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Am J Physiol Endocrinol Metab 254: E681-E686, 1988;
0193-1849/88 $5.00
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AJP - Endocrinology and Metabolism, Vol 254, Issue 6 E681-E686, Copyright © 1988 by American Physiological Society

ARTICLES

Bradykinin-induced vasoconstriction and thromboxane release in perfused human placenta

B. M. Wilkes and P. F. Mento
Department of Medicine, North Shore University Hospital, Manhasset, New York.

This investigation was performed to study the effects of bradykinin on the human fetoplacental circulation. The artery to a single placental cotyledon was perfused with RPMI medium (0.764 ml/min). Bradykinin caused a dose-related increase in vascular resistance. Because bradykinin is generally a vasodilator, we investigated the possibility that bradykinin-induced vasoconstriction was due to interactions with other pressor systems. Bradykinin and 9,11-dideoxy-9 alpha, 11 alpha-epoxymethanoprostaglandin F2 alpha (a stable thromboxane agonist) caused a dose-related increase in perfusion pressure. The bradykinin response was not mediated by angiotensin II, because bradykinin-induced vasoconstriction was not inhibited by saralasin, a competitive angiotensin antagonist. Bradykinin increased thromboxane B2 production by 62.0%. Prostaglandin E2 levels were increased by 86.7%, but prostaglandin E2 did not affect fetoplacental vascular resistance. Angiotensin II did not stimulate thromboxane B2 production and caused only a slight increase in prostaglandin E2. Indomethacin decreased the pressor response to angiotensin II. SQ29548, a specific thromboxane antagonist, caused a 61.6% inhibition of the bradykinin pressor response but did not change angiotensin II responsiveness. The data demonstrate that thromboxane is an important mediator of bradykinin-induced vasoconstriction in the isolated perfused human placenta.


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