Abstract
The present study examined the effect of sodium transport inhibition by amiloride, ouabain, and luminal sodium removal on potassium secretion in isolated cortical collecting tubules from adrenalectomized and DOCA-stimulated rabbits. Collecting tubules from adrenalectomized rabbits had a mean potassium secretion of 3.62 +/- 0.37 pmoles X mm-1 X min-1, which significantly decreased to 1.52 +/- 0.21 pmoles X mm-1 X min-1 after addition of amiloride, but no additional effect was observed after the addition of ouabain. The transepithelial voltage (VT) became less positive after exposure to amiloride. Cortical collecting tubules from DOCA-treated animals exhibited significantly greater potassium secretion (28.6 +/- 9.4 pmoles X mm-1 X mm-1). Amiloride totally inhibited potassium secretion, and VT reversed polarity in these tubules. In tubules from adrenalectomized rabbits the removal of luminal sodium inhibited potassium secretion by approximately 44% but had no effect on VT. There remained, however, a substantial amount of potassium secretion in the absence of transepithelial sodium flux. Thus, potassium secretion in the cortical collecting tubule is highly dependent on sodium reabsorption under conditions of mineralocorticoid stimulation but significantly less so in adrenalectomized animals. Potassium secretion in the cortical collecting tubule of adrenalectomized rabbits is inhibited independent of VT and occurs, in part, by an apparent electroneutral process. Chronic exposure to mineralocorticoids appears to stimulate electrogenic sodium reabsorption and potassium secretion.
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