Abstract
The endothelium-dependent vasodilators ACh, histamine, and bradykinin were studied in the isolated, perfused human placental cotyledon. Histamine caused a decrease in perfusion pressure that was attenuated by cimetidine. Bradykinin, at lower concentrations (10(-20) to 10(-14) M), produced a concentration-dependent decrease in perfusion pressure, whereas at higher concentrations it produced an increase in perfusion pressure. ACh was without any effect. The decrease in perfusion pressure observed with bradykinin was potentiated by captopril and was significantly attenuated in the presence of HOE-140, the B(2)-receptor antagonist, or by pretreatment with an inhibitor of nitric oxide synthase, but not by an inhibitor of cyclooxygenase. The decrease in perfusion pressure observed with bradykinin was potentiated by ANG I but not by ANG II. It is concluded that endothelium-dependent vasodilation can be demonstrated with histamine and bradykinin in the fetoplacental vessels, and at least for bradykinin, this is partly mediated by release of nitric oxide. The potentiation of the bradykinin response in the presence of ANG I may serve to buffer the vasoconstriction produced by ANG II in the fetoplacental circulation.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
