Effects of cyanide, Q0, and dinitrophenol on renal sodium reabsorption and oxygen consumption

Abstract

Effects on sodium reabsorption and oxygen consumption of the renal arterial injection of three metabolic inhibitors were studied by unilateral clearance techniques in anesthetized dogs. In control studies, 21.5 ± 2.3 mEq sodium were reabsorbed per millimole oxygen consumed within a range of sodium reabsorption of from 2 to 9 mEq/min. A total dose of 10^–4 m cyanide depressed both sodium reabsorption and oxygen consumption in the injected kidney. Administration of 10^–4 m Q₀, the quinone nucleus of coenzyme Q, reduced sodium reabsorption and had a variable effect on O₂ consumption. Dinitrophenol, in a total dose of 10^–3 m, increased oxygen consumption without affecting the per cent of filtered sodium that was reabsorbed. The resultant Na:O₂ ratios were 12:1. We conclude that the major fraction of O₂ consumption energizes sodium reabsorption in the kidney perhaps via the classic route of ATP synthesis and hydrolysis. However, all three compounds used in this study would be predicted to decrease renal ATP concentrations. Yet only cyanide and Q₀ decreased sodium reabsorption. Energy for sodium movement may come directly from oxidative metabolism bypassing synthesis and breakdown of ATP.