摘要
目的 探讨缝隙连接 (GJ)在苯肾上腺素 (PE)缩血管中的作用。方法 通过大鼠离体肠系膜动脉环 (superiormesentericarterialrings,MARs)试验 ,观察GJ阻断剂Hep tanol预处理对PE引起的去内皮和完整内皮MARs收缩及其量效曲线的影响。结果 Heptanol预处理可明显抑制 1 0× 10 - 7mol·L- 1PE的缩血管作用 ,并呈剂量依赖关系。 3 0× 10 - 5 mol·L- 1Heptanol抑制百分率分别为 11 70 %±3 2 5% (去内皮组 )和 15 2 4%± 7 87% (完整内皮组 ) ;3 0× 10 - 4mol·L- 1Heptanol预处理 ,抑制百分率分别为3 6 3 6%± 11 54% (去内皮组 )和 3 8 85%± 13 0 3 % (完整内皮组 ) ;同浓度Heptanol对PE致去内皮和完整内皮MAR收缩的抑制作用差异无显著性。 3 0× 10 - 5 ,1 0× 10 - 4,3 0× 10 - 4mol·L- 1Heptanol使PE的量效曲线右移 ,最大效应 (Emax)不变。结论 GJ参与介导苯肾上腺素的缩血管作用 ,GJ阻断剂Heptanol对PE缩血管的抑制作用无明显内皮依赖性 。
AIM To investigate the role of gap junction ( GJ) on the phenylephrine (PE)-induced vasoconstriction. METHODS By using isolated rings of rat superior mesenteric arteries (MARs), without and with endothelium, the effects of GJ blocker heptanol on the PE-induced vasoconstriction and concentra tion-effect curves were recorded as changes in isometric force. RESULTS Heptanol significantly inhibited the 1 0 ×10 -7 mol·L -1 PE-induced vaso constriction. The inhibitory percentage of 3 0×10 -5 mol·L -1 hept anol was respectively 11 70%±3 25%(in the absence of endothelium) or 15 24% ±7 87%(in the presence of endothelium). While pretreatment with 3 0 ×10 -4 mol·L -1 heptanol, the inhibitory percentage was respectively 36 36% ±11 54%(without endothelium) or 38 85%±13 03%(with endothelium). Statistica l data showed there was no significant difference between the effect of heptanol on PE-induced vasoconstriction without and with endothelium in MARs. A shift w as produced to the right of the concentration-effect curve of 1 0 ×10 -9 ～1 0 ×10 -4 mol·L -1 PE by pretreatment with 3 0×10 -5 , 1 0×10 -4 , 3 0×10 -4 mol·L -1 heptanol, the maximal response o f PE did not decrease. The EC 50 of PE was significantly increased. CONCLUSION The gap junction is involved in the PE-induced vasoconstric tion. The inhibitory effect of Heptanol is independent on endothelium significantly and concentration-dependent.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2003年第12期1358-1361,共4页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目No 3996 0 0 76
