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Activation of a Non‐Selective Cation Channel by Store‐Operated and Receptor‐Mediated Elevation of [Ca 2+ ] i in Rat Carotid Body Glomus Cells
Author(s) -
Kim Donghee,
Wang Jiaju,
Hogan James O
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.984.1
Subject(s) - thapsigargin , chemistry , glomus cell , biophysics , muscarine , depolarization , receptor , endocrinology , medicine , extracellular , biochemistry , chemoreceptor , biology , muscarinic acetylcholine receptor
Our recent studies show that a non‐selective cation channel (NSC) is highly expressed in rat glomus cells. An increase in Ca 2+ influx via the voltage‐dependent Ca 2+ channel (VDCC) caused by depolarizing stimuli such as hypoxia, low pH o and high [KCl] o activated NSC. The effect of [Ca 2+ ] i rise by mechanisms other than via VDCC on NSC activity is not yet known. Here we studied the role of store‐operated Ca 2+ entry (SOCE) and receptor‐mediated [Ca 2+ ] i rise on NSC activity. Patch‐clamp single channel recording and fura‐2 fluorescence signal were used. SOCE was produced by incubating cells in Ca 2+ ‐free solution containing 1 uM thapsigargin and then adding Ca 2+ back to the solution. The rapid rise in [Ca 2+ ] i associated with SOCE caused a strong activation of NSC. Receptor‐mediated [Ca 2+ ] i rise was produced using Angiotensin II (100 nM) and muscarine (10 uM), which stimulate the Gq‐PLC pathway and elevates [Ca 2+ ] i in glomus cells. Both Ang II and muscarine produced a significant activation of NSC. Caffeine that causes release of Ca 2+ from the endoplasimc reticulum also elevated [Ca 2+ ] i and activated NSC. GABA, dopamine, endothelin‐1, 5‐HT did not elevate [Ca 2+ ] i and did not activate NSC. Adenosine produced a weak elevation of [Ca 2+ ] i but did not activate NSC. Our results indicate that a stimulus that produces an increase in [Ca 2+ ] i , regardless of which signaling pathway (VDCC, SOCE and receptor‐mediated) is used, can activate NSC to help depolarize glomus cells. Support or Funding Information Supported by NIH grant