Hemodynamic effects of captopril in one-kidney, one clip hypertensive rabbits.

Hemodynamic effects of captopril were examined in chronic one-kidney, one clip renal hypertensive rabbits and normotensive controls either in normal sodium or in sodium depletion. The mean arterial pressure (MAP) of hypertensive and normotensive rabbits in sodium depletion did not differ from that in normal sodium, while plasma renin activity (PRA) was elevated by sodium depletion. The cardiac output of sodium depleted groups decreased slightly. The increase in total peripheral resistance was greater in hypertensive than in normotensive groups. The MAP in all groups was decreased by acute administration of captopril irrespective of sodium intake. The decrease in MAP in the sodium-depleted hypertensive group was correlated with the control values of PRA, but no correlation was observed in other groups. Captopril significantly reduced the cardiac output of the sodium-depleted hypertensive group, but not of the other groups. These results show that: (1) the lowering effect of captopril on arterial pressure is not mediated only by blocking of the renin-angiotensin system, and (2) the decrease in cardiac output with captopril in sodium depleted hypertensive rabbits is an important factor in the reduction in the arterial pressure.