Electrolyte and Water Metabolism of Rabbit Kidney Slices: Effect of Metabolic Inhibitors

Abstract

Thin slices of rabbit kidney cortex, depleted of K, reaccumulate K with a reciprocal loss of Na during incubation under optimal conditions. The effects of metabolic inhibitors on this process showed that all compounds which decrease O2 consumption likewise prevent the uptake of K. Anoxic anoxia, cyanide and arsenite depress these functions in a parallel manner. A larger group of compounds (including azide, HgCl2, organic mercurials, Benemid and theophylline) depress K uptake at concns. significantly lower than those required to depress O2 consumption. 2,4-Dinitrophenol and related compounds show a good correlation between depression of K uptake and inhibition of the generation of energy-rich phosphate bonds. Inhibitors of carbonic anhydrase, cholinesterase and alkaline phosphatase have no effect. Tissue hydration is slightly increased by anoxic anoxia but more so by certain inhibitors. In every expt. with a constant external osmotic pressure, the tissue osmotic pressure (estimated as the sum of Na plus K) remained essentially constant despite changes in water content. Depression of metabolic activity is, therefore, associated with an isomotic increase in cellular hydration. No evidence was found to support the concept that the cells are normally hypertonic to their environment. The mechanisms of tissue adjustments to changes in external osmotic pressure are discussed.