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巴比妥类药物对水蛭瑞氏细胞的钙可逆作用。

A calcium reversible action of barbiturates on the leech Retzius cell.

作者信息

Kleinhaus A L, Prichard J W

出版信息

J Pharmacol Exp Ther. 1977 May;201(2):332-9.

PMID:870678
Abstract

The Na salts of phenobarbital, barbital, pentobarbital, secobarbital, methohexital and thiopental in concentrations of 1 to 5 mM all caused prolonged action potentials in leech Retzius cells. The prolongation was favored by low Ca and was reversible by elevation of Ca. Barbiturate-prolonged action potentials were not affected by 50 micronm tetrodotoxin or replacement of Cl by propionate, but they were dependent on external Na. Their amplitudes were increased by steady hyperpolarization and input resistance was reduced during them. They were of shorter duration when elicited at a rapid rate. They were sometimes shortened by intracellular iontophoresis of Ca and by use of the ionophore X537A, but technical factors complicated the interpretation of both kinds of experiments. The results are consistent with the hypothesis that the barbiturates used blocked a voltage-dependent inward Ca current which activates a K conductance necessary for normal repolarization.

摘要

浓度为1至5毫摩尔的苯巴比妥、巴比妥、戊巴比妥、司可巴比妥、美索比妥和硫喷妥钠的钠盐均会使水蛭雷特修斯细胞的动作电位延长。低钙有利于这种延长,而升高钙可使其逆转。巴比妥类药物延长的动作电位不受50微摩尔河豚毒素的影响,也不受用丙酸盐替代氯离子的影响,但它们依赖于细胞外钠离子。稳定的超极化会增加其幅度,并且在动作电位期间输入电阻会降低。快速引发时,其持续时间较短。细胞内钙离子电离子导入和使用离子载体X537A有时会使其缩短,但技术因素使这两种实验的解释都变得复杂。这些结果与以下假设一致:所使用的巴比妥类药物阻断了一种电压依赖性内向钙电流,该电流激活了正常复极化所需的钾离子电导。

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