PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
21613605-1	2011	Bovine adrenocortical cells express bTREK-1 K(+) (bovine KCNK2) channels that are inhibited by ANG II through a Gq-coupled receptor by separate Ca(2+) and ATP hydrolysis-dependent signaling pathways.	Adenosine Triphosphate	155-158	ANG	Bos taurus	95-98
2521426-1	1989	The sustained aldosterone secretory response to angiotensin II (ANG II) depends on receptor-mediated increases in membrane diglyceride (DG) and an increase in calcium influx rate.	Diglycerides	123-134	ANG	Bos taurus	64-67
2521426-1	1989	The sustained aldosterone secretory response to angiotensin II (ANG II) depends on receptor-mediated increases in membrane diglyceride (DG) and an increase in calcium influx rate.	Calcium	159-166	ANG	Bos taurus	64-67
2521426-8	1989	In contrast to the effect of ANP, the calcium channel blocker nitrendipine abolished the ANG II-induced rise in 45Ca2+ influx rate, reduced the steady-state level of [Ca2+]i, and returned the phosphoproteins to their control states.	Nitrendipine	62-74	ANG	Bos taurus	89-92
21613605-5	2011	BAPTA was much more effective than EGTA at suppressing bTREK-1 inhibition by ANG II.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	0-5	ANG	Bos taurus	77-80
21613605-5	2011	BAPTA was much more effective than EGTA at suppressing bTREK-1 inhibition by ANG II.	Egtazic Acid	35-39	ANG	Bos taurus	77-80
21613605-6	2011	When intracellular Ca(2+) concentration ([Ca(2+)](i)) was buffered to 20 nM with either 11 mM BAPTA or EGTA, ANG II (10 nM) inhibited bTREK-1 by 12.0 +- 4.5% (n=11) and 59.3 +- 8.4% (n=4), respectively.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	94-99	ANG	Bos taurus	109-112
21613605-6	2011	When intracellular Ca(2+) concentration ([Ca(2+)](i)) was buffered to 20 nM with either 11 mM BAPTA or EGTA, ANG II (10 nM) inhibited bTREK-1 by 12.0 +- 4.5% (n=11) and 59.3 +- 8.4% (n=4), respectively.	Egtazic Acid	103-107	ANG	Bos taurus	109-112
12468568-1	2002	Recently, we demonstrated that the heptapeptide angiotensin-(1-7) (Ang-[1-7]) exhibits a favorable kinetic of nitric oxide (NO) release accompanied by extremely low superoxide (O2-) production.	Nitric Oxide	110-122	ANG	Bos taurus	67-70
14518593-5	2003	Telmisartan, a newly developed Ang II type 1 receptor antagonist, or an antioxidant N-acetylcysteine significantly inhibited PDGF-B gene induction in Ang II-exposed pericytes.	Telmisartan	0-11	ANG	Bos taurus	31-34
14518593-5	2003	Telmisartan, a newly developed Ang II type 1 receptor antagonist, or an antioxidant N-acetylcysteine significantly inhibited PDGF-B gene induction in Ang II-exposed pericytes.	Telmisartan	0-11	ANG	Bos taurus	150-153
14518593-5	2003	Telmisartan, a newly developed Ang II type 1 receptor antagonist, or an antioxidant N-acetylcysteine significantly inhibited PDGF-B gene induction in Ang II-exposed pericytes.	Acetylcysteine	84-100	ANG	Bos taurus	150-153
14518593-6	2003	The present results suggest that Ang II-type 1 receptor interaction could stimulate PDGF-B gene expression in cultured retinal pericytes through intracellular reactive oxygen species generation and could thus be involved in the progression of diabetic retinopathy.	Reactive Oxygen Species	159-182	ANG	Bos taurus	33-36
12468568-1	2002	Recently, we demonstrated that the heptapeptide angiotensin-(1-7) (Ang-[1-7]) exhibits a favorable kinetic of nitric oxide (NO) release accompanied by extremely low superoxide (O2-) production.	Superoxides	165-175	ANG	Bos taurus	67-70
12468568-1	2002	Recently, we demonstrated that the heptapeptide angiotensin-(1-7) (Ang-[1-7]) exhibits a favorable kinetic of nitric oxide (NO) release accompanied by extremely low superoxide (O2-) production.	Superoxides	177-179	ANG	Bos taurus	67-70
10067976-4	1999	The NO and PGI2 synthase inhibitors, 1-NOARG and flurbiprofen, respectively, were used to unmask Ang II vasoconstriction; the changes in vascular diameters were then measured.	1-noarg	37-44	ANG	Bos taurus	97-100
10572242-3	1999	Under normal culture conditions, BAEC efficiently internalized (125)I-Ang IV as assessed by acid-resistant binding.	baec	33-37	ANG	Bos taurus	70-73
10572242-4	1999	Internalization of (125)I-Ang IV was considerably decreased after pretreatment of cells with hyperosmolar sucrose or after pretreatment of BAEC with inhibitors of endosomal acidification such as monensin or NH(4)Cl.	Sucrose	106-113	ANG	Bos taurus	26-29
10572242-4	1999	Internalization of (125)I-Ang IV was considerably decreased after pretreatment of cells with hyperosmolar sucrose or after pretreatment of BAEC with inhibitors of endosomal acidification such as monensin or NH(4)Cl.	baec	139-143	ANG	Bos taurus	26-29
10572242-4	1999	Internalization of (125)I-Ang IV was considerably decreased after pretreatment of cells with hyperosmolar sucrose or after pretreatment of BAEC with inhibitors of endosomal acidification such as monensin or NH(4)Cl.	Monensin	195-203	ANG	Bos taurus	26-29
10572242-4	1999	Internalization of (125)I-Ang IV was considerably decreased after pretreatment of cells with hyperosmolar sucrose or after pretreatment of BAEC with inhibitors of endosomal acidification such as monensin or NH(4)Cl.	Ammonium Chloride	207-214	ANG	Bos taurus	26-29
10572242-6	1999	As expected, internalization of (125)I-Ang IV was completely abolished by divalinal-Ang IV, a known AT(4) receptor antagonist.	divalinal	74-83	ANG	Bos taurus	39-42
10572242-6	1999	As expected, internalization of (125)I-Ang IV was completely abolished by divalinal-Ang IV, a known AT(4) receptor antagonist.	divalinal	74-83	ANG	Bos taurus	84-87
10067976-7	1999	After the inhibition of endogenous NO and PGI2 synthesis by 1-NOARG and flurbiprofen, respectively, the vasoconstriction effects of Ang II became more pronounced.	Epoprostenol	42-46	ANG	Bos taurus	132-135
10067976-7	1999	After the inhibition of endogenous NO and PGI2 synthesis by 1-NOARG and flurbiprofen, respectively, the vasoconstriction effects of Ang II became more pronounced.	1-noarg	60-67	ANG	Bos taurus	132-135
12141944-10	2002	Treatment with 1/4 PGF(2alpha)/Ang II decreased plasma progesterone concentration, and induced luteolysis and oestrus.	Prostaglandins F	19-22	ANG	Bos taurus	31-34
12141944-10	2002	Treatment with 1/4 PGF(2alpha)/Ang II decreased plasma progesterone concentration, and induced luteolysis and oestrus.	Progesterone	55-67	ANG	Bos taurus	31-34
12141944-11	2002	The onset of oestrus in cows treated with full-dose (500 microg) PGF(2alpha) (3.1 +/- 0.2 (mean +/- SEM) days after treatment) was significantly earlier than that in cows treated with 1/4 PGF(2alpha)/Ang II (4.8 +/- 0.2 days after treatment) (P < 0.05).	Prostaglandins F	65-68	ANG	Bos taurus	200-203
10067976-4	1999	The NO and PGI2 synthase inhibitors, 1-NOARG and flurbiprofen, respectively, were used to unmask Ang II vasoconstriction; the changes in vascular diameters were then measured.	Flurbiprofen	49-61	ANG	Bos taurus	97-100
10067976-7	1999	After the inhibition of endogenous NO and PGI2 synthesis by 1-NOARG and flurbiprofen, respectively, the vasoconstriction effects of Ang II became more pronounced.	Flurbiprofen	72-84	ANG	Bos taurus	132-135
10067976-9	1999	Vasoactive doses of Ang II (10(-10) M to 10(-4) M) caused a dose-dependent increase in the release of NO and PGI2 from isolated bovine retinal vessels, indicating that the increase in EDRF may nullify direct Ang II-induced vasoconstriction.	Epoprostenol	109-113	ANG	Bos taurus	20-23
9765364-2	1998	In this study, structural properties of the AT4 receptor from bovine adrenals are described using a novel photoactive analog of Ang IV, [125I]Benzoylphenylalanine-Ang IV (BP-Ang IV), recently developed in our laboratory.	benzoylphenylalanine	142-162	ANG	Bos taurus	128-131
10067976-11	1999	CONCLUSIONS: This study demonstrates that the retinal vascular endothelium acts as a buffer against the vasoconstricting agent Ang II via release of vasodilators NO and PGI2, and the vasoconstriction effects due to Ang II are most prominent in the smallest diameter vessels.	Epoprostenol	169-173	ANG	Bos taurus	127-130
9605926-7	1998	Inhibition of PKC by staurosporine augmented Ang II-stimulated AT1-R phosphorylation, suggesting a negative regulatory role of PKC on the putative G protein-coupled receptor kinase(s) that mediates the majority of AT1-R phosphorylation.	Staurosporine	21-34	ANG	Bos taurus	45-48
9461224-1	1998	Prostaglandin E2 (PGE2) is an endogenous hormone of adrenal zona glomerulosa cells and is released in response to stimulation by agonists such as angiotensin II (Ang II).	Dinoprostone	0-16	ANG	Bos taurus	162-165
9461224-1	1998	Prostaglandin E2 (PGE2) is an endogenous hormone of adrenal zona glomerulosa cells and is released in response to stimulation by agonists such as angiotensin II (Ang II).	Dinoprostone	18-22	ANG	Bos taurus	162-165
9461224-12	1998	Using fura-2 loaded cells, PGE2 (2 micromol/L), dibutyryl cAMP (2 mmol/L), and Ang 11 (2 micromol/L) increased intracellular calcium over basal concentrations by 5.5-fold, 3-fold, and 6.2-fold, respectively.	Calcium	125-132	ANG	Bos taurus	79-82
9357777-5	1997	The antimitogenic effect of ANG II is partly mimicked by the AT2-selective agonist CGP-42112.	CGP 42112A	83-92	ANG	Bos taurus	28-31
8958583-6	1996	Physiological studies in which test compounds were injected into the internal carotid of the rat and cerebral blood flor (CBF) was measured by laser Doppler flowmetry indicated that pretreatment with Divalinal-Ang IV, but not DuP 753 or PD123177, blocked the increased flow observed with Ang IV infusion.	divalinal	200-209	ANG	Bos taurus	210-213
1986182-4	1991	Increases in [Ca2+]c produced by Ang II in cells continuously maintained in either HCO3(-) - or HEPES-buffered media were similar, and with the same monolayer the nature of the Ang II-stimulated Ca2+ signal was independent of the buffer employed.	Bicarbonates	83-90	ANG	Bos taurus	33-36
1986182-4	1991	Increases in [Ca2+]c produced by Ang II in cells continuously maintained in either HCO3(-) - or HEPES-buffered media were similar, and with the same monolayer the nature of the Ang II-stimulated Ca2+ signal was independent of the buffer employed.	HEPES	96-101	ANG	Bos taurus	33-36
1717781-2	1991	Exposure to nanomolar concentrations of saralasin, an Ang II agonist, attenuated the passage of the fluorophores across the monolayers by 50-75%.	Saralasin	40-49	ANG	Bos taurus	54-57
1717781-4	1991	Sarathrin, however, did inhibit the saralasin-induced reduction in transendothelial monolayer permeability and suggested specific Ang II binding site mediation.	sarathrin	0-9	ANG	Bos taurus	130-133
2006162-2	1991	Binding of 125I-labeled bovine angiogenin (125I-Ang) to AngBP occurs with an apparent Kd approximately 5 x 10(-10) M and is specific, saturable, and inhibited by excess unlabeled angiogenin.	Iodine-125	11-15	ANG	Bos taurus	48-51
2006162-3	1991	125I-Ang can be crosslinked efficiently to AngBP by a water-soluble carbodiimide, 1-ethyl-3-(3-dimethylaminopropyl)carbo-diimide.	Water	54-59	ANG	Bos taurus	5-8
2006162-3	1991	125I-Ang can be crosslinked efficiently to AngBP by a water-soluble carbodiimide, 1-ethyl-3-(3-dimethylaminopropyl)carbo-diimide.	Carbodiimides	68-80	ANG	Bos taurus	5-8
2006162-3	1991	125I-Ang can be crosslinked efficiently to AngBP by a water-soluble carbodiimide, 1-ethyl-3-(3-dimethylaminopropyl)carbo-diimide.	Ethyldimethylaminopropyl Carbodiimide	82-128	ANG	Bos taurus	5-8