Angiotensin II Increases Uterine Vascular Resistance in Pregnant and Nonpregnant Rabbits

Abstract

Uterine vascular responses to graded doses of angiotensin-II (A-II) injection directly into the uterine blood supply were studied in pregnant and nonpregnant rabbits anesthetized with pentobarbital. A segment of the uterus was isolated in situ and pump perfused at a constant rate of flow with the animal''s own arterial blood. Uterine perfusion pressure, and hence uterine vascular resistance, always increased when A-II was injected into the arterial perfusion system. Responses to A-II were dose dependent and similar in magnitude in pregnant and nonpregnant rabbits. These responses were virtually abolished in the presence of 1-sar-8-ala-angiotensin-II, a specific A-II antagonist. Responses to A-II were unaltered after .alpha.-adrenergic blockade with phentolamine. In contrast to earlier findings in which A-II was injected systemically, the uterine vasoconstriction induced with A-II was active, ascribable to direct interactions between A-II and its specific receptor, and the interactions were independent of .alpha.-adrenergic mechanisms.