Regulation of basolateral membrane potential after stimulation of Na+ transport in proximal tubules |
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Authors: | Jean-Yves Lapointe Marcelle Duplain |
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Affiliation: | (1) Membrane Transport Research Group, University of Montreal, C. P. 6128-A, H3C 3J7 Montreal, Quebec, Canada |
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Abstract: | Summary We have previously shown that stimulation of apical Na-coupled glucose and alanine transport produces a transient depolarization of basolateral membrane potential (Vbl) in rabbit proximal convoluted tubule (PCT. Sl segment). The present study is aimed at understanding the origin of the membrane repolarization following the intial effect of addition of luminal cotransported solutes. Luminal addition of 10–15mMl-alanine produced a rapid and highly significant depolarization ofVbl (20.3±1.1 mV,n=15) which was transient and associated with an increase in the fractional K+ conductance of the basolateral membrane (tK) from 8 to 29% (P<0.01,n=6). Despite the significant increase intK, the repolarization was only slightly reduced by the presence of basolateral Ba2+ (2mM,n=6) or quinine (0.5 mM,n=5). The repolarization was greatly reduced in the presence of 0.1 mM 4-acetamino-4isothiocyamostilbene-2,2-disulfonic acid (SITS) and blunted by bicarbonate-free solutions. Intracellular pH (pHi) determined with the fluorescent dye 2, 7-bis-2-carboxyethyl-5(and-6)-carboxyfluorescein (BCECF), averaged 7.39±0.02 in control solution (n=9) and increased to 7.50±0.03 in the first 15 sec after the luminal application of alanine. This was followed by a significant acidification averaging 0.16±0.01 pH unit in the next 3 min. In conclusion, we believe that, contrary to other leaky epithelia, rabbit PCT can regulate its basolateral membrane potential not only through an increase in K+ conductance but also through a cellular acidification reducing the basolateral HCO3– exit through the electrogenic Na-3(HCO3) cotransport mechanism. |
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Keywords: | electrophysiology potassium conductance intracellular pH bicarbonate transport Na-coupled transport |
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