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

被引:170
作者
Brown, AJ [1 ]
Zhong, M [1 ]
Finch, J [1 ]
Ritter, C [1 ]
McCracken, R [1 ]
Morrissey, J [1 ]
Slatopolsky, E [1 ]
机构
[1] WASHINGTON UNIV, DEPT MED, ST LOUIS, MO 63110 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY | 1996年 / 270卷 / 03期
关键词
calcium set point; hyperparathyroidism; vitamin D deficiency; calcitriol therapy;
D O I
10.1152/ajprenal.1996.270.3.F454
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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 D-3 [1,25-(OH)(2)D-3]. 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 mRNA was 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)(2)D-3 produced a dose-dependent increase in PTG CaR mRNA. Treatment of +D rats with 100 ng of 1,25-(OH)(2)D-3 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)(2)D-3 administration but returned to normal by 24 h. This upregulation of CaR expression by 1,25-(OH)(2)D-3 may be involved in the suppressive effects of vitamin D compounds on PTH secretion.
引用
收藏
页码:F454 / F460
页数:7
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