Benevolensky D S, Menshikova E V, Watras J, Levitsky D O, Ritov V B
USSR Cardiology Research Center, Academy of Medical Sciences, Moscow.
Biomed Biochim Acta. 1987;46(8-9):S393-8.
The effects of Ca2+ and inositol-1,4,5-trisphosphate (IP3) as putative inducers of Ca2+ release from sarcoplasmic reticulum (SR) vesicles were studied. Addition of Ca2+ (5-50 microM) or caffeine (5 mM) to calcium loaded SR vesicles from canine ventricular myocardium caused immediate release of Ca2+; whereas, no such Ca2+ release was observed in canine aortic SR vesicles. Fractionation of the cardiac SR by zonal centrifugation of calcium/oxalate-loaded SR vesicles showed that Ca2+-induced Ca2+ release was present in a caffeine-sensitive, ryanodine-sensitive, calsequestrin-enriched fraction, probably derived from the junctional SR. By contrast, IP3 (greater than 0.1 microM) stimulated Ca2+ release from aortic SR, but had no such effect on cardiac SR (even with 50 microM IP3. These data indicate a difference in Ca2+ release mechanisms in SR from the heart and vascular smooth muscle.
研究了Ca2+和肌醇-1,4,5-三磷酸（IP3）作为肌浆网（SR）囊泡中Ca2+释放的假定诱导剂的作用。向犬心室心肌的钙负载SR囊泡中添加Ca2+（5-50微摩尔）或咖啡因（5毫摩尔）会导致Ca2+立即释放；然而，在犬主动脉SR囊泡中未观察到这种Ca2+释放。通过对钙/草酸盐负载的SR囊泡进行区带离心对心脏SR进行分级分离表明，Ca2+诱导的Ca2+释放在一个对咖啡因敏感、对ryanodine敏感、富含钙结合蛋白的级分中存在，该级分可能来自连接SR。相比之下，IP3（大于0.1微摩尔）刺激主动脉SR释放Ca2+，但对心脏SR没有这种作用（即使使用50微摩尔IP3）。这些数据表明心脏和血管平滑肌SR中Ca2+释放机制存在差异。
