Your browser doesn't support javascript.
loading
Regulation of calcium sparks and spontaneous transient outward currents by RyR3 in arterial vascular smooth muscle cells.
Löhn, M; Jessner, W; Fürstenau, M; Wellner, M; Sorrentino, V; Haller, H; Luft, F C; Gollasch, M.
Afiliación
  • Löhn M; HELIOS Klinikum-Berlin, Franz Volhard Clinic and Max Delbrück Center for Molecular Medicine, Medical Faculty of the Charité, Humboldt University Berlin, Germany.
Circ Res ; 89(11): 1051-7, 2001 Nov 23.
Article en En | MEDLINE | ID: mdl-11717163
Intracellular Ca(2+) levels control both contraction and relaxation in vascular smooth muscle cells (VSMCs). Ca(2+)-dependent relaxation is mediated by discretely localized Ca(2+) release events through ryanodine receptor (RyR) channels in the sarcoplasmic reticulum (SR). These local increases in Ca(2+) concentration, termed sparks, stimulate nearby Ca(2+)-activated K(+) (BK) channels causing BK currents (spontaneous transient outward currents or STOCs). STOCs are hyperpolarizing currents that oppose vasoconstriction. Several RyR isoforms are coexpressed in VSMCs; however, their role in Ca(2+) spark generation is unknown. To provide molecular information on RyR cluster function and assembly, we examined Ca(2+) sparks and STOCs in RyR3-deficient freshly isolated myocytes of resistance-sized cerebral arteries from knockout mice and compared them to Ca(2+) sparks in cells from wild-type mice. We used RT-PCR to identify RyR1, RyR2, and RyR3 mRNA in cerebral arteries. Ca(2+) sparks in RyR3-deficient cells were similar in peak amplitude (measured as F/F(0)), width at half-maximal amplitude, and duration compared with wild-type cell Ca(2+) sparks. However, the frequency of STOCs (between -60 mV and -20 mV) was significantly higher in RyR3-deficient cells than in wild-type cells. Ca(2+) sparks and STOCs in both RyR3-deficient and wild-type cells were inhibited by ryanodine (10 micromol/L), external Ca(2+) removal, and depletion of SR Ca(2+) stores by caffeine (1 mmol/L). Isolated, pressurized cerebral arteries of RyR3-deficient mice developed reduced myogenic tone. Our results suggest that RyR3 is part of the SR Ca(2+) spark release unit and plays a specific molecular role in the regulation of STOCs frequency in mouse cerebral artery VSMCs after decreased arterial tone.
Asunto(s)
Buscar en Google
Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Arterias / Calcio / Canal Liberador de Calcio Receptor de Rianodina / Señalización del Calcio / Canales de Potasio Calcio-Activados / Músculo Liso Vascular Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Circ Res Año: 2001 Tipo del documento: Article País de afiliación: Alemania
Buscar en Google
Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Arterias / Calcio / Canal Liberador de Calcio Receptor de Rianodina / Señalización del Calcio / Canales de Potasio Calcio-Activados / Músculo Liso Vascular Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Circ Res Año: 2001 Tipo del documento: Article País de afiliación: Alemania