Contribution of sympathetic neural reflexes to mineralocorticoid escape.

The administration of aldosterone to normal subjects induces sodium retention, which is only transient inasmuch as sodium balance is restored shortly after extracellular fluid volume is expanded. This escape from sodium-retaining effects of mineralocorticoids, which is normally attended by sympathetic withdrawal, is not seen in some forms of secondary hyperaldosteronism that evolve with edema and increased sympathetic activity. The precise significance of the reflexly mediated changes in sympathetic activity on renal function has been difficult to assess. In fact, changes in cardiovascular volumes are known to be accompanied by alterations in other parameters that play a crucial role on salt and water equilibrium, such as renal perfusion pressure and renal renin. In this short paper we have analyzed the most probable integrated sequence of responses in neural activity, systemic pressure, and renal renin that lead to escape from high circulating levels of aldosterone. A major role is ascribed to volume expansion and to arterial pressure-induced natriuresis in the restoration of sodium balance. However, such responses are greatly facilitated by a selective inhibition of renal sympathetic activity mediated by cardiopulmonary receptors, and by a fall in postglomerular vascular resistance specifically mediated by a decrease in intrarenal angiotensin. These two modulatory factors are thought to assume a greater influence on sodium excretion during instances of secondary hyperaldosteronism.