Although the distal tubule is considered the target for aldosterone action, aldosterone receptors had been found in myocardium, vascular smooth muscle cells and glomeruli .In vitro studies of cultured mesangial cells revealed increased production of type IV collagen after incubation with aldosterone. In a double blind controlled study MacFadyen and colleagues observed that spironolactone treatment reduced circulating levels of procollagen type III N-terminal amino peptide, a marker of vascular collagen turnover. Weber and other investigators have observed that aldosterone caused myocardial fibrosis and this effect could be ameliorated by treatment with spironolactone. In addition to the classical genomic action through the type 1 mineralocorticoid receptor, aldosterone is now known to have significant non-genomic mediated action in many different tissues including kidney tubules and vascular smooth muscle cells. Aldosterone also up regulates Angiotensin II membrane receptors thereby multiplying the vascular effect of Ang II. This upregulation was inhibited by treatment with spironolactone. These findings are consistent with a synergistic action between Ang II and aldosterone in the production of vascular injury as first proposed by Masson et al almost 4 decades ago.