Kannan M S, Fenton A M, Prakash Y S, Sieck G C
Department of Veterinary Pathobiology, University of Minnesota, St. Paul 55108, USA.
Am J Physiol. 1996 Feb;270(2 Pt 2):H801-6. doi: 10.1152/ajpheart.1996.270.2.H801.
Cyclic ADP-ribose (cADPR) was shown to induce calcium release from the endoplasmic reticulum via ryanodine-sensitive pathways. In smooth muscle, two pathways for calcium release from the sarcoplasmic reticulum (SR) have been previously demonstrated: D-myo-inositol 1, 4, 5-trisphosphate-gated and ryanodine-gated. However, evidence for cADPR as a regulator for SR Ca2+ release in smooth muscle is lacking. We used permeabilized porcine coronary artery smooth muscle cells to directly examine the stimulation of SR Ca2+ release by cADPR. The results provide direct evidence that cADPR stimulates SR Ca2+ release and that this response is not inhibited by heparin, by depletion of the caffeine-sensitive Ca2+ pool, or by blockade or ryanodine receptors. These results indicate a novel mechanism for Ca2+ release from the SR of vascular smooth muscle.
环磷酸腺苷核糖（cADPR）已被证明可通过对ryanodine敏感的途径诱导内质网释放钙。在平滑肌中，先前已证明存在两种从肌浆网（SR）释放钙的途径：D-肌醇1,4,5-三磷酸门控途径和ryanodine门控途径。然而，缺乏cADPR作为平滑肌中SR钙释放调节剂的证据。我们使用透化的猪冠状动脉平滑肌细胞直接检测cADPR对SR钙释放的刺激作用。结果提供了直接证据，表明cADPR刺激SR钙释放，并且这种反应不受肝素、咖啡因敏感钙库耗竭、ryanodine受体阻断的抑制。这些结果表明了血管平滑肌SR钙释放的一种新机制。
