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Ca 2+ channel‐sarcoplasmic reticulum coupling: a mechanism of arterial myocyte contraction without Ca 2+ influx
Author(s) -
del ValleRodríguez Alberto,
LópezBarneo José,
Ureña Juan
Publication year - 2003
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/cdg432
Subject(s) - ryanodine receptor , endoplasmic reticulum , myocyte , biology , phospholipase c , depolarization , biophysics , contraction (grammar) , cytosol , inositol , calcium signaling , voltage dependent calcium channel , microbiology and biotechnology , phospholipase , calcium , medicine , signal transduction , receptor , endocrinology , biochemistry , enzyme
Contraction of vascular smooth muscle cells (VSMCs) depends on the rise of cytosolic [Ca 2+ ] owing to either Ca 2+ influx through voltage‐gated Ca 2+ channels of the plasmalemma or receptor‐mediated Ca 2+ release from the sarcoplasmic reticulum (SR). We show that voltage‐gated Ca 2+ channels in arterial myocytes mediate fast Ca 2+ release from the SR and contraction without the need of Ca 2+ influx. After sensing membrane depolarization, Ca 2+ channels activate G proteins and the phospholipase C–inositol 1,4,5‐trisphosphate (InsP 3 ) pathway. Ca 2+ released through InsP 3 ‐dependent channels of the SR activates ryanodine receptors to amplify the cytosolic Ca 2+ signal. These observations demonstrate a new mechanism of signaling SR Ca 2+ ‐release channels and reveal an unexpected function of voltage‐gated Ca 2+ channels in arterial myocytes. Our findings may have therapeutic implications as the calcium‐channel‐induced Ca 2+ release from the SR can be suppressed by Ca 2+ ‐ channel antagonists.
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