title: 1,25(OH)2-vitamin D3 reduces spontaneous and hypocalcemia-stimulated pulsatile component of parathyroid hormone secretion.
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.affiliation: Department of Pediatrics, University of Heidelberg, Germany.
authors.forename: C P
authors.initials: CP
authors.lastname: Schmitt
authors.forename: F
authors.initials: F
authors.lastname: Schaefer
authors.forename: D
authors.initials: D
authors.lastname: Huber
authors.forename: I
authors.initials: I
authors.lastname: Zahn
authors.forename: J D
authors.initials: JD
authors.lastname: Veldhuis
authors.forename: E
authors.initials: E
authors.lastname: Ritz
authors.forename: O
authors.initials: O
authors.lastname: Mehls
mesh_terms: D000284:Administration, Oral; D000328:Adult; D002117:Calcitriol / Q000494:pharmacology*; D005260:Female; D006801:Humans; D006996:Hypocalcemia / Q000378:metabolism*; D007275:Injections, Intravenous; D008297:Male; D010281:Parathyroid Hormone / Q000097:blood / Q000378:metabolism*; D011673:Pulsatile Flow / Q000187:drug effects
chemical_list: D010281:Parathyroid Hormone; D002117:Calcitriol