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Dihydropyridine‐ and voltage‐sensitive Ca 2+ entry in human parathyroid cells
Author(s) -
Yokoyama Keitaro,
Matsuba Douchi,
AdachiAkahane Satomi,
Takeyama Hiroshi,
Tabei Isao,
Suzuki Akifumi,
Shibasaki Toshiaki,
Iida Rinako,
Ohkido Ichiro,
Hosoya Tatsuo,
Suda Norio
Publication year - 2009
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2009.046813
Subject(s) - extracellular , chemistry , dihydropyridine , parathyroid chief cell , parathyroid hormone , biophysics , calcium , endocrinology , patch clamp , medicine , voltage dependent calcium channel , agonist , receptor , biochemistry , biology , organic chemistry
Patch‐clamp and fluorescence measurements of cytoplasmic Ca 2+ concentration ([Ca 2+ ] i ) were performed to directly detect extracellular Ca 2+ entry into cultured parathyroid cells from patients with secondary hyperparathyroidism. Cells loaded with fluo‐3 AM or fluo‐4 AM showed a transient increase in fluorescence (Ca 2+ transient) following 10 s exposure to 150 m m K + solution in the presence of millimolar concentrations of external Ca 2+ . The Ca 2+ transient was completely inactivated after 30–40 s exposure to the high‐K + solution, was reduced by dihydropyridine antagonists and was enhanced by FPL‐64176, an L‐type Ca 2+ channel agonist. The electrophysiological and pharmacological properties of the whole‐cell Ca 2+ and Ba 2+ currents were similar to those of L‐type Ca 2+ channels. The Ca 2+ transients induced by 10 s exposure to 3.0 m m extracellular Ca 2+ concentration ([Ca 2+ ] o ) were inhibited by dihydropyridine antagonists and were partly inactivated following 30–40 s exposure to the high‐K + solution. These results demonstrate, for the first time, that human parathyroid cells express L‐type‐like Ca 2+ channels that are possibly involved in the [Ca 2+ ] o ‐induced change in [Ca 2+ ] i . This Ca 2+ entry system might provide a compensatory pathway for the negative feedback regulation of parathyroid hormone secretion, especially in hyperplastic conditions in which the Ca 2+ ‐sensing receptor is poorly expressed.