In rat kidney the “secretory” isoform of the Na+-K+-2Cl−cotransporter (NKCC1) localizes to the basolateral membrane of the α-intercalated cell. The purpose of this study was to determine whether rat outer medullary collecting duct (OMCD) secretes Cl−and whether transepithelial Cl−transport occurs, in part, through Cl−uptake across the basolateral membrane mediated by NKCC1 in series with Cl−efflux across the apical membrane. OMCD tubules from rats treated with deoxycorticosterone pivalate were perfused in vitro in symmetrical HCO[Formula: see text]/CO2-buffered solutions. Cl−secretion was observed in this segment, accompanied by a lumen positive transepithelial potential. Bumetanide (100 μM), when added to the bath, reduced Cl−secretion by 78%, although the lumen positive transepithelial potential and fluid flux were unchanged. Bumetanide-sensitive Cl−secretion was dependent on extracellular Na+and either K+or NH[Formula: see text], consistent with the ion dependency of NKCC1-mediated Cl−transport. In conclusion, OMCD tubules from deoxycorticosterone pivalate-treated rats secrete Cl−into the luminal fluid through NKCC1-mediated Cl−uptake across the basolateral membrane in series with Cl−efflux across the apical membrane. The physiological role of NKCC1-mediated Cl−uptake remains to be determined. However, the role of NKCC1 in the process of fluid secretion could not be demonstrated.