Renal metabolism and ammoniagenesis during acute respiratory alkalosis in the dog

Publisher Website
Google Scholar
Abstract
Acute respiratory alkalosis (blood pH, 7.60; arterial PCO2 [CO2 partial pressure], 15 mm Hg (1 mm Hg = 133.322 Pa); plasma bicarbonate, 14 mM) was induced in 9 anesthetized dogs by increasing their respiratory rate and depth. Renal glutamine extraction and NH4 production expressed per 100 ml of glomerular filtration rate did not change during acute hypocapnia, whereas arterial glutamine concentration decreased significantly from 0.47 to 0.36 mM. Hypocapnia did not change plasma K concentration and its urinary excretion. Acute hypocapnia increased lactate extraction and pyruvate production, whereas citrate extraction and glutamate and alanine production did not change. Citraturia remained minimal. Renal cortical glutamine concentration fell from 0.64-0.38 mM during hypocapnia while .alpha.-ketoglutarate, glutamate, malate, oxaloacetate and citrate did not change. Lactate concentration rose from 1.1-2.0 mM. Glutamine concentration in the liver and muscle decreased following acute hypocapnia. The data are compatible with the hypothesis that an acute respiratory alkalosis might not result in any change in the H ion concentration and (or) gradient between the mitochondrial matrix and the cytosol. Renal glutamine extraction and NH4 production are not reduced, renal cortical concentrations of relevant metabolites in the ammoniagenic pathway are not changed, and renal handling of citrate remains unaffected.