Inhibition of transcellular NaCI reabsorption in dog kidneys during hypercalcemia

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Abstract
Reduced concentrating and diluting capacity of the kidney in acute and chronic hypercalcemia may partly be due to inhibition of transcellular sodium reabsorption (RNa) in the thick ascending limb of Henle's loop. To examine this hypothesis, local heat production and RNawere measured during normo‐and hypercalcemia at comparable glomerular filtration rate (GFR) in volume expanded, anesthetized dogs. Changes in proximal RNawhich might occur during CaCl2infusion, were minimized by infusing acetazolamide (75 mg/kg body wt iv). When ultrafiltrable calcium was increased from 1.12±0.09 to 2.95±0.10 mmol/1, cortical heat production was unchanged, whereas outer medullary heat production fell by 32±4%. RNawas reduced by 32±6%. Bicarbonate reabsorption did not change but calcium reabsorption and potassium excretion increased significantly. The potassium content of cortex and outer medulla increased during hypercalcemia, whereas ouabain, an inhibitor of Na+K+‐ATPase reduces the potassium content. We conclude that hypercalcemia does not inhibit transcellular RNain the diluting segment by a direct effect on the Na+K+‐ATPase or the mitochondria, but by interfering with the coupled NaCI transport across the luminal cell membrane.