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肾上腺素与绵羊心脏浦肯野纤维平台电位的起搏机制

Epinephrine and the pacemaking mechanism at plateau potentials in sheep cardiac Purkinje fibers.

作者信息

Pappano A J, Carmeliet E E

出版信息

Pflugers Arch. 1979 Oct;382(1):17-26. doi: 10.1007/BF00585899.

DOI:10.1007/BF00585899
PMID:574937
Abstract
  1. In 1.35 mM [K+]0, sheep cardiac Purkinje fibers depolarized to about -40 mV. Whereas some fibers oscillated spontaneously at plateau potentials, others could be made to oscillate when polarized by intracellular currents. Pacemaker activity at plateau potentials (-50 to 0 mV) was distinct from that caused by the iK2 pacemaker at more negative potentials (-60 to -100 mV). 2. Epinephrine induced spontaneously occurring action potentials and increased pacemaker activity in depolarized Purkinje fibers. The ED50 for the positive chronotropic effect of epinephrine was about 5 x 10(-7) M. This concentration is similar to that reported for the effect of epinephrine on plateau amplitude (Carmeliet and Vereecke, 1969) and the slow inward current (isi, Reuter, 1974). 3. In voltage clamp experiments, epinephrine, increased the magnitude of isi and of an outward plateau current, ixi. It is concluded that epinephrine effects pacemaking at plateau potentials by increasing isi and without shifting the voltage dependence of these currents. The onset of pacemaker activity by epinephrine was preceded by membrane depolarization that results from an inward shift of the steady-state current-voltage relation. This current may flow through isi channels that are activated but not completely inactivated.
摘要
  1. 在1.35 mM的[K⁺]₀浓度下,绵羊心脏浦肯野纤维去极化至约 -40 mV。一些纤维在平台电位下自发振荡,而其他纤维在被细胞内电流极化时也可被诱导振荡。平台电位(-50至0 mV)下的起搏活动与更负电位(-60至 -100 mV)下由IK₂起搏器引起的起搏活动不同。2. 肾上腺素可诱导去极化的浦肯野纤维自发产生动作电位并增加起搏活动。肾上腺素正性变时作用的半数有效浓度(ED50)约为5×10⁻⁷ M。该浓度与报道的肾上腺素对平台振幅的作用(Carmeliet和Vereecke,1969年)以及慢内向电流(isi,Reuter,1974年)的浓度相似。3. 在电压钳实验中,肾上腺素增加了isi和外向平台电流ixi的幅度。得出的结论是,肾上腺素通过增加isi来影响平台电位下的起搏,且不改变这些电流的电压依赖性。肾上腺素引发起搏活动之前,膜会发生去极化,这是由稳态电流 - 电压关系向内偏移导致的。该电流可能流经已激活但未完全失活的isi通道。

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