The role of aldosterone in renal sodium conservation during sodium depletion.

Abstract

SummaryThe effect of aldosterone infused intravenously at 2, 4, 8 and 16 μg./hr., i.e. over the physiological range, upon the renal retention of sodium was studied in adrenalectomized sheep during progressive sodium depletion over 32 hr. via a parotid fistula. The animals were given basal cortisol and corti‐costerone. The resulting patterns of renal sodium excretion were compared with the renal response to sodium loss in the same animals before bilateral adrenalectomy. With high renal output of sodium under high sodium load there was no evidence of aldosterone activation of sodium retention, but as sodium loss progressed there was evidence of increased sensitivity to aldosterone of the renal sodium retention mechanism. The dose/effect relation between rate of aldosterone infusion and renal excretion of sodium at this stage showed (a) a threshold dosage for this effect, (b) a proportionality between dosage and degree of sodium retention, (c) that the effective dosage is similar to the aldosterone secretion rate from the adrenal when present under similar circumstances of sodium toss. The results demonstrate that the normal rate of release of aldosterone in the sodium replete animal, 0·64 ± 0·36 ± 0·10 (14) μg./hr, is not sufficient to allow a maximal sodium retention by the kidney. Therefore, aldosterone secretion is commensurate and causal to normal renal sodium conservation during sodium loss.