Expression of the na-cl cotransporter in osteoblast-like cells: effects of thiazide diuretics. Barry, Elizabeth L. R., Frank A. Gesek, Mark R. Kaplan, Steven C. Hebert, and Peter A. Friedman. Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, New Hampshire 03755; and Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115
APStracts 3:0264C, 1996.
The use of thiazide diuretics is associated with increased bone mineral density and, in some studies, with reduced incidence of fractures suggesting a potential role for these drugs in the treatment of osteoporosis. Our objective was to examine the effects of thiazides on osteoblast-like cells using the rat UMR-106 osteosarcoma cell line. Treatment of UMR-106 cells with chlorothiazide caused membrane depolarization and a rise of intracellular calcium ([Ca2+]i), but had no effect on cAMP accumulation. The rise of [Ca2+]i was partially inhibited by nifedipine and removal of extracellular calcium, indicating calcium uptake from the extracellular media, as well as by thapsigargin or dantrolene, indicating contributions from calcium release from intracellular stores. Reverse transcriptase-PCR was used to isolate a partial cDNA clone for the thiazide-sensitive sodium-chloride cotransporter from UMR-106 cells that hybridized to 5.0 and 11.0 kB mRNAs upon Northern blot analysis. Antisense oligonucleotides to the sodium-chloride cotransporter specifically inhibited the chlorothiazide-induced depolarization and rise of [Ca2+]i, and reduced immunofluorescence staining for the sodium-chloride cotransporter protein in UMR-106 cells. We conclude that thiazide diuretics inhibit sodium-chloride cotransporter activity in UMR-106 cells thereby altering intracellular calcium regulation. These results provide evidence for direct effects of thiazide diuretics on bone cells.

Received 11 April 1996; accepted in final form 24 July 1996.
APS Manuscript Number C200-6.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 21 August 1996