Rat calcium-sensing receptor is regulated by vitamin D but not by calcium

A. J. Brown, M. Zhong, J. Finch, C. Ritter, R. McCracken, J. Morrissey, E. Slatopolsky

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216 Scopus citations

Abstract

Parathyroid hormone (PTH) secretion is regulated by extracellular calcium acting through a cell surface calcium receptor (CaR). We have examined the potential regulation of the CaR in the parathyroid glands (PTG) and kidney by calcium and 1,25-dihydroxyvitamin D3 [1,25-(OH2D3]. Rats fed vitamin D-deficient ( -D) diets containing 0.02, 0.4, or 2.0% Ca had a wide range of serum ionized Ca (2.5-5.2 mg/dl) and PTH (22-590 pg/ml) concentrations. PTG CaR mRNA did not vary significantly with ionized calcium or PTH, indicating that hypocalcemia and hyperparathyroidism may not alter CaR expression. However, PTG CaR mRNAwas 40% lower in the -D rats than in age-matched rats fed a vitamin D-replete (+D) diet (P < 0.002). Repletion of -D rats with 1,25-(OH)2D3 produced a dose-dependent increase in PTG CaR mRNA. Treatment of +D rats with 100 ng of 1,25-(OH)2D3 increased CaR mRNA by 33% (P < 0.05) and 54% (P < 0.002) in the PTG and by 89% (P < 0.02) and 91% (P < 0.02) in the kidney in two independent experiments. PTG CaR peaked at 16 h (150% of control, P 0.05) after 1,25-(OH)2D3 administration but returned to normal by 24 h. This upregulation of CaR expression by 1,25-(OH)2D3 may be involved in the suppressive effects of vitamin D compounds on PTH secretion.

Original languageEnglish
Pages (from-to)F454-F460
JournalAmerican Journal of Physiology
Volume270
Issue number3 PART 2
DOIs
StatePublished - 1996

Keywords

  • Calcitriol therapy
  • Calcium set point
  • Hyperparathyroidism
  • Vitamin D deficiency

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