Potassium channels in adrenocortical cells

Abstract

Excessive aldosterone secretion, so-called primary aldosteronism, is the most common form of secondary hypertension. For the regulation of aldosterone secretion in adrenal glomerulosa cells, the control of membrane voltage is of paramount importance. Physiologically, resting glomerulosa cells are hyperpolarized and secretion of aldosterone is low. On the other hand, depolarization of the plasma membrane leads to Ca2+ influx and activation of signals that enhance aldosterone secretion. In glomerulosa cells, K+ channels serve several functions: (i) they hyperpolarize the membrane and, together with depolarizing ion conductances, participate in membrane voltage oscillations, (ii) they are targets of hormones regulating aldosterone production, and (iii) they are the molecular correlate underlying the unique K+ sensitivity of glomerulosa cells that respond to small rises of plasma K+ with finely tuned increases in aldosterone secretion. The importance of the precise control of membrane voltage and ion transport for adrenal pathophysiology has been highlighted by recent discoveries showing that mutations in membrane transporters and ion channels cause aldosterone-producing adenomas. In this short review, we summarize the physiology of K+ channels in glomerulosa cells and discuss their pathophysiological relevance and possible clinical implications.