Pendrin (Slc26a4) localizes to type B and non-A, non-B intercalated cells in the distal convoluted tubule, the connecting tubule, and the cortical collecting duct (CCD), where it mediates apical Cl⁻/HCO₃⁻ exchange. The purpose of this study was to determine whether angiotensin II increases transepithelial net chloride transport, J_Cl, in mouse CCD through a pendrin-dependent mechanism. J_Cl and transepithelial voltage, V_T, were measured in CCDs perfused in vitro from wild-type and Slc26a4 null mice ingesting a NaCl-replete diet or a NaCl-replete diet and furosemide. In CCDs from wild-type mice ingesting a NaCl-replete diet, V_T and J_Cl were not different from zero either in the presence or absence of angiotensin II (10⁻⁸ M) in the bath. Thus further experiments employed mice given the high-NaCl diet and furosemide to upregulate renal pendrin expression. CCDs from furosemide-treated wild-type mice had a lumen-negative V_T and absorbed Cl⁻. With angiotensin II in the bath, Cl⁻ absorption doubled although V_T did not become more lumen negative. In contrast, in CCDs from furosemide-treated Slc26a4 null mice, Cl⁻ secretion and a V_T of ∼0 were observed, neither of which changed with angiotensin II application. Inhibiting ENaC with benzamil abolished V_T although J_Cl fell only ∼50%. Thus substantial Cl⁻ absorption is observed in the absence of an electromotive force. Attenuating apical anion exchange with the peritubular application of the H⁺-ATPase inhibitor bafilomycin abolished benzamil-insensitive Cl⁻ absorption. In conclusion, angiotensin II increases transcellular Cl⁻ absorption in the CCD through a pendrin- and H⁺-ATPase-dependent process.