Effects of interrupting the renin-angiotensin system on sodium excretion in man.

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Abstract
1. Twelve normal volunteers were studied on 2 separate days, having taken a range of diets providing 50-300 mmol sodium per day for 3 days and having been dehydrated overnight. Each volunteer received a background intravenous infusion of arginine vasopressin (5 .times. 10-7 i.u. kg-1 min-1) on both days, and also received 6 mg captopril orally on one day and a placebo tablet on the other. The ensuing changes in arterial pressure, and in urinary solute and solute-free water excretion were recorded. 2. Captopril did not significantly alter arterial pressure. It increased the rate of excretion of sodium but not of potassium, and it did not significantly change urinary osmolality or creatinine clearance. 3. Captopril increased the rate of solute-free water reabsorption and did so in direct proportion to its effect of increasing sodium excretion. 4. A further twelve normal, dehydrated volunteers on free diets were studied on each of 2 days, after taking 500 mg lithium carbonate on the previous evening. On each day, they also received a loading dose and maintenance infusion of insulin. On one day they received 50 mg captopril orally, and, on the other, they received a placebo tablet. The arterial pressure, urinary excretion of electrolytes, and inulin clearance were recorded. 5. Captopril increased the rates of excretion of sodium, lithium and potassium, but there were no significant changes in inulin clearance or arterial pressure. 6. The natriuretic effect of captopril in either group of twelve volunteers was not significantly less in those volunteers who were already excreting more sodium, at least over the range of dietary sodium loading to which the volunteers were subjected. 7. Six normal volunteers were studied on a further 2 days, having taken a diet supplying 30 mmol sodium per day for 3 days and being dehydrated overnight. Each volunteer received a background intravenous infusion of arginine vasopressin (5 .times. 10-7 i.u. kg-1 min-1) on both days and also received an intravenous infusion of saralasin acetate (50 ng kg-1 min-1) plus carrier on one day and carrier alone on the other. The ensuing changes in arterial pressure, and in urinary solute and solute-free water excretion were recorded. 8. There was a small but significant fall in systolic arterial pressure during the infusion of saralasin. As with captopril, saralasin increased both solute-free water excretion and sodium excretion, and the increasing solute-free water excretion was directly proportional to the increasing sodium excretion. 9. These results suggest that interrupting the renin-angiotensin system with either captopril or saralasin produced an acute increase of sodium excretion mainly by decreasing the reabsorption of filtered sodium from the proximal tubule.