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1 Endocrine Research Unit, Department of Medicine, Veterans Affairs Medical Center, University of California, San Francisco, California 04121; 3 Institution of Molecular Pharmacology and Biophysics, University of Cincinnati Medical Center, Cincinnati, Ohio 45267; 2 Division of Clinical Pharmacology, First Department of Internal Medicine, Imre Haynal University of Health, H-1135 Budapest, Hungary
Parathyroid cells express
Ca2+-conducting currents that are activated by raising the
extracellular Ca2+ concentration
([Ca2+]o). We investigated the sensitivity of
these currents to dihydropyridines, the expression of voltage-dependent
Ca2+ channel (VDCC) subunits, and the effects of
dihydropyridines on the intracellular free [Ca2+]
([Ca2+]i) and secretion in these cells.
Dihydropyridine channel antagonists dose dependently suppressed
Ca2+-conducting currents, and agonists partially reversed
the inhibitory effects of the antagonists in these cells. From a bovine
parathyroid cDNA library, we isolated cDNA fragments encoding parts of
an
1S- and a
3-subunit of L-type
Ca2+ channels. The
1S-subunit cDNA from the
parathyroid represents an alternatively spliced variant lacking exon 29 of the corresponding gene. Northern blot analysis and
immunocytochemistry confirmed the presence of transcripts and proteins
for
1- and
3-subunits in the parathyroid
gland. The addition of dihydropyridines had no significant effects on
high [Ca2+]o-induced changes in
[Ca2+]i and parathyroid hormone (PTH)
release. Thus our studies indicate that parathyroid cells express
alternatively spliced L-type Ca2+ channel subunits, which
do not modulate acute intracellular Ca2+ responses or
changes in PTH release.
intracellular Ca2+ mobilization; Ca2+ receptor; Ca2+ sensing
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K. Yokoyama, D. Matsuba, S. Adachi-Akahane, H. Takeyama, I. Tabei, A. Suzuki, T. Shibasaki, R. Iida, I. Ohkido, T. Hosoya, et al. Dihydropyridine- and voltage-sensitive Ca2+ entry in human parathyroid cells Exp Physiol, July 1, 2009; 94(7): 847 - 855. [Abstract] [Full Text] [PDF] |
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