title: Proximal tubular acidification in metabolic alkalosis.
abstract: Metabolic alkalosis was induced in rats by acute bicarbonate loading in the presence and absence of extracellular volume (ECV) expansion. Proximal tubular acidification was studied by stopped-flow microperfusion and the determination of luminal pH by antimony microelectrodes. Stationary pH and bicarbonate were markedly increased in proximal tubules of alkalotic rats, and acidification half-times were increased, leading to a fall in net bicarbonate reabsorption (JHCO-3) to 36% of control values. Net H+ ion secretion (JH+) into phosphate buffer fell to 56% of controls, whereas alkalinization t/2 and H+ fluxes, measured during perfusion with acid phosphate, were unaltered. ECV expansion reduced proximal JHCO-3 36% in control rats, without affecting JH+, and caused a fall in alkalinization t/2, compatible with increased bicarbonate back-flux into the lumen. However, it did not affect JHCO3 and JH+ in alkalotic rats. Carbonic anhydrase inhibition did not significantly reduce acidification in alkalotic rats. An analysis of the components of bicarbonate reabsorption showed that alkalosis reduced catalyzed H+ -ion secretion to 7% of the control values. It is concluded that proximal H+ ion secretion is significantly reduced in metabolic alkalosis leading to lower JHCO-3. No evidence for modification of H+/HCO-3 apparent permeabilities was obtained. The effects of alkalosis were not significantly altered by ECV expansion or by carbonic anhydrase inhibition.
mesh_terms: D000136:Acid-Base Equilibrium; D000471:Alkalosis / Q000503:physiopathology*; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D008297:Male; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D001639:Bicarbonates; D002257:Carbonic Anhydrase Inhibitors