The last two decades have witnessed a growing number of experimental observations regarding the
mineralocorticoid physiopathology, leading to a new understanding of the molecular basis of the aldosterone-induced
target organ damage. As a matter of fact, although it has long been known that the combined administration of
mineralocorticoids and salt leads to extensive vascular lesions in the target organs, the recognition that aldosterone is able
to induce direct toxic effects on the various cell types that make up the cardiovascular organ has built up recently.
Moreover, non-genomic effects have been attributed to aldosterone, i.e. effects which do not depend on the activation of
the cellular transcription machinery, whose physiopathologic relevance is still being investigated. These advances in our
understanding of aldosterone physiopathology have shed light on the biological reasons which are at the base of the
impressive results obtained in clinical trials of aldosterone antagonism.