Effects of certain inhibitors on renal excretion of salt and water

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Abstract
The direct proportionality between renal oxygen consumption and sodium reabsorption suggests a linkage between cation transport and the electron transport system (ETS). We have studied the effects of in vitro inhibitors of the ETS on sodium reabsorption in the dog kidney. Compounds known to block O2 consumption or reduce tissue levels of adenosine triphosphate (ATP) were infused in millimolar quantities into a renal artery of anesthetized dogs. We observed a unilateral diuresis following the administration of cyanide, antimycin-A and iodoacetamide; no diuresis was observed following administration of 2,4-dinitrophenol, azide, and phlorizin. These latter agents block the synthesis or facilitate the degradation of ATP. Negative results were also observed with phthiocol (a naphthoquinone), malonate, and Amytal, inhibitors of specific substrates of ETS. We interpret our results as follows. Inhibition of sodium reabsorption by cyanide and antimycin-A supports the hypothesis that renal cation transport is dependent in part upon oxidative metabolism. The failure of phlorizin and 2,4-dinitrophenol to affect sodium reabsorption suggests that cation transport may be independent of ATP synthesis or concentration in renal tissues.