1. Ca2+ channel-sarcoplasmic reticulum coupling: a mechanism of arterial myocyte contraction without Ca2+ influx.
- Author
-
del Valle-Rodríguez A, López-Barneo J, and Ureña J
- Subjects
- Animals, Calcium Signaling, GTP-Binding Proteins metabolism, In Vitro Techniques, Inositol 1,4,5-Trisphosphate metabolism, Membrane Potentials, Muscle Contraction physiology, Muscle, Smooth, Vascular cytology, Muscle, Smooth, Vascular physiology, Rats, Rats, Wistar, Ryanodine Receptor Calcium Release Channel metabolism, Type C Phospholipases metabolism, Calcium Channels metabolism, Myocytes, Smooth Muscle physiology, Sarcoplasmic Reticulum metabolism
- Abstract
Contraction of vascular smooth muscle cells (VSMCs) depends on the rise of cytosolic [Ca2+] owing to either Ca2+ influx through voltage-gated Ca2+ channels of the plasmalemma or receptor-mediated Ca2+ release from the sarcoplasmic reticulum (SR). We show that voltage-gated Ca2+ channels in arterial myocytes mediate fast Ca2+ release from the SR and contraction without the need of Ca2+ influx. After sensing membrane depolarization, Ca2+ channels activate G proteins and the phospholipase C-inositol 1,4,5-trisphosphate (InsP3) pathway. Ca2+ released through InsP3-dependent channels of the SR activates ryanodine receptors to amplify the cytosolic Ca2+ signal. These observations demonstrate a new mechanism of signaling SR Ca(2+)-release channels and reveal an unexpected function of voltage-gated Ca2+ channels in arterial myocytes. Our findings may have therapeutic implications as the calcium-channel-induced Ca2+ release from the SR can be suppressed by Ca(2+)-channel antagonists.
- Published
- 2003
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