Effect of captopril on bradykinin inactivation by human foetal placental circulation.
The inactivation of bradykinin on passage across the human foetal placental circulation was investigated in six full-term human placentas. The placentas were perfused with a modified Krebs-Henseleit solution and placenta perfusion pressure was recorded. Samples collected at the arterial inflow and at the venous effluent were assayed on the isolated guinea-pig ileum as an estimation of bradykinin activity. Bradykinin (100 ng ml-1) was infused through the foetal placental vessels before and during captopril 4 X 10(-7) M. Bradykinin produced a transient increase in placental vascular resistance that was not potentiated by captopril. Bradykinin activity was completely abolished after passage through the foetal placental circulation, and the inactivation was blocked by captopril. These data suggest that angiotensin I converting enzyme (kininase II) might occur in the foetal placental vessels.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001920:Bradykinin / Q000097:blood* / Q000494:pharmacology; D002216:Captopril / Q000494:pharmacology*; D005260:Female; D006168:Guinea Pigs; D006801:Humans; D007082:Ileum / Q000187:drug effects; D066298:In Vitro Techniques; D008431:Maternal-Fetal Exchange; D009119:Muscle Contraction / Q000187:drug effects; D010920:Placenta / Q000098:blood supply* / Q000187:drug effects / Q000502:physiology; D011247:Pregnancy; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects
D002216:Captopril; D001920:Bradykinin