L-palmitylcarnitine and calcium ions act similarly on excitatory ionic currents in avian ventricular muscle.
L-palmitylcarnitine and calcium ions act similarly on excitatory ionic currents in avian ventricular muscle.
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L-棕榈基肉碱和钙离子对禽类心室肌的兴奋性离子电流的作用类似。
DOI：
10.1161/01.res.52.6.625
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发表时间：
1983
影响因子：
20.1
通讯作者：
Pappano,AJ
中科院分区：
文献类型：
--
作者：
Inoue,D;Pappano,AJ
棕榈肉碱是一种两亲性物质，在缺血心脏组织中蓄积和泄漏，影响了禽类心室肌的快钠离子通道和慢钙离子通道。在5.4 mM外钾离子存在的情况下，棕榈肉碱在不改变静息电位的情况下，降低了动作电位的最大上升速率，增加了动作电位在高原水平的持续时间。棕榈基肉碱使稳态失活的最大上升速率（快速钠离子电流的指标）向更正的电位移动了3 ~ 6 mV。外钙离子升高至5.4 mM（正常= 1.8 mM），与棕榈肉碱一样，降低了最大上升速率，使动作电位为最大值的一半的电压移动了3 mV，使电位更正，但未改变静息电位。与棕榈肉碱不同，升高的外钙离子减少了静息电位- 80mv引发的动作电位持续时间。在25 mM [K+]0完全灭活快速钠离子通道的情况下，棕榈肉碱和升高的外部钙离子增加了钙离子依赖动作电位的幅度、最大上升速率和持续时间。当初始外钙离子为0.9 mM时，棕榈肉碱（3mv）和外钙离子升高（6mv）使钙依赖性动作电位最大上升速率的稳态失活持续向更正的电位转移。棕榈肉碱与升高的钙一样，在普萘洛尔存在时引起正性肌力效应。棕榈基肉碱（3 × 10（-5）至3 × 10(-4)M）的作用与外钙升高的作用相似，这与棕榈基肉碱与外钙升高一样，通过对膜表面电荷的影响来影响钠和钙通道运作的假设是一致的。
Palmitylcarnitine, an amphiphile that accumulates in and leaks from ischemic heart tissue, affected the fast sodium ion channel and the slow calcium channel in avian ventricular muscle. In the presence of 5.4 mM external potassium ion, palmitylcarnitine reduced the maximum rate of rise of the action potential and increased action potential duration at the plateau level without changing the resting potential. Steady state inactivation of the maximum rate of rise, an index of fast sodium ion current, was shifted by 3-6 mV to more positive potentials by palmitylcarnitine. Elevation of external calcium ion to 5.4 mM (normal = 1.8 mM), like palmitylcarnitine, reduced the maximum rate of rise and shifted the voltage at which the action potential was half maximum by 3 mV to more positive potentials without changing the resting potential. Elevated external calcium ion, unlike palmitylcarnitine, reduced the duration of action potentials initiated from a resting potential of -80 mV. Palmitylcarnitine and elevated external calcium ion increased the amplitude, the maximum rate of rise, and duration of calcium ion dependent action potentials recorded in the presence of 25 mM [K+]0 that completely inactivated the fast sodium ion channel. Steady state inactivation of the maximum rate of rise of calcium-dependent action potentials was consistently shifted to more positive potentials by palmitylcarnitine (3 mV) and by elevated external calcium ion (6 mV) when the initial external calcium ion was 0.9 mM. Palmitylcarnitine, like elevated calcium, evoked a positive inotropic effect in the presence of propranolol. The similarity of the effects of palmitylcarnitine (3 X 10(-5) to 3 X 10(-4)M) with those of elevated external calcium is consistent with the hypothesis that palmitylcarnitine, like elevated external calcium, influences sodium and calcium channel operation by an effect on membrane surface charge.