Su J Y, Chang Y I
Department of Anesthesiology, University of Washington, Seattle 98195.
Pflugers Arch. 1993 May;423(3-4):300-6. doi: 10.1007/BF00374409.
Ryanodine causes depression of the caffeine-induced tension transient (ryanodine depression) in skinned muscle fibers, because it blocks the sarcoplasmic reticulum (SR) Ca(2+)-release channels [Su, J. Y. (1988) Pflügers Arch 411:132-136, 371-377; (1992) Pflügers Arch 421:1-6]. This study was performed to examine the sensitivity of SR Ca(2+)-release channels to ryanodine in fetal compared to adult myocardium and to investigate the influence of Ca2+, caffeine, and Mg2+ on ryanodine depression in skinned fibers. Ryanodine (0.3 nM-1 microM) caused a dose-dependent depression in skinned myocardial fibers of the rat, and the fetal fibers (IC50 approximately 74 nM) were 26-fold less sensitive than those of the adult (IC50 approximately 2.9 nM). The depression induced by 0.1 microM or 1 microM ryanodine was a function of [caffeine], or [Ca2+] (pCa < 6.0), which was potentiated by caffeine, and an inverse function of [Mg2+]. At pCa > 8.0 plus 25 mM caffeine, a 20% ryanodine depression was observed in both the fetal and adult fibers, indicating independence from Ca2+. Ryanodine depression in skinned fibers of the fetus was less affected than that seen in the adult by pCai, [caffeine]i, or 25 mM caffeine plus pCai or plus pMgi (IC50 approximately pCa 4.5 versus 5.1; caffeine 12.7 mM versus 2 mM; pCa 6.7 versus 7.3; and pMg 3.9 versus 3.3 respectively). The results show that the SR Ca(2+)-release channel in both fetal and adult myocardium is modulated by Ca2+, caffeine, and Mg2+.(ABSTRACT TRUNCATED AT 250 WORDS)
雷诺丁可使去皮肤肌纤维中咖啡因诱导的张力瞬变降低（雷诺丁抑制），因为它阻断肌浆网（SR）的Ca(2+)释放通道[苏，J.Y.（1988年）《普弗吕格氏文献》411:132 - 136，371 - 377；（1992年）《普弗吕格氏文献》421:1 - 6]。本研究旨在比较胎儿心肌与成人心肌中SR Ca(2+)释放通道对雷诺丁的敏感性，并研究Ca2+、咖啡因和Mg2+对去皮肤纤维中雷诺丁抑制的影响。雷诺丁（0.3 nM - 1 microM）在大鼠去皮肤心肌纤维中引起剂量依赖性抑制，胎儿纤维（IC50约74 nM）的敏感性比成纤维（IC50约2.9 nM）低26倍。0.1 microM或1 microM雷诺丁诱导的抑制是[咖啡因]或[Ca2+]（pCa < 6.0）的函数，由咖啡因增强，且是[Mg2+]的反函数。在pCa > 8.0加25 mM咖啡因时，胎儿和成纤维中均观察到20%的雷诺丁抑制，表明与Ca2+无关。胎儿去皮肤纤维中的雷诺丁抑制受pCai、[咖啡因]i或25 mM咖啡因加pCai或加pMgi的影响小于成纤维（IC50分别约为pCa 4.5对5.1；咖啡因12.7 mM对2 mM；pCa 6.7对7.3；pMg 3.9对3.3）。结果表明，胎儿和成人心肌中的SR Ca(2+)释放通道均受Ca2+、咖啡因和Mg2+调节。（摘要截短于250字）
