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AJP - Renal Physiology, Vol 253, Issue 1 76-F88, Copyright © 1987 by American Physiological Society
ARTICLES |
J. A. Schafer and S. L. Troutman
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 microU/ml in the bathing solution increased the bath-to-lumen flux (Jb----l; pmol X min-1 X mm-1) from 16.9 +/- 2.3 to 43.2 +/- 4.6 (n = 16). The lumen-to-bath flux (Jl----b) fell from 3.2 +/- 0.7 to 1.3 +/- 0.4 with ADH due to hyperpolarization of the transepithelial voltage from -12.6 +/- 1.3 to -39.3 +/- 2.0 mV, but the calculated Rb+ permeability was unaltered at 0.20-0.26 micron/s. Although 2 mM lumen Ba2+ inhibited Jb----l by 55 +/- 6%, the flux ratio (Jb----l/Jl----b) of 28 +/- 8 was larger than predicted for passive exchange. In the absence of ADH 2 mM Ba2+ reduced Jb----l to the level predicted for passive movement, but addition of ADH with Ba2+ still present increased Jb----l by an amount identical to that observed without Ba2+, although the absolute Jb----l was less. Simultaneous addition of 2 mM luminal and 4 mM bath Ba2+ also inhibited Jl----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.
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