Renal intercalated cells mediate the secretion or the absorption of OH-/H+ equivalents and Cl- in the distal convoluted tubule (DCT), the connecting tubule (CNT) and the cortical collecting duct (CCD). In so doing, they regulate acid-base balance, vascular volume and blood pressure. In type B and non-A, non-B intercalated cells, Cl- absorption and HCO3- secretion are accomplished through the apical Na+-independent Cl-/HCO3- exchanger, pendrin. With increased circulating aldosterone or angiotensin II, pendrin abundance and function are up-regulated. In the absence of pendrin (Slc26a4 (-/-) or pendrin null mice), aldosterone- and angiotensin II-stimulated Cl- absorption are reduced, which attenuates the blood pressure response to these hormones. Pendrin also modulates aldosterone-induced changes in ENaC abundance and function through a kidney-specific mechanism that does not involve changes in the concentration of a circulating hormone. Instead, pendrin changes ENaC abundance and function, at least in part, by altering luminal HCO3-. Thus, aldosterone and angiotensin II modulate the renal regulation of blood pressure, in part, by regulating pendrin-mediated Cl- absorption and ENaC-mediated Na+ absorption. This review summarizes the contribution of the Cl-/HCO3- exchanger, pendrin, in the renal regulation of blood pressure.