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. t 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, 3 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.