The role of vascular reactivity in normotensive and hypertensive rats.

An increase in reactivity of the blood vessels is a feature in many types of hypertension and may be of importance in the pathogenesis of high blood pressure. The literature on experimental hypertension, the renin-angiotensin system and vascular reactivity in human and various experimental models of hypertension are reviewed. Vascular responsiveness was examined using an isolated hindlimb preparation of rat and perfused with the animal's own blood. Plasma renin concentration was inversely related with dietary sodium in normal rats. Pressor responsiveness to angiotensin II was reciprocally related to endogenous levels of renin in the normotensive rats and the differences were abolished by blockade of the renin-angiotensin system. The results favour the hypothesis that prior occupancy and or "up" regulation of endogenous receptors determine the pressor responsiveness to angiotensin II in normotensive animals. Inhibition of converting enzyme with captopril significantly decreased the formation of angiotensin II and potentiated the vascular responses to pressor agents. Removal of a kidney and either acute administration of salt and deoxycorticosterone or clipping the remaining kidney significantly enhanced pressor responsiveness in hypertensive animals. Hypersensitivity was not present in the early phase of 2-kidney 1-clip Goldblatt hypertension but it was demonstrated in the chronic phase of hypertension. These differences may be explained by occupancy and availability of angiotensin II receptors and medial hypertrophy. Relief of ischaemia restored arterial pressure and hindlimb vascular resistance to normal at one day but hypersensitivity to pressor agents was still present in the chronic and to the same extent in the early renovascular hypertension. This may be due to subnormal vascular tone when structural changes are still present. 60 days after unclipping, pressor reactivity returned to normal suggesting regression of structural vascular changes. These studies suggest that structural hypertrophy is a consequence of hypertension and may have an additional effect after prolonged hypertension.