Suarez-Kurtz G
Departamento de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Brasil.
Braz J Med Biol Res. 1994 Nov;27(11):2661-6.
Heavy sarcoplasmic reticulum (SR) membrane fractions from rabbit and porcine skeletal muscle were incorporated into planar lipid bilayers and the activity of the Ca2+ release channels was recorded under voltage clamp, using Cs+ as the current carrier. The effects of the nucleotides adenosine triphosphate (ATP) and uridine triphosphate (UTP) on channel activity were studied at a holding potential of +30 mV. UTP (0.1-1.0 mM) had no effect per se on the conductance or the gating properties of the Ca2+ release channels. In contrast, ATP (> 0.1 mM) increased P(o), the open channel probability, and both tau o1 and tau o2, the open time constants, and decreased tau c1 and tau c2, the closed time constants. The Ca2+ channel conductance, however, was not affected by ATP. Ruthenium red (1-2 microM), a well-known inhibitor of the SR Ca2+ release channel, abolished the ATP-induced channel activation. These electrophysiological data provide support for our contention (G. Suarez-Kurtz et al. (1993). Anais da Academia Brasileira de Ciências, 65:330) that the UTP-induced tension in mammalian "skinned" muscle fibers is not due to stimulated release of SR-stored Ca2+ via the release channel.
将来自兔和猪骨骼肌的重肌质网（SR）膜组分整合到平面脂质双分子层中，并在电压钳制下，以铯离子（Cs⁺）作为电流载体记录钙释放通道的活性。在+30 mV的保持电位下研究了三磷酸腺苷（ATP）和三磷酸尿苷（UTP）对通道活性的影响。UTP（0.1 - 1.0 mM）本身对钙释放通道的电导或门控特性没有影响。相比之下，ATP（> 0.1 mM）增加了开放通道概率P(o)以及开放时间常数tau o1和tau o2，并降低了关闭时间常数tau c1和tau c2。然而，钙通道电导不受ATP影响。钌红（1 - 2 microM）是一种著名的SR钙释放通道抑制剂，它消除了ATP诱导的通道激活。这些电生理数据支持了我们的观点（G. Suarez - Kurtz等人，（1993年）。巴西科学院学报，65:330），即UTP诱导的哺乳动物“去皮”肌纤维张力不是由于通过释放通道刺激SR储存的钙释放所致。
