Lactate oxidation and sodium reabsorption by dog kidney in vivo.
Lactate uptake (Qlact) and oxidation (QCO2lact), oxygen consumption (QO2) and net tubular Na+ reabsorption (TNa), were estimated in pentobarbital-anesthetized dogs under control conditions and following unilateral intrarenal injection of ouabain or intravenous infusion of acetazolamide, ethacrynic acid, or furosemide. QCO2lact accounted for approximately half of simultaneous Qlact and for about one-third of QO2 in control periods. Ouabain injection resulted in significant decreases in several functions of the injected kidney: TNa, 46%; TNa/FNa, 36%; QO2, 40%; Qlact, 59%; and QCO2lact, 70%. Acetazolamide infusion decreased TNa, 33%; TNa/FNa, 12%; QO2, 10%; and QCO2lact, 38%; but did not change Qlact. Ethacrynic acid diminished TNa, 60%; TNa/FNa, 36%; QO2, 45%; Qlact, 31%; and QCO2lact, 73%. Furosemide lowered TNa, 37%; TNa/FNa, 28%; QO2, 25%; and Qlact, 48%; but did not change QCO2lact, 2%. Results indicate that decarboxylation is a major pathway of renal lactate metabolism, that lactate oxidation is a substantial source of aerobic energy for the kidney, and that QCO2lact is probably functionally related to sodium reabsorption. This relationship appears to be closer for a fraction of TNa associated with ouabain- and ethacrynic acid-sensitive mechanisms.
D000042:Absorption; D000086:Acetazolamide / Q000494:pharmacology; D000818:Animals; D004285:Dogs; D004976:Ethacrynic Acid / Q000494:pharmacology; D005260:Female; D005665:Furosemide / Q000494:pharmacology; D007668:Kidney / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism*; D010042:Ouabain / Q000494:pharmacology; D010084:Oxidation-Reduction; D012964:Sodium / Q000378:metabolism*
D007773:Lactates; D010042:Ouabain; D005665:Furosemide; D012964:Sodium; D004976:Ethacrynic Acid; D000086:Acetazolamide