The interaction of pendrin and the epithelial sodium channel in blood pressure regulation

Purpose of review This review summarizes the contribution of the Cl-/HCO3- exchanger pendrin in the renal regulation of blood pressure. Recent findings Intercalated cells are found in the distal convoluted tubule, the connecting tubule and the collecting duct. These cells regulate acid-base balance by secreting or absorbing OH-/H+ equivalents and regulate vascular volume and blood pressure by absorbing chloride ions. In type B and non-A, non-B intercalated cells chloride absorption and HCO3- secretion are accomplished through the apical sodium-independent Cl-/HCO3- exchanger pendrin. With increased circulating aldosterone, pendrin abundance and transport are upregulated. In the absence of functional pendrin (Slc26a4 (-/-) mice), aldosterone-stimulated chloride absorption is reduced, which attenuates the blood pressure response to this steroid hormone. Pendrin also regulates aldosterone-induced changes in epithelial sodium channel abundance and function through a kidney-specific mechanism that does not involve changes in concentration of a circulating hormone. In vitro, angiotensin II increases sodium chloride absorption in the collecting duct by increasing the driving force for pendrin-mediated chloride absorption and the epithelial sodium channel-mediated sodium absorption through greater electrogenic hydrogen secretion. Summary Aldosterone and angiotensin II modulate the renal regulation of blood pressure, in part, by regulating pendrin-mediated chloride absorption and the epithelial sodium channel-mediated sodium absorption. Pendrin also modulates stimulation of the epithelial sodium channel by aldosterone.