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银诱导的青蛙骨骼肌收缩及其受钙拮抗剂硝苯地平和非洛地平以及钙激动剂 Bay K 8644 的调节。

Silver-induced frog skeletal muscle contraction and its modulation by calcium antagonists nifedipine and felodipine and calcium agonist Bay K 8644.

作者信息

Lu A, Oba T, Yamano S, Sako T, Yamaguchi M

机构信息

Department of Veterinary Anatomy and Cellular Biology, Ohio State University, Columbus 43210.

出版信息

Gen Pharmacol. 1992 Jul;23(4):747-52. doi: 10.1016/0306-3623(92)90160-l.

Abstract
  1. Ag+ induces one phase of a transient contracture in frog skeletal muscle (0.3-10 microM) and potentiates twitch tension when the fiber is given continuous stimulation. 2. The potentiation of fiber contraction by Ag+ is similar to the effect of Ca2+ antagonists nifedipine and felodipine. 3. Bay K 8644 (100 nM) potentiates and accelerates Ag(+)-induced tension development and the inactivation occurs more rapidly than in the control (Ag+ alone). 4. Two factors can be considered to be essential for the induction of Ag+ contracture: (1) a certain number of Ag+ ions must bind to free SH groups of the voltage sensor; and (2) the binding must occur within a limited time to raise the mechanical threshold to induce contracture. 5. All results suggest that Ag+ binding to crucial SH groups on the Ca2+ channel may be responsible for the activation of muscle contraction, potentiation, and the inhibition of excitation-contraction coupling in skeletal muscle.
摘要
  1. 银离子(Ag+)在青蛙骨骼肌中(0.3 - 10微摩尔)可诱导一个短暂挛缩阶段,并且当纤维受到持续刺激时会增强抽搐张力。2. Ag+对纤维收缩的增强作用类似于钙拮抗剂硝苯地平和非洛地平的作用。3. 贝前列素K 8644(100纳摩尔)增强并加速了Ag(+)诱导的张力发展,且失活比对照组(仅Ag+)更快发生。4. 可以认为有两个因素对于诱导Ag+挛缩至关重要:(1)一定数量的Ag+离子必须与电压传感器的游离巯基结合;(2)这种结合必须在有限时间内发生,以提高诱导挛缩的机械阈值。5. 所有结果表明,Ag+与钙通道上关键巯基的结合可能是骨骼肌中肌肉收缩激活、增强以及兴奋 - 收缩偶联抑制的原因。

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