Salt and Aldosterone

A very large number of experimental and human studies independently link high dietary salt intake and aldosterone excess to the development and progression of end-organ damage. Observational and dietary interventional studies clearly establish high diet salt intake as an important contributor to the development of hypertension, cardiac hypertrophy, and proteinuria. Likewise, observational data and studies of aldosterone blockade demonstrate that hyperaldosteronism significantly relates to level of blood pressure, intracardiac volumes, left ventricular mass, and urinary protein excretion. As such, these studies establish both high dietary salt intake and excess aldosterone to be important and independent mediators of cardiovascular risk. It is interesting, however, that animal models of hyperaldosteronism have consistently demonstrated that the unfavorable target-organ effects of aldosterone are in fact dependent on the concomitant dietary sodium intake. Beginning with landmark studies by Brilla and Weber, it has been repeatedly demonstrated that the proinflammatory and profibrotic effects of excess aldosterone induced in end organs, including the heart, vasculature, and kidney, do not manifest unless the dietary salt intake is also excessive. That is, the deleterious tissue effects of aldosterone could be largely avoided by maintaining the rats on a low-salt diet. Until recently, such an interaction between sodium and aldosterone in humans, while anticipated, had not been clearly observed. Now, however, a growing body of data, including the article by du Cailar et al in this edition of Hypertension, demonstrates that the blood pressure and target-organ effects of excess aldosterone and excess dietary sodium are in large part dependent on each other. That is, as had been predicted by animal models of excess aldosterone, endogenous aldosterone and dietary sodium consumption in hypertensive patients do not contribute in solo but instead act in concert to accelerate target-organ decline.