Aldosterone in fluid and electrolyte disorders: Hyper- and hypoaldosteronism

Abstract

Aldosterone plays a major role in regulating the amount of sodium and potassium in the body through its direct effects on the renal tubule. When hypersecretion of aldosterone occurs in an otherwise normal subject, a syndrome characterized by hypertension and by potassium depletion is produced. Marked hypersecretion of aldosterone occurs in the edematous states of cirrhosis and nephrosis. The means by which this hypersecretion occurs is not known, but it is clearly secondary to disturbances in the circulation which promote transudation. Hypersecretion in this setting leads instead to marked and sustained renal retention of sodium. Hypertension and potassium depletion are not produced. In patients with advanced congestive heart failure, hypersecretion may not be present. This finding perhaps suggests a fundamental difference in the nature of the stimulus to aldosterone secretion in heart failure as compared with that in nephrosis and cirrhosis. The secretion of aldosterone is related directly or indirectly to potassium balance, to blood volume change, and perhaps to ACTH. These factors do not adequately account, however, for the hypersecretion of aldosterone noted in various clinical and experimental situations. There is now evidence which suggests that pressure changes within the vascular tree, not necessarily related to over-all volume change, may serve as an important stimulus. The relationship between pressure changes and electrolyte metabolism is obscure, but it is clear that aldosterone can participate in acute hemodynamic adjustment and that it may play a role in the maintenance of blood pressure. Recent work indicates that the syndrome of malignant hypertension is often associated with hypersecretion of aldosterone. In contrast, the secretion of aldosterone has been found to be normal in benign hypertension. Hypersecretion of aldosterone in human malignant hypertension could prove to be a secondary phenomenon, but the possibility that it plays a causal role cannot be excluded. A word about the role of aldosterone in homeostasis may be in order. It is important to remember that the secretion of aldosterone falls to very low, addisonism-like levels when the dietary sodium content is high and, also, that certain adrenalectomized patients given cortisone do not require mineralocorticoid for well-being. Thus, aldosterone secretion may become important only when the body is threatened by hypotension, by sodium and water depletion, or by excessive accumulation of potassium. Accordingly, the syndrome of pure hypoaldosteronism may be difficult to identify.