Vol. 277, Issue 2, H842-H847, August 1999
Effects of selected endothelium-dependent vasodilators on
fetoplacental vasculature: physiological implications
Saral
Amarnani,
Belinda
Sangrat, and
Gautam
Chaudhuri
Departments of Obstetrics and Gynecology and of Molecular and
Medical Pharmacology, University of California, Los Angeles,
California 90095
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
1014 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
B2-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.
bradykinin; human cotyledon perfusion; nitric oxide
