Effects of angiotensin I and II and their interactions with some prostanoids in perfused human umbilical arteries.
In perfused human umbilical arteries both angiotensin I and II induced vasoconstriction with a monophasic response. Angiotensin I and II induced vasoconstrictions at doses greater than or equal to 10(-8) M and 10(-9) M respectively. Captopril inhibited the angiotensin I response while the angiotensin II receptor blocker Sar1-Ala8 AII inhibited the effect of both angiotensins. PGI2 attenuated the angiotensin II response in a dose dependent pattern. PGE2 and PGF2 alpha in concentrations below the critical levels for creating pressure responses per se, also attenuated the angiotensin II response. The cyclooxygenase inhibitor indomethacin potentiated the angiotensin II response indicating that endogenous production of prostanoids is of importance in the modulation of angiotensin effects.
D000803:Angiotensin I / Q000494:pharmacology*; D000804:Angiotensin II / Q000494:pharmacology*; D000809:Angiotensins / Q000494:pharmacology*; D002216:Captopril / Q000494:pharmacology; D004347:Drug Interactions; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D010477:Perfusion; D011247:Pregnancy; D011453:Prostaglandins / Q000494:pharmacology*; D012504:Saralasin / Q000494:pharmacology; D014469:Umbilical Arteries / Q000187:drug effects* / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects
D000809:Angiotensins; D011453:Prostaglandins; D000804:Angiotensin II; D000803:Angiotensin I; D002216:Captopril; D012504:Saralasin; D007213:Indomethacin