Influence of alterations in acid-base conditions on intracellular pH of intact renal cortex.
Intracellular pH (pHI) of intact rat renal cortex was estimated using [14C]-5,5-dimethyl-2,4-oxazolidinedione and 22Na+ under conditions of metabolic acidosis and alkalosis, potassium depletion and carbonic anhydrase inhibition. In metabolic acidosis and alkalosis, pHI and bicarbonate concentration changed in the same direction as occurred in plasma. In potassium depletion, systemic acid-base balance was unaltered but a marked intracellular acidosis developed. Carbonic anhydrase inhibition with acetazolamide was associated with an extracellular respiratory acidosis and a rise in intracellular bicarbonate concentration. Another carbonic anhydrase inhibitor, benzolamide, caused no change in systemic acid-base state but produced a decrease in intracellular bicarbonate concentration. When appropriate corrections were made for predicted change in tubular fluid bicarbonate and for intracellular sodium, modification in the absolute values of the above changes occurred but the directions of the changes in pHI and bicarbonate concentration were unaltered.
D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000503:physiopathology; D000471:Alkalosis / Q000503:physiopathology; D000818:Animals; D001826:Body Fluids / Q000502:physiology*; D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D007424:Intracellular Fluid / Q000502:physiology*; D007672:Kidney Cortex / Q000502:physiology* / Q000503:physiopathology; D008297:Male; D011191:Potassium Deficiency / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains
D002257:Carbonic Anhydrase Inhibitors