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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Influence of T-type Ca2+ (mibefradil) and Cl- (indanyloxyacetic acid 94) channel antagonists on alpha1-adrenoceptor mediated contractions in rat aorta.
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Influence of T-type Ca2+ (mibefradil) and Cl- (indanyloxyacetic acid 94) channel antagonists on alpha1-adrenoceptor mediated contractions in rat aorta.

机译：T型Ca2 +（咪贝拉地尔）和Cl-（茚满基氧乙酸94）通道拮抗剂对大鼠主动脉中α1-肾上腺素受体介导的收缩的影响。

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摘要

The effects of the T-type and L-type Ca2+ channel antagonists, mibefradil and nifedipine, respectively, and those of a Cl- channel antagonist, indanyloxyacetic acid 94, on mechanical responses elicited by selective activation of alpha1-adrenoceptors using cirazoline were examined in rat isolated aortic rings. The presence of mibefradil (300 nM), indanyloxyacetic acid, 94 (30 microM) and nifedipine (300 nM) alone inhibited mechanical responses elicited by cirazoline. The concentration-response curves to cirazoline were displaced to the right with significant increases in the EC50 and significant depressions of the maximal responses in the presence of the individual agents mibefradil, indanyloxyacetic acid 94, or nifedipine. A combination of mibefradil and indanyloxyacetic acid 94 further inhibited the mechanical activity produced by cirazoline. The further reduction in the maximal response to cirazoline, in the presence of mibefradil and nifedipine, was insignificant when compared with the effects of nifedipine alone. In addition, maximal mechanical responses produced by cirazoline were not significantly affected by a combination of nifedipine and indanyloxyacetic acid 94 when compared with either nifedipine alone or mibefradil and indanyloxyacetic acid 94 combined. Our current findings indicate that mibefradil, indanyloxyacetic acid 94, and nifedipine can inhibit cirazoline-induced contractions to a varying degree. Moreover, based on our present data it would be reasonable to suggest that the contribution of T-type versus L-type Ca2+ channels to contractile responses obtained with cirazoline are approximately 21% and 35%, respectively, of the Emax. It would appear that L-type Ca2+ channels play a greater role in processes that are involved in excitation-contraction coupling subsequent to stimulation of alpha1-adrenoceptors. In addition, Cl- channels also appear to be involved in the process of contraction following alpha1-adrenoceptor activation.
机译：分别考察了T型和L型Ca2 +通道拮抗剂米贝拉地尔和硝苯地平以及Cl通道拮抗剂茚满基氧乙酸94对通过使用cirazoline选择性激活α1-肾上腺素受体引起的机械反应的影响。大鼠离体主动脉环。咪贝拉地尔（300 nM），茚满基氧基乙酸94（30 microM）和硝苯地平（300 nM）的存在单独抑制了环唑啉引起的机械反应。在单独使用米贝拉地尔，茚满基氧乙酸94或硝苯地平的情况下，对cirazoline的浓度-响应曲线向右移动，EC50显着增加，最大响应显着下降。咪贝拉地尔和茚满基氧基乙酸94的组合进一步抑制了环唑啉产生的机械活性。与单独使用硝苯地平相比，在存在米贝拉地尔和硝苯地平的情况下，对西拉唑啉的最大反应的进一步降低微不足道。另外，与单独的硝苯地平或咪贝拉地尔和茚满基氧乙酸94相比，硝苯地平和茚满基氧乙酸94的组合对环唑啉产生的最大机械反应没有显着影响。我们目前的发现表明，米贝拉地尔，茚满基氧乙酸94和硝苯地平可以不同程度地抑制环唑啉引起的收缩。此外，根据我们目前的数据，有理由建议T型与L型Ca2 +通道对使用cirazoline获得的收缩反应的贡献分别约为Emax的21％和35％。似乎L型Ca2 +通道在刺激α1-肾上腺素能受体后参与激发-收缩偶联的过程中起着更大的作用。另外，在α1-肾上腺素受体激活后，Cl-通道似乎也参与了收缩过程。

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