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Vitamin D and parotid gland function in the rat

This thesis examines the hypothesis that the parotid gland is a target organ for vitamin D. Employing methods previously used to characterize 1,25-dihydroxyvitamin D$ sb{ rm 3}$ (1,25(OH)$ sb{ rm 2}$D$ sb{ rm 3}$) receptors in established target tissues, classical receptors for this sterol were demonstrated in acinar cells of normal rat parotid gland. Submandibular gland, lacrimal gland and pancreatic acinar cells did not contain 1,25(OH)$ sb{ rm 2}$D$ sb{ rm 3}$ receptors. Vitamin D deprivation caused a decrease in the rate of production of pilocarpine-stimulated and auriculotemporal nerve-stimulated parotid saliva, which persisted when serum concentrations of calcium, parathyroid hormone and 1,25(OH)$ sb{ rm 2}$D$ sb{ rm 3}$ were maintained within normal limits, yet was reversed by treatment with vitamin D$ sb{ rm 3}$ (D$ sb{ rm 3}$). The concentration of calcium in pilocarpine-stimulated saliva did not correlate with decreased salivary flow, but appeared to vary with changes in the serum concentration of this ion. Amylase secretion and calcium release by exocytosis were normal in vitamin D-deprived rats. These findings suggested that fluid secretion but not protein secretion by parotid gland was vitamin D dependent, but that 1,25(OH)$ sb{ rm 2}$D$ sb{ rm 3}$ was not the active metabolite for this effect. Examination of the relative abilities of D$ sb{ rm 3}$, 25-hydroxyvitamin D$ sb{ rm 3}$ (25OHD$ sb{ rm 3}$), 24,25-dihydroxyvitamin D$ sb3$ (24,25(OH)$ sb{ rm 2}$D$ sb{ rm 3}$) and 1,25(OH)$ sb{ rm 2}$D$ sb{ rm 3}$ to correct abnormal parotid function in vitamin D-deprived rats revealed that 24,25(OH)$ sb{ rm 2}$D$ sb{ rm 3}$ was the active metabolite, and essential for normal water and electrolyte secretion by parotid gland. Carbachol-stimulated potassium efflux from parotid glands from vitamin D-deprived rats was normal, suggesting that the site of action of 24,25(OH)$ sb{ rm 2}$D$ sb{ rm 3}$ was later in the sequence of fluid secretion. Sucrose density grad

Identiferoai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.75930
Date January 1988
CreatorsPeterfy, Charles G.
PublisherMcGill University
Source SetsLibrary and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada
LanguageEnglish
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation
Formatapplication/pdf
CoverageDoctor of Philosophy (Department of Pharmacology and Therapeutics.)
RightsAll items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated.
Relationalephsysno: 000911100, proquestno: AAINL52334, Theses scanned by UMI/ProQuest.

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