Aldosterone and its receptor, the mineralocorticoid receptor (MR), play a key role in the regulation of reno-cardiovascular function as well as in the regulation of normal and abnormal reno-cardiovascular function, which are responsible for the variety of its functional responses. The underlying mechanisms are of genomic and nongenotropic nature. Prevention of critical arterial hypotension by NaCl retention and regulation of potassium homeostasis, which is of eminent importance for cardiovascular electrophysiology and rhythmogenesis, represent the good face of aldosterone in the cardiovascular system. Triggering of persistent arterial hypertension with all the detrimental secondary effects on heart, kidney, vessels, and brain represents the bad face of aldosterone/MR in the cardiovascular system. Blood pressure-independent reno-cardiovascular end organ damage represents the ugly face of MR activation and does not depend on elevated aldosterone concentrations. In this way, aldosterone/MR induces or facilitates inflammatory and fibrotic processes in a permissive milieu, created for example by angiotensin II or NaCl and characterized by enhanced oxidative stress, in vascular walls.