Watras J, Benevolensky D
Department of Medicine, University of Connecticut Health Center, Farmington 06032.
Biochim Biophys Acta. 1987 Dec 10;931(3):354-63. doi: 10.1016/0167-4889(87)90227-8.
Inositol 1,4,5-trisphosphate-induced calcium release from canine aortic smooth muscle sarcoplasmic reticulum vesicles was examined using the calcium indicator antipyrylazo III. Calcium release was initiated by addition of inositol 1,4,5-trisphosphate (IP3) to aortic vesicles 7 min after initiation of ATP-supported calcium uptake. Half-maximal calcium release occurred at 1 microM IP3, with maximal calcium release amounting to 25 +/- 2% of the intravesicular calcium (n = 12, 9 preparations). Ruthenium red (10-20 microM), which has been reported to block IP3-induced calcium release from skeletal muscle sarcoplasmic reticulum, did not inhibit aortic IP3-induced calcium release. Elevation of Mg2+ concentration from 0.06 to 7.8 mM inhibited aortic IP3-induced calcium release 75%, which contrasts with the Mg2+-insensitive IP3-induced calcium release from platelet reticular membranes. The IP3-dependence of aortic calcium release suggested that Mg2+ acted as a noncompetitive inhibitor. Thus, aortic sarcoplasmic reticulum vesicles contain an IP3-sensitive calcium pathway which is inhibited by millimolar concentrations of Mg2+, but which is not inhibited by Ruthenium red and so differs from the previously described IP3-sensitive calcium pathways in skeletal muscle and platelet reticular membranes.
使用钙指示剂安替比拉宗III检测了1,4,5-三磷酸肌醇诱导犬主动脉平滑肌肌浆网囊泡释放钙的情况。在ATP支持的钙摄取开始7分钟后,向主动脉囊泡中加入1,4,5-三磷酸肌醇(IP3)引发钙释放。半最大钙释放发生在1μM IP3时,最大钙释放量相当于囊泡内钙的25±2%(n = 12,9个标本)。据报道,钌红(10 - 20μM)可阻断IP3诱导的骨骼肌肌浆网钙释放,但不抑制主动脉IP3诱导的钙释放。将Mg2+浓度从0.06 mM提高到7.8 mM可抑制主动脉IP3诱导的钙释放75%,这与血小板网状膜中Mg2+不敏感的IP3诱导的钙释放形成对比。主动脉钙释放对IP3的依赖性表明Mg2+起非竞争性抑制剂的作用。因此,主动脉肌浆网囊泡含有一条IP3敏感的钙途径,该途径受到毫摩尔浓度Mg2+的抑制,但不受钌红的抑制,因此与先前描述的骨骼肌和血小板网状膜中的IP3敏感钙途径不同。