Tags

Type your tag names separated by a space and hit enter

1,25(OH)2-vitamin D3 reduces spontaneous and hypocalcemia-stimulated pulsatile component of parathyroid hormone secretion.
J Am Soc Nephrol. 1998 Jan; 9(1):54-62.JA

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 microgram/d). In addition, acute effects of 1,25(OH)2D3 were examined by a single intravenous bolus of 2 micrograms 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.

Authors+Show Affiliations

Department of Pediatrics, University of Heidelberg, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9440087

Citation

Schmitt, C P., et al. "1,25(OH)2-vitamin D3 Reduces Spontaneous and Hypocalcemia-stimulated Pulsatile Component of Parathyroid Hormone Secretion." Journal of the American Society of Nephrology : JASN, vol. 9, no. 1, 1998, pp. 54-62.
Schmitt CP, Schaefer F, Huber D, et al. 1,25(OH)2-vitamin D3 reduces spontaneous and hypocalcemia-stimulated pulsatile component of parathyroid hormone secretion. J Am Soc Nephrol. 1998;9(1):54-62.
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 : JASN, 9(1), 54-62.
Schmitt CP, et al. 1,25(OH)2-vitamin D3 Reduces Spontaneous and Hypocalcemia-stimulated Pulsatile Component of Parathyroid Hormone Secretion. J Am Soc Nephrol. 1998;9(1):54-62. PubMed PMID: 9440087.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 1,25(OH)2-vitamin D3 reduces spontaneous and hypocalcemia-stimulated pulsatile component of parathyroid hormone secretion. AU - Schmitt,C P, AU - Schaefer,F, AU - Huber,D, AU - Zahn,I, AU - Veldhuis,J D, AU - Ritz,E, AU - Mehls,O, PY - 1998/1/24/pubmed PY - 1998/1/24/medline PY - 1998/1/24/entrez SP - 54 EP - 62 JF - Journal of the American Society of Nephrology : JASN JO - J. Am. Soc. Nephrol. VL - 9 IS - 1 N2 - 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 microgram/d). In addition, acute effects of 1,25(OH)2D3 were examined by a single intravenous bolus of 2 micrograms 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. SN - 1046-6673 UR - https://www.unboundmedicine.com/medline/citation/9440087/125_OH_2_vitamin_D3_reduces_spontaneous_and_hypocalcemia_stimulated_pulsatile_component_of_parathyroid_hormone_secretion_ L2 - http://jasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=9440087 DB - PRIME DP - Unbound Medicine ER -