Potassium transport in cortical collecting tubules from mineralocorticoid-treated rat

Unidirectional fluxes of 86Rb+ were used to examine the stimulation of K+ secretion produced by arginine vasopressin (ADH) in isolated perfused cortical collecting tubules from rats treated with desoxycorticosterone. ADH at 100 μU/ml in the bathing solution increased the bath-to-lumen flux (J/sub b→1/; pmol /center dot/ min-1 /center dot/ mm-1) from 16.9 /plus minus/ 2.3 to 43.2 /plus minus/ 4.6. The lumen-to-bath flux (J/sub 1→b/) fell from 3.2 /plus minus/ 0.7 to 1.3 /plus minus/ 0.4 with ADH due to hyperpolarization of the transepithelial voltage from -12.6 /plus minus/ 1.3 to /minus/39.3 /plus minus/ 2.0 mV, but the calculated Rb+ permeability was unaltered at 0.20-0.26 μm/s. Although 2 mM lumen Ba2+ inhibited J/sub b→1/ by 55 /plus minus/ 6%, the flux ratio (J/sub b→1//J/sub 1→b/) of 28 /plus minus/ 8 was larger than predicted for passive exchange. In the absence of ADH 2 mM Ba2+ reduced J/sub b→1/ to the level predicted for passive movement, but addition of ADH with Ba2+ still present increased J/sub 1→1/ by an amount identical to that observed without Ba2+, although the absolute J/sub b→1/ was less. Simultaneous addition of 2 mM luminal and 4 mM bath Ba2+ also inhibited J/sub 1→b/ for 22Na+ but not to passive levels. These results indicate either that the concentrations of Ba2+ used were insufficient to block K+ conductances completely or that K+/Rb+ secretion can occur through a Ba2+-insensitive pathway