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Research Article Free access | 10.1172/JCI106379

Evidence for suppression of parathyroid gland activity by hypermagnesemia

Shaul G. Massry, Jack W. Coburn, and Charles R. Kleeman

Cedars-Sinai Medical Research Institute, Los Angeles, California 90048

Department of Medicine, Cedars-Sinai Medical Center, Veterans Administration Center, Los Angeles, California 90048

Department of Medicine, University of California at Los Angeles School of Medicine, Los Angeles, California 90048

Find articles by Massry, S. in: PubMed | Google Scholar

Cedars-Sinai Medical Research Institute, Los Angeles, California 90048

Department of Medicine, Cedars-Sinai Medical Center, Veterans Administration Center, Los Angeles, California 90048

Department of Medicine, University of California at Los Angeles School of Medicine, Los Angeles, California 90048

Find articles by Coburn, J. in: PubMed | Google Scholar

Cedars-Sinai Medical Research Institute, Los Angeles, California 90048

Department of Medicine, Cedars-Sinai Medical Center, Veterans Administration Center, Los Angeles, California 90048

Department of Medicine, University of California at Los Angeles School of Medicine, Los Angeles, California 90048

Find articles by Kleeman, C. in: PubMed | Google Scholar

Published September 1, 1970 - More info

Published in Volume 49, Issue 9 on September 1, 1970
J Clin Invest. 1970;49(9):1619–1629. https://doi.org/10.1172/JCI106379.
© 1970 The American Society for Clinical Investigation
Published September 1, 1970 - Version history
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Abstract

The effect of hypermagnesemia, produced by MgCl2 infusion, on the activity of parathyroid glands, as assessed by changes in levels of serum calcium (SCa) and in the fraction of filtered phosphate excreted (CP/CCr), was studied in 11 intact and 4 thyroparathyroidectomized (T-PTX) dogs. To exclude the effect of diurnal variation in CP/CCr on the results, studies were initiated in both morning and afternoon hours and each study with MgCl2 infusion was paired with a control experiment in the same dog not receiving MgCl2. During MgCl2 infusion, serum phosphorus rose progressively. Despite this rise, the levels of CP/CCr fell in all experiments and were significantly different from values observed at the same time of the day in the paired control experiments. The concentrations of total SCa fell by 1.0-2.4 mg/100 ml with a proportional decrease in the levels of the diffusible and ionized fractions. The pattern of the fall in CP/CCr during MgCl2 resembled that observed after CaCl2 infusion (seven dogs) and that which acutely followed thyroparathyroidectomy (seven dogs). When parathyroid extract was given to dogs receiving MgCl2 infusion both CP/CCr and SCa rose, and MgCl2 infusion did not affect CP/CCr and SCa in T-PTX dogs. These results indicate that hypermagnesemia suppresses the activity of the parathyroid glands, probably, by inhibiting production and (or) release of the hormone, without interfering with end-organ response. An increase in serum magnesium of 1.7-2.0 mg/100 ml was capable of producing the suppressive effect. Evaluation of the effect of simultaneous modest hypocalcemia and hypermagnesemia suggests that a decrease in the level of serum calcium is more potent than an increase in the concentration of serum magnesium in the regulation of parathyroid activity.

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