Ito K, Takakura S, Sato K, Sutko J L
Circ Res. 1986 May;58(5):730-4. doi: 10.1161/01.res.58.5.730.
We have examined the effects of ryanodine, an inhibitor of the release of sarcoplasmic reticulum calcium in cardiac muscle, on contractile tension and calcium-45 movement in aortic smooth muscle of guinea pigs to learn whether this agent also modifies the release of stored calcium in vascular smooth muscle. Ryanodine (3-100 microM) suppressed the phasic contractions induced by caffeine and norepinephrine in calcium-free medium and prevented the stimulation of calcium-45 efflux by these agonists. Ryanodine did not significantly alter either the contractile response or the increased cellular influx of calcium-45 caused by high potassium in more than 1 mM calcium, suggesting that this agent does not affect depolarization-induced calcium entry into the cells. In a calcium-free, high potassium solution, the addition of calcium at concentrations of 1 mM and less resulted in a contraction which appeared to depend largely on the release of calcium from intracellular stores. This contraction was blocked by ryanodine. These data are consistent with the hypothesis that ryanodine causes a diminished release of calcium from the intracellular store in vascular smooth muscle, as it does in cardiac muscle. Moreover, our results indicate that a calcium-induced calcium release may exist in smooth muscle, and that this release is antagonized by ryanodine.
我们研究了雷诺丁(一种心肌肌浆网钙释放抑制剂)对豚鼠主动脉平滑肌收缩张力和钙-45移动的影响,以了解该药物是否也会改变血管平滑肌中储存钙的释放。雷诺丁(3 - 100微摩尔)抑制了无钙培养基中咖啡因和去甲肾上腺素诱导的相性收缩,并阻止了这些激动剂对钙-45外流的刺激。在钙浓度超过1毫摩尔时,雷诺丁对高钾引起的收缩反应或细胞内钙-45流入增加均无显著影响,这表明该药物不影响去极化诱导的钙进入细胞。在无钙的高钾溶液中,添加浓度为1毫摩尔及更低的钙会导致收缩,这种收缩似乎很大程度上依赖于细胞内储存钙的释放。这种收缩被雷诺丁阻断。这些数据与以下假设一致:雷诺丁会减少血管平滑肌细胞内储存钙的释放,就像它在心肌中所起的作用一样。此外,我们的结果表明,平滑肌中可能存在钙诱导的钙释放,并且这种释放会被雷诺丁拮抗。