Escape from the sodium-retaining effects of mineralocorticoids: Role of ANF and intrarenal hormone systems

Abstract

A number of interrelated mechanisms modulate the response that leads to escape. The time course of escape is dependent on the conditions under which mineralocorticoid action leads to extracellular fluid volume expansion. The basic hemodynamic changes of pressure natriuresis following chronic volume expansion are needed for the expression of the central circulatory modulation of ANF and sympathetic withdrawal. Intrarenal modulation by the renal prostaglandins and a decreased antinatriuretic action of angiotensin II are likely to contribute to escape. The intrarenal modulatory mechanisms in escape need to be further defined. Escape from the sodium-retaining effects of mineralocorticoids is due to the decreased sodium reabsorption of nephron segments other than those of mineralocorticoid action. The decreased reabsorption of sodium, especially by the proximal tubule, results in increased distal delivery of the cation, overcoming the sustained effect of the mineralocorticoid. The discovery of ANF has greatly added to our understanding of escape. Its precise role as it interrelates with the other modulatory mechanisms of escape needs further investigation.