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Hypoxia inhibits the recombinant alpha 1C subunit of the human cardiac L‐type Ca2+ channel.
Author(s) -
Fearon I M,
Palmer A C,
Balmforth A J,
Ball S G,
Mikala G,
Schwartz A,
Peers C
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1997.sp022041
Subject(s) - patch clamp , recombinant dna , biophysics , hek 293 cells , protein subunit , hypoxia (environmental) , chemistry , membrane potential , l type calcium channel , g alpha subunit , electrophysiology , microbiology and biotechnology , myocyte , voltage dependent calcium channel , biology , receptor , calcium , biochemistry , neuroscience , oxygen , gene , organic chemistry
1. Whole‐cell patch clamp recordings were used to investigate the effects of hypoxia on recombinant human L‐type Ca2+ channel alpha 1C subunits stably expressed in human embryonic kidney (HEK 293) cells. 2. Ca2+ channel currents were reversibly inhibited by hypoxia (PO2 < 90 mmHg). The degree of inhibition depended on the charge carrier used, Ca2+ currents being more O2 sensitive than Ba2+ currents. 3. Hypoxic inhibition of Ca2+ channel currents was more pronounced at lower activating membrane potentials (< or = +30 mV), and was associated with a slowing of activation kinetics. Current inactivation and deactivation were unaffected by hypoxia. 4. Since hypoxia similarly regulates native L‐type Ca2+ channels in vascular smooth muscle cells, our results suggest that hypoxic regulation of L‐type Ca2+ channels arises from modification of structural features of the alpha 1 subunit common to cardiac and smooth muscle L‐type channels.
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