Aldosterone stimulates reabsorption of sodium, sustaining blood volume and pressure in the face of salt deprivation or extracellular fluid depletion. The steroid also stimulates excretion of potassium, protecting extracellular fluid from excessive levels of that ion. These two actions are relatively rapid and clearly adaptive when appropriately initiated and terminated, but maladaptive when prolonged or excessive, causing hypertension and electrolyte imbalance. Aldosterone and other mineralocorticoids exert slower, direct effects on cells in the heart, kidneys, and vessels, leading to hypertrophy, fibrosis, and dysfunction contributing to degenerative cardiovascular diseases. The maladaptive actions of aldosterone are exacerbated by sodium chloride, angiotensin, endothelin, and certain growth factors. Damage can be minimized by antagonists of aldosterone receptors, inhibitors of the renin system, depletion of salt, and repletion of potassium and magnesium. Specific inhibitors of fibrosis and hypertrophy, and more effective inhibitors of the renin system should be useful in the future.