PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 24925526-11 2014 Thus, BK stimulates both EDHF-dependent vasodilation and t-PA release. edhf 25-29 kininogen 1 Homo sapiens 6-8 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 15361764-14 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 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 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 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 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 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 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 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 < 0.01). edhf 23-27 kininogen 1 Homo sapiens 0-2 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 < 0.05), but not by EET(11,12) (18.4% +/- 3.3% versus 25.1% +/- 4.9%; p > 0.05) was significantly reduced. edhf 45-49 kininogen 1 Homo sapiens 81-91 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 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 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 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 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 11522609-14 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 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 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. 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 10924042-7 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 10924042-13 2000 Dilation to BK was virtually abolished when administered concomitantly with SNP during L-NMMA and Indo (P < 0.01 vs. before SNP), suggesting that NO inhibits EDHF-induced dilation. edhf 161-165 kininogen 1 Homo sapiens 12-14 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 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 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 10919570-5 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 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 10511133-0 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 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 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 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 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 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. edhf 47-51 kininogen 1 Homo sapiens 99-109 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 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 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 9338651-9 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 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 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 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 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 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 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 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