1,25(OH)2-vitamin D3 reduces spontaneous and hypocalcemia-stimulated pulsatile component of parathyroid hormone secretion

Claus P. Schmitt, Franz Schaefer, Daniela Huber, Ingrid Zahn, Johannes D Veldhuis, Eberhard Ritz, Otto Mehls

Research output: Contribution to journalArticle

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Abstract

To investigate the effects of 1,25(OH)2-vitamin D3 (1,25(OH)2D3) on pulsatile parathyroid hormone (PTH) release, minute-to-minute intact PTH secretion was examined in nine healthy adults under baseline conditions and during hypocalcemia (sodium citrate clamp) before and after 5 d of oral 1,25(OH)2D3 treatment (1 μg/d). In addition, acute effects of 1,25(OH)2D3 were examined by a single intravenous bolus of 2 μg of 1,25(OH)2D3. Pulsatile and tonic PTH secretion rates were calculated by the multiparameter deconvolution technique. During baseline, 68% of circulating PTH was attributable to tonic, and 32% to pulsatile, secretion. During induction of hypocalcemia, a selective increase in pulsatile secretion (+1100%), mediated by a combined increase in burst frequency and burst mass, was observed. During the subsequent steady-state hypocalcemic period, burst frequency and mass decreased and tonic secretion increased to 3 times the baseline level. Intravenous 1,25(OH)2D3 did not affect the temporal pattern of PTH secretion. In contrast, oral 1,25(OH)2D3 decreased baseline plasma PTH by 30% without a detectable change in Ca2+. This suppression was accounted for mainly by a decrease in PTH burst frequency. During hypocalcemia induction, a significantly lower (30%) increase in burst mass occurred compared with the pretreatment study. During steady-state hypocalcemia, PTH burst mass (-45%) and pulsatile (-50%) and total (-35%) secretion rate were lower than before treatment. In conclusion, acute hypocalcemia selectively increases pulsatile PTH release by stimulating both burst frequency and mass via a Ca2+ rate-sensitive mechanism. Oral 1,25- (OH)2D3 suppresses pulsatile baseline PTH release and reduces the pulsatile secretory capacity of the parathyroids during a hypocalcemic stimulus.

Original languageEnglish (US)
Pages (from-to)54-62
Number of pages9
JournalJournal of the American Society of Nephrology
Volume9
Issue number1
StatePublished - Jan 1998
Externally publishedYes

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Hypocalcemia
Cholecalciferol
Parathyroid Hormone

ASJC Scopus subject areas

  • Nephrology

Cite this

Schmitt, C. P., Schaefer, F., Huber, D., Zahn, I., Veldhuis, J. D., Ritz, E., & Mehls, O. (1998). 1,25(OH)2-vitamin D3 reduces spontaneous and hypocalcemia-stimulated pulsatile component of parathyroid hormone secretion. Journal of the American Society of Nephrology, 9(1), 54-62.

1,25(OH)2-vitamin D3 reduces spontaneous and hypocalcemia-stimulated pulsatile component of parathyroid hormone secretion. / Schmitt, Claus P.; Schaefer, Franz; Huber, Daniela; Zahn, Ingrid; Veldhuis, Johannes D; Ritz, Eberhard; Mehls, Otto.

In: Journal of the American Society of Nephrology, Vol. 9, No. 1, 01.1998, p. 54-62.

Research output: Contribution to journalArticle

Schmitt, CP, Schaefer, F, Huber, D, Zahn, I, Veldhuis, JD, Ritz, E & Mehls, O 1998, '1,25(OH)2-vitamin D3 reduces spontaneous and hypocalcemia-stimulated pulsatile component of parathyroid hormone secretion', Journal of the American Society of Nephrology, vol. 9, no. 1, pp. 54-62.
Schmitt, Claus P. ; Schaefer, Franz ; Huber, Daniela ; Zahn, Ingrid ; Veldhuis, Johannes D ; Ritz, Eberhard ; Mehls, Otto. / 1,25(OH)2-vitamin D3 reduces spontaneous and hypocalcemia-stimulated pulsatile component of parathyroid hormone secretion. In: Journal of the American Society of Nephrology. 1998 ; Vol. 9, No. 1. pp. 54-62.
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abstract = "To investigate the effects of 1,25(OH)2-vitamin D3 (1,25(OH)2D3) on pulsatile parathyroid hormone (PTH) release, minute-to-minute intact PTH secretion was examined in nine healthy adults under baseline conditions and during hypocalcemia (sodium citrate clamp) before and after 5 d of oral 1,25(OH)2D3 treatment (1 μg/d). In addition, acute effects of 1,25(OH)2D3 were examined by a single intravenous bolus of 2 μg of 1,25(OH)2D3. Pulsatile and tonic PTH secretion rates were calculated by the multiparameter deconvolution technique. During baseline, 68{\%} of circulating PTH was attributable to tonic, and 32{\%} to pulsatile, secretion. During induction of hypocalcemia, a selective increase in pulsatile secretion (+1100{\%}), mediated by a combined increase in burst frequency and burst mass, was observed. During the subsequent steady-state hypocalcemic period, burst frequency and mass decreased and tonic secretion increased to 3 times the baseline level. Intravenous 1,25(OH)2D3 did not affect the temporal pattern of PTH secretion. In contrast, oral 1,25(OH)2D3 decreased baseline plasma PTH by 30{\%} without a detectable change in Ca2+. This suppression was accounted for mainly by a decrease in PTH burst frequency. During hypocalcemia induction, a significantly lower (30{\%}) increase in burst mass occurred compared with the pretreatment study. During steady-state hypocalcemia, PTH burst mass (-45{\%}) and pulsatile (-50{\%}) and total (-35{\%}) secretion rate were lower than before treatment. In conclusion, acute hypocalcemia selectively increases pulsatile PTH release by stimulating both burst frequency and mass via a Ca2+ rate-sensitive mechanism. Oral 1,25- (OH)2D3 suppresses pulsatile baseline PTH release and reduces the pulsatile secretory capacity of the parathyroids during a hypocalcemic stimulus.",
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