Sodium in renal tubular acidification kinetics.
Renal proximal tubules and their peritubular capillaries were perfused with mammalian Ringer solutions containing different sodium concentrations. In stop-flow microperfusion experiments, the pH was measured by means of antimony microelectrodes, permitting calculation of rates of H ion secretion and bicarbonate reabsorption. These rates, as well as transepithelial pH and bicarbonate gradients, were significantly reduced at ambient concentrations of 20 and 4 meq/liter Na+. However, even at the lowest sodium concentrations (4 meq/liter), H ion secretion was still 74%, and bicarbonate reabsorption of 64% of control rates. In similar conditions, sodium reabsorption as measured by the split-droplet technique fell to practically zero. Ouabain, 10(-3) M, in capillaries reduced bicarbonate reabsorption by 31%, and 3 X 10(-4) M furosemide in lumen and capillaries reduced acidification by 29%. At pH 8--9 in capillaries, sodium transport was normal while acidification was markedly reduced. These data show that low sodium levels impair renal tubular acidification, but they do not support a rigid coupling of these transport processes.
D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D001693:Biological Transport, Active / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D006859:Hydrogen / Q000378:metabolism*; D066298:In Vitro Techniques; D007684:Kidney Tubules / Q000378:metabolism* / Q000502:physiology; D008297:Male; D008564:Membrane Potentials; D008839:Microelectrodes; D008871:Microvilli / Q000378:metabolism; D010477:Perfusion; D051381:Rats; D012964:Sodium / Q000494:pharmacology*
D001639:Bicarbonates; D006859:Hydrogen; D012964:Sodium