Tissue distribution of electrolytes, Ca47, and Mg28 in acute hypercalcemia

Abstract

The in vivo effects of acute hypercalcemia on plasma and tissue distribution of electrolytes, radiocalcium, and radiomagnesium were studied in acutely renal-ligated dogs. Hypercalcemia abruptly increased plasma potassium and phosphorus concentrations but had no significant effect on plasma concentrations of other electrolytes. Skeletal muscle and myocardial sodium decreased 15%, skeletal muscle chloride decreased 22%, and pancreatic and aortic potassium increased 12%. Tissue phosphorus concentrations were unchanged. Total cellular calcium increased 40–70% in liver, myocardium, nerve, and aorta, was suggestively increased in skeletal muscle, and was unchanged in pancreas, brain, and bone. Exchangeable cellular calcium increased 35–75% in liver, skeletal muscle, myocardium, nerve, and aorta and was unchanged in pancreas and brain. Bone exchangeable calcium increased 260%. Exchangeable cellular magnesium of skeletal muscle and pancreas decreased 28% but total cellular magnesium concentrations were unaltered. The changes noted in individual tissues were reflected by 50% increases in exchanged able body and over-all tissue calcium pools and in unchanged exchangeable body and over-all tissue magnesium pools. No significant changes in fractional rates of calcium and magnesium turnover occurred. These data indicate that hypercalcemia causes 1) cellular accumulation of calcium by many but not all tissues, 2) inhibition of magnesium uptake by certain cells, and 3) changes in tissue sodium and potassium distribution which are compatible with known in vitro inhibitory effects of calcium on cellular electrolyte transport.