Renal intercalated cells mediate the secretion or absorption of Cl⁻ and OH⁻/H⁺ equivalents in the connecting segment (CNT) and cortical collecting duct (CCD). In so doing, they regulate acid-base balance, vascular volume, and blood pressure. Cl⁻ absorption is either electrogenic and amiloride-sensitive or electroneutral and thiazide-sensitive. However, which Cl⁻ transporter(s) are targeted by these diuretics is debated. While epithelial Na⁺ channel (ENaC) does not transport Cl⁻, it modulates Cl⁻ transport probably by generating a lumen-negative voltage, which drives Cl⁻ flux across tight junctions. In addition, recent evidence indicates that ENaC inhibition increases electrogenic Cl⁻ secretion via a type A intercalated cells. During ENaC blockade, Cl⁻ is taken up across the basolateral membrane through the Na⁺-K⁺−2Cl⁻ cotransporter (NKCC1) and then secreted across the apical membrane through a conductive pathway (a Cl⁻ channel or an electrogenic exchanger). The mechanism of this apical Cl⁻ secretion is unresolved. In contrast, thiazide diuretics inhibit electroneutral Cl⁻ absorption mediated by a Na⁺-dependent Cl⁻/HCO₃⁻ exchanger. The relative contribution of the thiazide and the amiloride-sensitive components of Cl⁻ absorption varies between studies and probably depends on the treatment model employed. Cl⁻ absorption increases markedly with angiotensin and aldosterone administration, largely by upregulating the Na⁺-independent Cl⁻/HCO₃⁻ exchanger pendrin. In the absence of pendrin [Slc26a4^(−/−) or pendrin null mice], aldosterone-stimulated Cl⁻ absorption is significantly reduced, which attenuates the pressor response to this steroid hormone. 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⁻. This review summarizes mechanisms of Cl⁻ transport in CNT and CCD and how these transporters contribute to the regulation of extracellular volume and blood pressure.