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Am J Physiol Renal Physiol 284: F381-F388, 2003. First published October 22, 2002; doi:10.1152/ajprenal.00236.2002
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Vol. 284, Issue 2, F381-F388, February 2003

Role of luminal anion and pH in distal tubule potassium secretion

J. B. O. Amorim1, M. A. Bailey2, R. Musa-Aziz3, G. Giebisch2, and G. Malnic3

1 Basic Science Department, Faculdade de Odontologia de São José dos Campos, and 3 Department of Physiology and Biophysics, Instituto de Ciências Biomédicas, Universidade de São Paulo, 05508-900 São Paulo, Brazil; and 2 Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06510

Potassium secretory flux (JK) by the distal nephron is regulated by systemic and luminal factors. In the present investigation, JK was measured with a double-barreled K+ electrode during paired microperfusion of superficial segments of the rat distal nephron. We used control solutions (100 mM NaCl, pH 7.0) and experimental solutions in which Cl- had been replaced with a less permeant anion and/or pH had been increased to 8.0. JK increased when Cl- was replaced by either acetate (~37%), sulfate (~32%), or bicarbonate (~62%), and also when the pH of the control perfusate was increased (~26%). The majority (80%) of acetate-stimulated JK was Ba2+ sensitive, but furosemide (1 mM) further reduced secretion (~10% of total), suggesting that K+-Cl- cotransport was operative. Progressive reduction in luminal Cl- concentration from 100 to 20 to 2 mM caused increments in JK that were abolished by inhibitors of K+-Cl- cortransport, i.e., furosemide and [(dihydroindenyl)oxy]alkanoic acid. Increasing the pH of the luminal perfusion fluid also increased JK even in the presence of Ba2+, suggesting that this effect cannot be accounted for only by K+ channel modulation of K+ secretion in the distal nephron of the rat. Collectively, these data suggest a role for K+-Cl- cotransport in distal nephron K+ secretion.

distal tubule; collecting duct; potassium secretion; postassium-chloride cotransport


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