Hypophysectomy and saralasin on mesenteric vasoconstrictor response to vasopressin

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Abstract
The dose-response relationship of the mesenteric resistance vessels to vasopressin was studied in anesthetized laparotomized cats before and after hypophysectomy and again during the plateau phase of the response to prolonged infusion of [Sar1-Ala8] angiotensin II (saralasin), a competitive antagonist of angiotensin II. Hypophysectomy and saralasin each caused increased superior mesenteric arterial conductance. Before hypophysectomy infusion of 0.5 mU[units]/(min .cntdot. kg) of vasopressin caused mesenteric conductance to decrease from 0.168 to 0.156 ml/(min .cntdot. kg .cntdot. mm Hg), a change of 0.012 units. After hypophysectomy, the same dose reduced conductance from 0.227 to 0.179 mU/(min .cntdot. kg .cntdot. mm Hg), a change of 0.048 units. During the plateau phase of the response to saralasin, 0.5 mU/(min .cntdot. kg) of vasopressin reduced conductance from 0.281 to 0.201 ml/(min .cntdot. kg .cntdot. mm Hg), a change of 0.079 units. Hypophysectomy and saralasin had little effect on mesenteric vasoconstrictor response to high doses of vasopressin (2.0-10 mU/(min .cntdot. kg)). Ineffectiveness of low doses of vasopressin on mesenteric resistance vessels of intact anesthetized, surgically-stressed animal may be due to the already constricted state of the bed caused by endogenous vasopressin and angiotensin and to an opposing vasodilator influence, the reflex withdrawal of the vasoconstrictor effect of endogenous vasopressin.