"CONTRACTION" ALKALOSIS AFTER DIURESIS OF EDEMATOUS PATIENTS WITH ETHACRYNIC ACID.
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Biomedical subjects
Publications and source records attributed to R W WINTERS.
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Twice washed mitochondria from rat kidney cortex can accumulate sulfate ions from low (10(-7)M) ambient concentrations to create virtual gradients of several hundred to one. This sulfate is subsequently released. The activation energy for the uptake is 12,000 calories per mole; for release it is about 30,000 calories per mole. Variations in the sulfate concentration of the medium show that there is a straight line Freundlich adsorption isotherm over a million-fold range of concentration of sulfate in the medium. There are 9 x 10(4) sites at 10(-5)M and 9 x 10(5) sites at 10(-3)M sulfate per average single mitochondrion. Preincubation at 30 degrees C rapidly destroys the ability to accumulate sulfate. Partial protection occurs if oxidative phosphorylation is proceeding during the preincubation. The concentration of the endogenous inorganic sulfate of twice washed mitochondria is 4.2 x 10(-4) moles per liter of mitochondrial pellet water; 99.85 per cent of this endogenous sulfate is inexchangeable with external sulfate in vitro. It is all exchangeable in vivo. The pH optimum for accumulation of radiosulfate from dilute external sulfate concentrations is 5.5. These observations show that there is a delicate and specific mechanism in mitochondria from kidney cortex which accumulates sulfate. The chemical nature of the accumulated sulfate is unknown.
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Potassium accumulation occurred in leached slices of the inner medulla of the dog kidney incubated under anaerobic conditions at 37 degrees C with glucose as substrate, but was blocked by inhibitors of glycolysis. Aerobically, only slight accumulation occurred with succinate as substrate at 37 degrees C, and this was blocked by dinitrophenol. These findings were in contrast to those obtained with kidney cortex slices under the same conditions.
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Potassium depletion in rats augments the specific renal lesions of phosphate loading. Since it has been shown that phosphate loading increases the specific cardiac lesions of potassium deficiency (12), it is concluded that the similar types of electrolyte imbalance (potassium depletion-phosphate load) act conversely in the two organs.
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