Ca2+ channel-sarcoplasmic reticulum coupling: a mechanism of arterial myocyte contraction without Ca2+ influx

• Published in: The EMBO journal 2003-09, Vol.22 (17), p.4337-4345
• Main Authors: del Valle-Rodríguez, Alberto, López-Barneo, José, Ureña, Juan
• Format: Article
• Language: English
• Subjects: Animals; arterial myocytes; Ca2+ channels; Calcium channels; Calcium Channels - metabolism; Calcium Signaling; calcium-channel-induced Ca2+ release; EMBO20; EMBO37; GTP-Binding Proteins - metabolism; In Vitro Techniques; Inositol 1,4,5-Trisphosphate - metabolism; inositol trisphosphate; Membrane Potentials; Muscle Contraction - physiology; Muscle, Smooth, Vascular - cytology; Muscle, Smooth, Vascular - physiology; Myocytes, Smooth Muscle - physiology; Rats; Rats, Wistar; Ryanodine Receptor Calcium Release Channel - metabolism; Sarcoplasmic Reticulum - metabolism; Type C Phospholipases - metabolism; voltage sensor
• ISSN: 0261-4189; 1460-2075; 1460-2075
• DOI: 10.1093/emboj/cdg432

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.