中文摘要：

本文旨在观察1813．甘草次酸（18β-glycyrrhetinticacid，1813-GA）对Kcl和苯肾上腺素（phenylephrine，PE）诱导的离体大鼠肾脏叶间动脉（renalinterlobarartery，RIA）收缩的影响。急性分离大鼠RIA，应用压力肌动图技术，观察1813-GA预处理后大鼠RIA对内皮非依赖血管收缩剂KCl和PE的反应情况。用微动脉段标本的全细胞膜片钳技术，观察100Imaol／L1813-GA对血管段上平滑肌细胞的膜电容（Gispul）、膜电导（Ginput）和膜电阻僻inpul）的影响。结果显示，KCl（30～100mmol／L）SNPE（0．1～30μmol／L）均可以引起大鼠RIA浓度依赖的收缩；100gmol／L的1813-GA预处理后，KCl和PE对大鼠RIA的缩血管作用明显降低妒〈0．01）。给予100μmaol／L18B．GA后，RIAn~管段上平滑肌细胞的R，μm1、Ginput和Clinpul与单个平滑肌细胞数值十分接近。以上结果提示，18β．GA可抑制KCl和PE对大鼠RIA的收缩作用，其机制可能涉及1813-GA对缝隙连接的抑制。

英文摘要：

The aim of the present study is to investigate the effect of 1813-glycyrrhetinic acid （18β-GA） on KC1- and PE-induced con- striction of rat renal interlobar artery （RIA）. Pressure myograph system was used to observe the constriction induced by KC1 and PE （endothelial independent vasoconstrictor） in acutely separated RIA of Wistar rats with or without 18β-GA pretreatment. Whole-cell patch clamp recordings were used to observe the effect of 1813-GA on membrane input capacitance （Ci,put）, membrane input conduct- ance （Ginput） or membrane input resistance （Rinput） of smooth muscle cells embedded in arteriole segment. The results showed that both KC1 （30-100 mmol/L） and PE （0.1-30 μmol/L） induced contraction of RIA in a concentration-dependent way. After pretreatment with 1813-GA （100 μmol/L）, KC1- or PE-induced constriction of RIA was significantly decreased. After application of 1813-GA （100 gmol/L）, the Cinput, Ginput and Rinput of the in situ smooth muscle cells were very close to those of dispersed single smooth muscle cells. These results suggest 18β-GA inhibits the contraction induced by KC1 and PE, and the underlying mechanism may involve the inhibitory effect of 18β-GA on gap junction.