Aldosterone influences independently the vascular environment in humans, acting through structural and functional modifications of the arterial wall as derived from mineralocorticoid receptors. In rats, aldosterone infusion increases arterial stiffness in the presence of high-sodium intake, together with development of extracellular matrix and inflammatory factors. A selective increase in systolic and pulse pressure ensues, causing predominant organ damage on the heart, kidney and large arteries. In humans at rest, but independently of mean arterial pressure, arterial stiffness and wave reflections are associated with a steeper increase in these parameters with age. This finding is observed mainly with the CC genotype and not the TT or the TC genotype of the aldosterone synthase gene polymorphism. Early identification of individuals presenting this genotype could be important to detect hypertension.