Systemic hemodynamic and hormonal responses during angiotensin II blockade with saralasin.

The effect of saralasin infusion on systemic hemodynamics, plasma renin activity (PRA), and aldosterone levels was studied under various conditions of sodium balance in 25 patients with essential hypertension. The results of 66 paired observations were statistically analyzed, to elucidate some controversial aspects of the mechanisms of saralasin action. The total peripheral resistance index (TPRI) increased when saralasin had an agonistic effect on blood pressure (BP) and decreased when it acted as an antagonist. The TPRI changed more than the BP by an inversely directed change in the cardiac index (CI). In addition, the changes in the CI were only weakly correlated with the changes in MAP; CI decreased consistently when BP increased but showed no distinct pattern when saralasin acted as an antagonist. The pulse rate did not change under any of the conditions applied. The present findings suggest that in addition to its antagonistic effects on peripheral circulation, saralasin has some action on the heart and autonomic nervous system. The observed changes in the plasma aldosterone level were in accordance with the changes in TPRI and did not point to a difference between adrenal and vascular sensitivity to saralasin or angiotensin II. The overall hemodynamic responses were related to the existing level of PRA. No correlation was found between the degree of volume depletion and the blood pressure response during saralasin after elimination of the effect of PRA by partial regression analysis. These findings do not support the concept that more information about the renin dependency of the BP is provided by the BP reaction to saralasin than by determination of the PRA.