Abstract
Summary
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 both pregnant and nonpregnant rabbits. These responses were virtually abolished in the presence of l-sar-8-ala-angiotensin-II, a specific A-II antagonist. In contrast, responses to A-II were unaltered after a-adre-nergic blockade with phentolamine. The present findings, in contrast to earlier studies in which A-II was injected systemically, suggest that uterine vasoconstriction induced with A-II was active, ascribable to direct interactions between A-II and its specific receptor, and that such interactions were independent of α-adrenergic mechanisms.
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