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AJP - Renal Physiology, Vol 256, Issue 1 136-F142, Copyright © 1989 by American Physiological Society
ARTICLES |
S. C. Sansom, S. Agulian, S. Muto, V. Illig and G. Giebisch
Department of Physiology, Yale University School of Medicine, New Haven, Connecticut 06510.
We used liquid ion exchanger and conventional microelectrodes to evaluate the effects of mineralocorticoids on the intracellular K activity (aiK) and K transport properties of principal cells (PC) of isolated cortical collecting ducts (CCDs). Hoffman modulation optics and electrophysiological methods were used to identify PC. K activity was measured with two single-barreled electrodes. We found that aiK of PC from deoxycorticosterone acetate (DOCA)-treated rabbits (97.6 mM) was not different from controls (94.8 mM). The driving forces for K transport across the basolateral membrane favored cell to bath (reabsorption) in PCs from controls and bath to cell (secretion) in PCs from DOCA-treated rabbits. However, the driving force for K secretion across the apical membrane was not significantly different between the two groups. We used the intracellular aiKs and bath ion substitutions (gluconate for Cl and K for Na) to evaluate the effects of DOCA on the ion-selective properties of the basolateral membrane of PC. DOCA increased PK/PCl from 0.33 to 0.89. Our conclusion was as follows: in PC of control rabbits K is above electrochemical equilibrium across the basolateral membrane. However, the basolateral K conductance is probably too small for significant K recycling. In PC of DOCA-treated rabbits the aiK is below electrochemical equilibrium across the basolateral membrane and the K conductance is increased. These effects enhance K secretion across this border while maintaining cell K constant.
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