Nature of Renal Escape from the Sodium-Retaining Effect of Aldosterone in Primary Aldosteronism and in Normal Subjects1

Six patients with primary aldosteronism have been subjected to a series of standardized saline infusion tests and various indices have been studied in an attempt to clarify the mechanism of renal escape. Similar studies have been made in 5 normal control subjects who have been tested under 4 experimental situations: a) while consuming 10 mEq of dietary sodium per day, b) while consuming 180 mEq of sodium per day, c) 24 hr after the onset of administration of d-aldosterone while on the high intake of sodium, and d) 5–7 days after the onset of administration of aldosterone, while on the high intake of sodium, when escape had fully developed. The maximum mean rate of sodium excretion in response to the intravenous saline load (UNsV) in the control subjects was decreased below base line at the end of the first day of administration of aldosterone. It was significantly increased above base-line values after escape had developed and while aldosterone was still being given. UNaV was even higher in patients with proven aldosterone-producing tumors. The increased rate of excretion of salt load during the escape phase could not be correlated with further increases in extracellular fluid volume, glomerular filtration rate, plasma volume, renal plasma flow, blood pressure or changes in aldosterone secretion. Indirect evidence suggests the existence of a humoral mechanism which induces renal tubular rejection of sodium and which is evoked by chronic excess of aldosterone either of endogenous or of exogenous origin. The existence of a similar ‘sodium-excreting phenomenon’ in essential hypertension suggests that the same humoral mechanism may be operating.