Relative Influence of Acute Sodium and Volume Depletion on Aldosterone Secretion in Nephrectomized Man
Plasma aldosterone concentration can increase in anephric man during hemodialysis despite the lack of kidneys to produce renin. Because the metabolic clearance rate of aldosterone does not change during hemodialysis, aldosterone secretion must increase in response to sodium depletion, volume depletion, or both. This study was designed to determine the relative influence of sodium and volume depletion by ultrafiltration and hemodialysis on plasma aldosterone concentration in anephric man. Fluid (547 ml) was removed from 13 anephric subjects during 4 hours of ultrafiltration in the absence of hemodialysis. Plasma sodium and potassium concentration did not change during ultrafiltration, but total body sodium and potassium decreased. Plasma aldosterone concentration did not change significantly. Each subject was then hemodialyzed for 8 hours. In 5 subjects, an additional liter of fluid was removed without a significant change in plasma sodium concentration. Plasma aldosterone concentration also did not change in response to the reduction in fluid volume. In 8 subjects, an additional liter of fluid was removed, and plasma sodium concentration decreased from 138.5 to 130.0 mEq/liter. Plasma aldosterone concentration increased from 8.3 to 19.6 ng/100 ml plasma. Three additional anephric subjects were hemodialyzed against a dialysate containing 125.0 mEq sodium/liter for 8 hours. Plasma potassium and total body fluid volume were held constant. Plasma sodium concentration decreased from 138.5 to 125.0 mEq/liter, and plasma aldosterone concentration increased from 7.4 to 24.3 ng/100 ml plasma. These data indicate that acute sodium depletion by hemodialysis accompanied by decreased plasma sodium concentration without a change in plasma potassium concentration or fluid volume can stimulate aldosterone secretion independently of the renal renin-angiotensin system.
- angiotensin II
- fluid volume
- metabolic clearance rate
- Received May 18, 1973.
- Accepted September 12, 1973.
- © 1973 American Heart Association, Inc.