The mineralocorticoid aldosterone is a major factor controlling the salt and water balance and thereby also the arterial blood pressure. Accordingly, primary aldosteronism characterized by an inappropiately high aldosterone secretion is the most common form of secondary hypertension. The physiological stimulation of aldosterone synthesis in adrenocortical glomerulosa cells by angiotensin II and an increased plasma K+ concentration depends on a membrane depolarization and an increase of the cytosolic Ca2+ activity. Recurrent gain‐of‐function mutations of ion channels and transporters have been identified in a majority of cases of aldosterone producing adenomas and in familial forms of primary aldosteronism. In this review, the physiological role of these genes in the regulation of aldosterone synthesis and the altered function of the mutant proteins as well are described. The specific changes of the membrane potential and the cellular ion homeostasis in adrenal cells expressing the different mutants are compared and their impact on autonomous aldosterone production and proliferation is discussed. This article is protected by copyright. All rights reserved.