Changes in the biological activity of autacoids during passage through the human perfused fetoplacental lobule.
Changes in the biological activities of a number of autacoids after a single passage through the human perfused fetoplacental lobule have been assessed by bioassay, whilst recording fetal vascular resistance. Bradykinin did not affect vascular resistance, but its biological activity on the superfused bioassay tissues fell by approximately 98%, whereas des-Asp1-angiotensin I activity increased at least 80-fold and the vascular resistance rose. All these effects were inhibited by captopril. Angiotensin II increased vascular resistance but its activity on the bioassay tissues was not changed. 5-Hydroxytryptamine activity was reduced by 67-90% and resistance to flow was not affected. The activities of prostaglandins D2, E2, and F2 alpha were slightly reduced. Prostaglandins D2 and F2 alpha caused vasoconstriction, their maximum effects being greater than those of either of the angiotensins. The TxA2-mimetic U46619 was approximately 90 times more potent than PGF2 alpha, as a vasoconstrictor, but the maximal effects were comparable. Thus, autacoid activity can be reduced, augmented or not affected during passage through the human perfused fetal placental vasculature.
D000803:Angiotensin I / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D012898:Autacoids / Q000494:pharmacology*; D001920:Bradykinin / Q000494:pharmacology; D015237:Dinoprost; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D010477:Perfusion; D010920:Placenta / Q000098:blood supply*; D011247:Pregnancy; D011460:Prostaglandins F / Q000494:pharmacology; D012039:Regional Blood Flow / Q000187:drug effects; D012701:Serotonin / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects
D012898:Autacoids; D011460:Prostaglandins F; D000804:Angiotensin II; D012701:Serotonin; D000803:Angiotensin I; D015237:Dinoprost; D001920:Bradykinin