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Articles in PresS, published online ahead of print October 22, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00236.2002
Submitted on June 25, 2002
Accepted on October 15, 2002
1 Basic Science Department, Faculdade de Odontologia de Sao Jose dos Campos, Sao Jose dos Campos, SP, Brazil
2 Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT, USA
3 Department of Physiology and Biophysics, Instituto de Ciencias Biomedicas, University Sao Paulo, Sao Paulo, SP, Brazil
* To whom correspondence should be addressed. E-mail: gemalnic{at}usp.br.
Potassium secretion (JK) by the distal nephron is regulated by systemic and luminal factors. In the present investigation, JK was measured with a double-barrelled K electrode during paired microperfusion of superficial segments of the rat distal nephron. We used control solutions (100 mmol/l NaCl, pH 7.0) and experimental solutions in which chloride had been replaced with a less permeant anion and/or pH had been increased to 8.0. JK increased when chloride 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 barium-sensitive but furosemide (1 mmol/l) further reduced secretion (~10% of total), suggesting KCl cotransport was operative. Progressive reduction in lumen chloride concentration from 100 to 20 to 2 mmol/l caused increments in JK which were abolished by inhibitors of KCl cortransport, i.e. furosemide and DioA. Increasing the pH of the lumen perfusion fluid also increased JK even in the presence of barium, suggesting that this effect cannot be accounted for only by K channel modulation of potassium secretion in the distal nephron of the rat. Collectively, these data suggest a role for KCl cotransport in distal nephron K secretion.
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