Zhang Wen, Ma Ke-Tao, Wang Yang, Si Jun-Qiang, Li Li
Department of Physiology/Key Laboratory of Education Ministry of Xinjiang Endemic and Ethnic Diseases, Medical College of Shihezi University, Shihezi 832002, China.
Sheng Li Xue Bao. 2014 Apr 25;66(2):195-202.
The aim of the present study is to investigate the effect of 18β-glycyrrhetinic acid (18β-GA) on KCl- and PE-induced constriction of rat renal interlobar artery (RIA). Pressure myograph system was used to observe the constriction induced by KCl 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 18β-GA on membrane input capacitance (C(input)), membrane input conductance (G(input)) or membrane input resistance (R(input)) of smooth muscle cells embedded in arteriole segment. The results showed that both KCl (30-100 mmol/L) and PE (0.1-30 μmol/L) induced contraction of RIA in a concentration-dependent way. After pretreatment with 18β-GA (100 μmol/L), KCl- or PE-induced constriction of RIA was significantly decreased. After application of 18β-GA (100 μmol/L), the C(input), G(input) and R(input) 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 KCl and PE, and the underlying mechanism may involve the inhibitory effect of 18β-GA on gap junction.
本研究旨在探讨18β-甘草次酸（18β-GA）对氯化钾（KCl）和苯肾上腺素（PE）诱导的大鼠肾叶间动脉（RIA）收缩的影响。采用压力肌动描记系统，观察在有或无18β-GA预处理的情况下，Wistar大鼠急性分离的RIA中KCl和PE（内皮非依赖性血管收缩剂）诱导的收缩。采用全细胞膜片钳记录技术，观察18β-GA对嵌入小动脉段的平滑肌细胞膜输入电容（C(input)）、膜输入电导（G(input)）或膜输入电阻（R(input)）的影响。结果表明，KCl（30 - 100 mmol/L）和PE（0.1 - 30 μmol/L）均以浓度依赖性方式诱导RIA收缩。用18β-GA（100 μmol/L）预处理后，KCl或PE诱导的RIA收缩显著降低。应用18β-GA（100 μmol/L）后，原位平滑肌细胞的C(input)、G(input)和R(input)与分散的单个平滑肌细胞非常接近。这些结果表明，18β-GA抑制KCl和PE诱导的收缩，其潜在机制可能涉及18β-GA对缝隙连接的抑制作用。
