Hwang K S, van Breemen C
Pflugers Arch. 1987 Apr;408(4):343-50. doi: 10.1007/BF00581127.
The effects of ryanodine on isometric tension development, net cellular Ca content and 45Ca efflux were measured in the isolated rabbit aorta. Pretreatment of the tissue with 10 microM ryanodine for 30 min reduced the norepinephrine (NE)-induced tension of the aortic rings bathed in the absence of extracellular Ca2+ in parallel with a reduction in the NE-stimulated 45Ca efflux. Ryanodine alone caused a delayed moderate increase in 45Ca efflux, slowly increasing the fractional loss from 0.02/min to 0.03/min, without any increase in tension. The increased 45Ca efflux was accompanied by a decrease in the net cellular Ca content. When ryanodine and NE were administered in sequence during 45Ca efflux, we found a quantitative correlation between the ryanodine induced loss of 45Ca and the inhibition of the NE-induced 45Ca release. We conclude that the inhibition of the NE-induced contraction by 10 microM ryanodine is the result of depletion of Ca from intracellular stores rather than inhibition of Ca2+ release.
在离体兔主动脉中测量了兰尼碱对等长张力发展、细胞内钙净含量和45Ca外流的影响。用10微摩尔兰尼碱预处理组织30分钟，可降低去甲肾上腺素（NE）诱导的、浸浴在无细胞外Ca2+溶液中的主动脉环的张力，同时降低NE刺激的45Ca外流。单独使用兰尼碱会导致45Ca外流延迟适度增加，从0.02/分钟缓慢增加到0.03/分钟，而张力无任何增加。45Ca外流增加伴随着细胞内钙净含量的减少。当在45Ca外流期间依次给予兰尼碱和NE时，我们发现兰尼碱诱导的45Ca损失与NE诱导的45Ca释放抑制之间存在定量相关性。我们得出结论，10微摩尔兰尼碱对NE诱导收缩的抑制是细胞内钙库中钙耗尽的结果，而非Ca2+释放的抑制。
