Decreased distal acidification in acute hypercapnia in the dog.
The present studies evaluate the effect of acute hypercapnia on distal nephron H+ secretion (DNH+S) in vivo by means of the urine-blood PCO2 difference (U-B PCO2) in alkaline urine. Bicarbonaturia was induced by either a sodium bicarbonate infusion or L-lysine administration. Our results demonstrate that the U-B PCO2, as a function of the urinary bicarbonate concentration, was significantly lower during acute respiratory acidosis; this effect was not dependent on changes in glomerular filtration rate and/or fractional excretion of sodium, potassium, and chloride. Infusion of the sodium salts of sulfate, a nonreabsorbable anion, did not correct the diminished U-B PCO2. Amiloride caused the U-B PCO2 to fall in normocapnic dogs but not in hypercapnic dogs. When hypercapnia was superimposed in dogs with extracellular fluid volume contraction, there were no changes in the U-B PCO2. This study indicates that acute hypercapnia in the intact dog decreases DNH+S and is compatible with an effect of hypercapnia on the voltage-dependent component of urine acidification. The mechanism appears to be direct rather than secondary to factors that influence the rate of sodium delivery to the distal nephron.
D000142:Acidosis, Respiratory / Q000503:physiopathology; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology / Q000652:urine; D002245:Carbon Dioxide / Q000097:blood / Q000652:urine; D004231:Diuresis / Q000187:drug effects; D004285:Dogs; D005110:Extracellular Space / Q000502:physiology; D005260:Female; D006863:Hydrogen-Ion Concentration; D006935:Hypercapnia / Q000503:physiopathology*; D008239:Lysine / Q000494:pharmacology; D008297:Male; D009399:Nephrons / Q000503:physiopathology*; D011188:Potassium / Q000652:urine; D012964:Sodium / Q000652:urine; D017693:Sodium Bicarbonate
D001639:Bicarbonates; D002245:Carbon Dioxide; D000584:Amiloride; D017693:Sodium Bicarbonate; D012964:Sodium; D008239:Lysine; D011188:Potassium