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依他尼酸对豚鼠结肠带平滑肌收缩性及钙通量的影响(作者译)

[Effect of ethacrynic acid on contractility and Ca flux of guinea pig taenia coli smooth muscle (author's transl)].

作者信息

Tokita S

出版信息

Nihon Seirigaku Zasshi. 1977;39(10):389-404.

PMID:599491
Abstract

The effects of ethacrynic acid (ETCA) which has been known as an -SH groups inhibitor on the contractility and the Ca flux of guinea pig taenia coli were investigated. The results obtained were as follow: 1) Contractures induced by 10(-4) M ACh, or the tonic component of 150 mM K-contractures were markedly suppressed by previous treatment with a low concentration (2 X 10(-4) M) of ETCA for 40 min. Conversely with the same treatment, the phasic component of this K-contracture was only slightly suppressed. The inhibitory effects of ETCA in both cases were reversed by the repetitive washing out of ETCA from taenia coli with normal tris-buffered solution. 2) ETCA, at concentrations higher than 10(-3) M, more markedly inhibited the ACh-, and the K-contractures. In this case these inhibitions were irreversible. 3) Cysteine in an equimolar concentration of ETCA prevented the inhibitory effects of ETCA on both contractures. 4) ETCA (10(-4) M) inhibited the ACh-contracture in Ca2+-free isotonic KCl solution to approximately the same degree as that in normal solution. 5) Inhibition of ACh-contracture by ETCA in Na+-free isotonic LiCl solution was less than that in normal solution. 6) ETCA (2 X 10(-4), or 10(-3) M) markedly stimulated 45Ca efflux from taenia coli in 20 mM Ca-EGTA tris-buffered solution. 7) 45Ca efflux acceleration by ETCA in Na+-free (replaced by Li+) 20 mM Ca-EGTA tris-buffered solution was less than that in 20 mM Ca-EGTA tris-buffered solution. These results may be explained by assuming that the inhibitory effect of ETCA on ACh-contracture can be attributed to the depletion of stored intracellular Ca and the acceleration of Ca efflux as a result of ETCA treatment.

摘要

已知作为一种-SH基团抑制剂的依他尼酸(ETCA)对豚鼠结肠带的收缩性和钙通量的影响进行了研究。得到的结果如下:1)用低浓度(2×10⁻⁴ M)的ETCA预先处理40分钟,可显著抑制由10⁻⁴ M乙酰胆碱(ACh)诱导的挛缩或150 mM钾挛缩的张力成分。相反,经过相同处理,这种钾挛缩的相位成分仅略有抑制。通过用正常的三羟甲基氨基甲烷缓冲溶液反复冲洗结肠带中的ETCA,可逆转ETCA在两种情况下的抑制作用。2)浓度高于10⁻³ M的ETCA更显著地抑制ACh和钾挛缩。在这种情况下,这些抑制作用是不可逆的。3)与ETCA等摩尔浓度的半胱氨酸可防止ETCA对两种挛缩的抑制作用。4)ETCA(10⁻⁴ M)在无钙等渗氯化钾溶液中对ACh挛缩的抑制程度与在正常溶液中大致相同。5)在无钠等渗氯化锂溶液中,ETCA对ACh挛缩的抑制作用小于在正常溶液中的抑制作用。6)ETCA(2×10⁻⁴或10⁻³ M)在20 mM钙-乙二醇双乙酸盐三羟甲基氨基甲烷缓冲溶液中显著刺激结肠带中45Ca的外流。7)在无钠(用锂替代)的20 mM钙-乙二醇双乙酸盐三羟甲基氨基甲烷缓冲溶液中,ETCA对45Ca外流的加速作用小于在20 mM钙-乙二醇双乙酸盐三羟甲基氨基甲烷缓冲溶液中的作用。这些结果可以通过假设ETCA对ACh挛缩的抑制作用可归因于细胞内储存钙的耗尽以及ETCA处理导致的钙外流加速来解释。

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