited a nearly twofold increase in the cGMP content of these arteries, which was abolished by both NG-nitro-L-arginine and removal of the endothelium.	moexiprilat	25-36	kininogen 1	Homo sapiens	5-15
8426080-4	1993	In addition, cleavage of high-molecular weight kininogen was detected by sodium dodecyl sulfate polyacrylamide gel electrophoresis analysis and quantified by densitometry.	Sodium Dodecyl Sulfate	73-95	kininogen 1	Homo sapiens	25-56
8426080-4	1993	In addition, cleavage of high-molecular weight kininogen was detected by sodium dodecyl sulfate polyacrylamide gel electrophoresis analysis and quantified by densitometry.	polyacrylamide gels	96-114	kininogen 1	Homo sapiens	25-56
8419709-5	1993	Endothelium-dependent relaxations to bradykinin (55% +/- 13% versus 99% +/- 1% = maximum relaxation of the preconstricted diameter in cardioplegia-reperfusion vessels versus control vessels, respectively; p &lt; 0.05) and the calcium ionophore A 23187 (33% +/- 6% versus 90% +/- 4%; p &lt; 0.05) were markedly impaired while endothelium-independent relaxation to sodium nitroprusside was similar to control value.	Calcium	226-233	kininogen 1	Homo sapiens	37-47
8419709-5	1993	Endothelium-dependent relaxations to bradykinin (55% +/- 13% versus 99% +/- 1% = maximum relaxation of the preconstricted diameter in cardioplegia-reperfusion vessels versus control vessels, respectively; p &lt; 0.05) and the calcium ionophore A 23187 (33% +/- 6% versus 90% +/- 4%; p &lt; 0.05) were markedly impaired while endothelium-independent relaxation to sodium nitroprusside was similar to control value.	Nitroprusside	363-383	kininogen 1	Homo sapiens	37-47
18475525-3	1993	[des-arg(9)]-Bradykinin and vehicle placebo (V) were without effect on any of these indices.	des-arg	1-8	kininogen 1	Homo sapiens	13-23
8437890-7	1993	In the presence of amiloride, the response to both apical and basolateral bradykinin was reduced by &gt; 50% in 8 out of 18 layers, and the mean response was reduced by approximately 25%.	Amiloride	19-28	kininogen 1	Homo sapiens	74-84
1467832-8	1992	Bradykinin and SIN 1 (a donor of nitric oxide) reduced contractions induced by prostaglandin F2 alpha in an additive fashion in the presence of nitro-L-arginine.	Dinoprost	79-101	kininogen 1	Homo sapiens	0-10
1467832-8	1992	Bradykinin and SIN 1 (a donor of nitric oxide) reduced contractions induced by prostaglandin F2 alpha in an additive fashion in the presence of nitro-L-arginine.	Nitroarginine	144-160	kininogen 1	Homo sapiens	0-10
1467832-10	1992	Bradykinin (in the presence of nitro-L-arginine) relaxed the tissues contracted with tetraethylammonium, prostaglandin F2 alpha, phorbol 12, 13-diacetate or endothelin, with similar pD2 values.	Nitroarginine	31-47	kininogen 1	Homo sapiens	0-10
1467832-10	1992	Bradykinin (in the presence of nitro-L-arginine) relaxed the tissues contracted with tetraethylammonium, prostaglandin F2 alpha, phorbol 12, 13-diacetate or endothelin, with similar pD2 values.	Tetraethylammonium	85-103	kininogen 1	Homo sapiens	0-10
1467832-10	1992	Bradykinin (in the presence of nitro-L-arginine) relaxed the tissues contracted with tetraethylammonium, prostaglandin F2 alpha, phorbol 12, 13-diacetate or endothelin, with similar pD2 values.	Dinoprost	105-127	kininogen 1	Homo sapiens	0-10
1467832-10	1992	Bradykinin (in the presence of nitro-L-arginine) relaxed the tissues contracted with tetraethylammonium, prostaglandin F2 alpha, phorbol 12, 13-diacetate or endothelin, with similar pD2 values.	phorbol-12,13-diacetate	129-153	kininogen 1	Homo sapiens	0-10
1467832-6	1992	Bradykinin induced comparable endothelium-dependent relaxations of proximal and distal rings of porcine coronary arteries contracted with prostaglandin F2 alpha in the presence of nitro-L-arginine.	Nitroarginine	180-196	kininogen 1	Homo sapiens	0-10
1334969-4	1992	PGI2 synthesis maximally stimulated by bradykinin, A23187, and arachidonic acid were also attenuated at low PO2, by 35%, 33%, and 35%, respectively.	Epoprostenol	0-4	kininogen 1	Homo sapiens	39-49
1334969-4	1992	PGI2 synthesis maximally stimulated by bradykinin, A23187, and arachidonic acid were also attenuated at low PO2, by 35%, 33%, and 35%, respectively.	PO-2	108-111	kininogen 1	Homo sapiens	39-49
1467832-8	1992	Bradykinin and SIN 1 (a donor of nitric oxide) reduced contractions induced by prostaglandin F2 alpha in an additive fashion in the presence of nitro-L-arginine.	Nitric Oxide	33-45	kininogen 1	Homo sapiens	0-10
1487709-8	1992	Endo-oligopeptidase A cleaved the bonds Phe-Ser of bradykinin, Met-Arg of BAM-12P and Arg-Arg of neurotensin as described for rabbit brain and heart and bovine brain enzymes.	Phenylalanine	40-43	kininogen 1	Homo sapiens	51-61
1487709-8	1992	Endo-oligopeptidase A cleaved the bonds Phe-Ser of bradykinin, Met-Arg of BAM-12P and Arg-Arg of neurotensin as described for rabbit brain and heart and bovine brain enzymes.	Serine	44-47	kininogen 1	Homo sapiens	51-61
1487709-8	1992	Endo-oligopeptidase A cleaved the bonds Phe-Ser of bradykinin, Met-Arg of BAM-12P and Arg-Arg of neurotensin as described for rabbit brain and heart and bovine brain enzymes.	Arginine	67-70	kininogen 1	Homo sapiens	51-61
1331550-5	1992	Indomethacin (10 microM) enhanced the response to both bradykinin and FMLP.	Indomethacin	0-12	kininogen 1	Homo sapiens	55-65
1331550-3	1992	The response to bradykinin was antagonized by HOE 140, a bradykinin receptor antagonist, while it was unaffected by MEN 10,376, a tachykinin receptor antagonist, hCGRP(8-37) a calcitonin gene-related peptide (CGRP) receptor antagonist and N-t-BOC-Phe-DLeu-Phe-DLeu-Phe (BPLPLP), an FMLP antagonist.	4-hydroxy-2-octenal	46-49	kininogen 1	Homo sapiens	16-26
1331550-11	1992	The effect of bradykinin but not that of FMLP was abolished by indomethacin.	Indomethacin	63-75	kininogen 1	Homo sapiens	14-24
1331550-3	1992	The response to bradykinin was antagonized by HOE 140, a bradykinin receptor antagonist, while it was unaffected by MEN 10,376, a tachykinin receptor antagonist, hCGRP(8-37) a calcitonin gene-related peptide (CGRP) receptor antagonist and N-t-BOC-Phe-DLeu-Phe-DLeu-Phe (BPLPLP), an FMLP antagonist.	4-hydroxy-2-octenal	46-49	kininogen 1	Homo sapiens	57-67
1331550-15	1992	Direct neurochemical evidence was obtained for activation of capsaicin-sensitive primary afferents in the renal pelvis: such a mechanism could be involved in the genesis of ureteral pain whenever bradykinin or FMLP come into contact with sensory nerves in the pyeloureteral wall.	Capsaicin	61-70	kininogen 1	Homo sapiens	196-206
1491860-2	1992	In rat, bradykinin has been postulated to cause hyperalgesia to mechanical stimuli by releasing prostaglandin from sympathetic post-ganglionic terminals.	Prostaglandins	96-109	kininogen 1	Homo sapiens	8-18
1359319-2	1992	We have studied the effect of a tachykinin receptor antagonist (FK-224) on bronchoconstriction induced by inhalation of bradykinin in asthmatic patients.	FK 224	64-70	kininogen 1	Homo sapiens	120-130
1359319-6	1992	Inhalation of bradykinin caused coughing in three subjects, which was inhibited by FK-224 in all three.	FK 224	83-89	kininogen 1	Homo sapiens	14-24
1359319-7	1992	Antagonism of the tachykinin receptor by FK-224 greatly inhibited both bronchoconstriction and coughing induced by bradykinin in asthmatic patients, suggesting that tachykinin release from the airway sensory nerves is involved in responses to bradykinin.	FK 224	41-47	kininogen 1	Homo sapiens	115-125
1359319-7	1992	Antagonism of the tachykinin receptor by FK-224 greatly inhibited both bronchoconstriction and coughing induced by bradykinin in asthmatic patients, suggesting that tachykinin release from the airway sensory nerves is involved in responses to bradykinin.	FK 224	41-47	kininogen 1	Homo sapiens	243-253