Regional haemodynamic effects of neuropeptide Y, vasopressin and angiotensin II in conscious, unrestrained, Long Evans and Brattleboro rats.

The regional haemodynamic responses to equipressor doses of neuropeptide Y (NPY), vasopressin (AVP) and angiotensin II (AII) were assessed in conscious Long Evans and Brattleboro rats, chronically instrumented with miniaturized, pulsed Doppler probes. NPY caused particularly potent renal vasoconstrictions in intact rats of both strains. However, there were differential changes in regional vascular sensitivity of NPY following administration of pentolinium and captopril, indicating that 'buffer' mechanisms were an important determinant of responses to NPY. A marked mesenteric and low renal sensitivity to AVP was seen in both strains in all conditions. AVP was the most potent of the 3 pressor agents, and no evidence was found for it interacting uniquely with buffer mechanisms. The pressor action of AII was offset by a tendency towards hindquarters vasodilatation that was converted to a marked vasoconstriction when pentolinium and captopril were administered. It is feasible that, in the intact rat, AII stimulated adrenal medullary adrenal release which caused beta-adrenoceptor-mediated vasodilatation that acted to offset the direct vasoconstrictor effects of AII.