Key result
Histamine and bradykinin demonstrated endothelium-dependent vasodilation in isolated human fetoplacental vessels, with bradykinin's effect partly mediated by nitric oxide release.
Why the study?
Do endothelium-dependent vasodilators (ACh, histamine, bradykinin) alter perfusion pressure in isolated human placental cotyledons?
Do endothelium-dependent vasodilators (ACh, histamine, bradykinin) alter perfusion pressure in isolated human placental cotyledons?
Endothelium-dependent vasodilation by histamine and bradykinin occurs in fetoplacental vessels, with bradykinin's effect partly mediated by nitric oxide and potentiated by angiotensin I.
Answers are grounded in this paper and cite their sources.
Supports further study of fetoplacental endothelial function; leaves open in vivo relevance and clinical translation.
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.
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Amarnani et al. (1999) studied Isolated, perfused human placental cotyledon. Endothelium-dependent vasodilators (ACh, histamine, bradykinin) was evaluated on Perfusion pressure. Histamine and bradykinin demonstrated endothelium-dependent vasodilation in isolated human fetoplacental vessels, with bradykinin's effect partly mediated by nitric oxide release.
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