Tissue Distribution of Electrolytes,47Ca and28Mg in Experimental Hyper- and Hypoparathyroidism
- 1 January 1966
- journal article
- research article
- Published by The Endocrine Society in Endocrinology
- Vol. 78 (1) , 16-28
- https://doi.org/10.1210/endo-78-1-16
Abstract
The effects of experimental hyper- and hypoparathyroidism on plasma and tissue distribution of electrolytes and tissue exchangeability with Ca47 and Mg28 were studied in dogs following acute renal pedicle ligation. In hyperparathyroidlsm, plasma concentrations of Mg and inorganic phosphorus as well as Ca were increased. A greater accumulation of Ca occurred in some tissues and a lesser accumulation in others than in acute hyper-calcemia of comparable severity and the fractional rate of exchange of tissue Ca was 30% more rapid than in control and acute hyper-calcemic dogs. Bone exchange of Ca was not significantly increased. Cell Mg concentrations were not appreciably altered by hyperpara-thyroidism except for a significant 9% decrease in myocardium, but the fractional rate of exchange of tissue Mg was increased. Acid-soluble phosphorus concentrations were decreased in 3 tissues and Na and Cl concentrations were decreased by 10 to 25% in 4 tissues. In hypoparathyroidism, in addition to a decreased plasma Ca, the increment in plasma inorganic phosphorus that usually occurs after renal pedicle ligation was 75% less than in control dogs. Cell Ca concentration were decreased by 10 to 40% but the fractional rate of exchange of tissue Ca was unaltered. Although cell Mg concentrations were unaltered, a 40% increase occurred in the exchangeability of skeletal muscle Mg. Tissue Na and Cl concentrations were decreased by 20% in 2 tissues. It has been previously reported that hypercalcemia increases cell Ca concentrations by raising the extracellular calcium concentration gradient. Evidence has also been presented that hypercalcemia directly inhibits cell influx of Mg and Na and cell efflux of K. With altered parathyroid activity, 2 types of effects are observed: those which are dependent upon an abnormal extracellular calcium concentration and those which appear to be due to intrinsic effects of parathormone on cell cation transport. The present data are compatible with the hypotheses that parathormone stimulates bidirectional transport of cell Ca and phosphorus, stimulates cell influx of Mg and opposes the effects of hypercalcemia on cell transport of univalent ions.This publication has 26 references indexed in Scilit:
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