PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
3117523-3	1987	After 1 day of dexamethasone treatment, the urinary excretion of PGE2 and PGF2 alpha was reduced to about 50% of the control value (P less than 0.05), and angiotensin II-induced release of arachidonic acid and PGs from renal medulla slices was blunted (P less than 0.05).	Phosphatidylglycerols	210-213	angiotensinogen	Rattus norvegicus	155-169	
1329556-7	1992	Infusion of PGs reduced the vasoconstrictor effect of ANG II in WKY, but had no effect in SHR.	Phosphatidylglycerols	12-15	angiotensinogen	Rattus norvegicus	54-60	
6689628-9	1983	Progesterone inhibited the synthesis of PGs caused by A-II in non-decidualized uterus but stimulated the release of PG in the decidualized uterus.	Phosphatidylglycerols	40-43	angiotensinogen	Rattus norvegicus	54-58	
6414846-11	1983	These studies suggest not only an important physiological feedback role of vasodilatory PGs, as modulators of AII-induced glomerular contraction, but also a direct mesangial contractile effect of the arachidonate metabolite TxA2.	Phosphatidylglycerols	88-91	angiotensinogen	Rattus norvegicus	110-113	
709751-8	1978	Thus, endogenous PGs attenuate the vasoconstrictor actions of A II on the superficial renal microvasculature and minimize changes in QA, SNGFR, and total GFR.	Phosphatidylglycerols	17-20	angiotensinogen	Rattus norvegicus	62-66	
12529274-9	2003	In conclusion, this study shows that LH rats exhibit an altered MBF response to ANG II compared with LL rats and indicates that the AT(1) receptor-mediated medullary vasodilator response to low doses of ANG II is mainly due to the release of PGs, whereas the dilator response to high doses of ANG II has additional nitric oxide- and kinin-dependent components.	Phosphatidylglycerols	242-245	angiotensinogen	Rattus norvegicus	203-209	
12529274-9	2003	In conclusion, this study shows that LH rats exhibit an altered MBF response to ANG II compared with LL rats and indicates that the AT(1) receptor-mediated medullary vasodilator response to low doses of ANG II is mainly due to the release of PGs, whereas the dilator response to high doses of ANG II has additional nitric oxide- and kinin-dependent components.	Phosphatidylglycerols	242-245	angiotensinogen	Rattus norvegicus	203-209