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Aldosterone, a vasculotoxic agent--novel functions for an old hormone.

In 1955, the syndrome of primary aldosteronism was described by and subsequently named after J. W. Conn [1]. It was defined as high aldosterone concentrations in the presence of adrenal adenoma or bilateral hyperplasia. Recently, the definition of the syndrome has been expanded and the—claimed or real—frequency has risen sharply [2]. An animated discussion is going on whether we are really dealing with a true rise in the frequency of primary aldosteronism as originally defined. New data allow a more sophisticated and broader interpretation of the role of aldosterone. In the Framingham offspring study, it had been documented that the frequency of a rise in blood pressure and the incidence of hypertension increase progressively from the first to the fourth quartile of serum aldosterone concentrations [3]. This led recently to the comment ‘whether primary aldosteronism is as widespread as some believe may not be as relevant as whether the commonly prevailing level of aldosterone is too high for the amount of sodium we consume’ [4]. In line with the idea that aldosterone plays a more general role in the genesis of hypertension, it was also stated that ‘aldosterone . . . contributes to the development of hypertension . . .more than even the most generous estimates for the prevalence of primary hyperaldosteronism’ [4]. This interpretation finds support in some recent experimental data. Makhanova [5] created salt-sensitive blood pressure in mice by increasing the expression of aldosterone synthase by manipulating the untranslated regions of aldosterone synthase gene in mice, raising aldosterone synthase mRNA by a factor of 1.5. On low salt, such mice had normal blood pressure but less activation of RAS than wild type. On high salt, however, blood pressure was higher by 10 mmHg, accompanied by hypokalaemia and increased expression of collecting duct sodium channel (ENaC). Along these lines, a study in humans [6] found a correlation between an aldosterone synthase polymorphism (344T/C) and aldosterone excretion as well as hypertension; this observation has recently been confirmed by one study [7] but not by another one [8]. It is likely that the blood pressureraising effect of aldosterone is not only the result of natriuresis and sodium balance; in anuric dialysis patients, 50 mg spironolactone lowered systolic blood pressure by 11mmHg, remarkably without a change in serum potassium and presumably as a result of a direct vascular effect [9].