Contribution of the Na(+)-K(+)-2Cl(-) cotransporter (NKCC1) to transepithelial transport of H(+), NH(4)(+), K(+), and Na(+) in rat outer medullary collecting duct.

In rat kidney, the "secretory" isoform of the Na-K-Cl cotransporter, NKCC1 (BSC-2), localizes to the basolateral membrane of the alpha intercalated cell, the acid secreting cell of the outer medullary collecting duct (OMCD). This laboratory has reported that NKCC1 mediates Cl(-) uptake across the basolateral membrane in series with Cl(-) secretion across the apical membrane in rat OMCD. NKCC1 transports NH(4)(+), K(+), and Na(+) as well as Cl(-); therefore, a role for the cotransporter in the process of HCl, NH(4)Cl, KCl, and NaCl secretion has been suggested. Thus, it was determined if bumetanide, an inhibitor of NKCC1, alters transepithelial cation transport in rat OMCD. OMCD tubules from deoxycorticosterone pivalate (DOCP)-treated rats were perfused in vitro. Hydration of CO(2), rather than NH(4)(+), provides the principle source of H(+) for net acid secretion. In HCO(3)(-)/CO(2)-buffered solutions, no effect of bumetanide on net K(+) flux was detected. Under some conditions, bumetanide addition resulted in a small reduction in secretion of net H(+) equivalents. Transepithelial Na(+) flux, J(Na), was -1.5 +/- 1.7 pmol/mm per min, values not different from zero. However, with the application of bumetanide to the bath, J(Na) was +5.2 +/- 1.3 pmol/mm per min (P < 0.05), which indicates net Na(+) absorption. In conclusion, inhibition of NKCC1 in rat OMCD changes transepithelial movement of Na(+) and Cl(-). The role of NKCC1 in the secretion of net H(+) equivalents is small.