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Gitelman’s syndrome (GS) is a rare inherited tubulopathy characterized by hypokalemia, hypomagnesemia, and metabolic alkalosis due to inactivating mutations of the distal convoluted tubule sodium chloride cotransporter. This entails reduced extracellular volume and consequent activation of counterbalancing systems such as the renin–angiotensin–aldosterone system. Although with high levels of angiotensin II, Gitelman’s patients do not display hypertension or its cardiovascular and renal remodeling complications related to overactivation of those systems. The present review will explore the available experimental evidence on angiotensin II signaling in GS. The understanding of these mechanisms might be useful to track the rationale for novel treatments of Gitelman’s syndrome. These peculiar characteristics make GS a human model to investigate the angiotensin II signaling in humans to give deeper insights into the pathophysiology of hypertension. Current treatment for GS includes potassium and magnesium supplements with additional tailored treatments for concomitant chondrocalcinosis or prolonged QT interval; however, additional nutritional approaches could be considered that might minimize possible supplements’ side effects.

Molecular aspects of the altered Angiotensin II signaling in Gitelman’s syndrome