摘要
目的研究文多灵对大鼠肾血管的舒张效应及作用机制。方法快速分离大鼠肾动脉并固定于多通道微血管肌动扫描仪中,预孵育不同的受体抑制剂或离子通道阻断剂,记录给药后血管环等张力的变化。结果文多灵对由苯肾上腺素、KCl预收缩的血管呈剂量依赖性地舒张;四乙铵(TEA+)、Ro-32-0432能部分拮抗文多灵的舒张血管效应,而格列本脲、BaCl2或Y-27632对其舒张作用没有明显的影响;文多灵在无钙的高钾溶液中能浓度依赖性地抑制CaCl2的血管收缩作用以及舒张由(-)Bay K8644预收缩的血管。此外,与文多灵舒血管效应与内皮细胞无关。结论文多灵在体外可能通过抑制血管平滑肌细胞外钙内流、TEA+-敏感的钾离子通道或蛋白激酶C途径舒张大鼠肾血管。
Aim To explore the underlying relaxatmn mechanisms of vindoline in isolated rat renal arteries. Methods Rings were quickly isolated and suspended in a Multi Myograph System and changes of isometric tension were recorded in the absence or presence of different receptor inhibitors or ion channel blockers. Results Vindoline produced a dose-dependent relaxa- tion in rings with or without endothelia contracted by phenylephrine or KC1. Treatment with TEA + or Ro-34- 0432 slightly blunt the relaxation induced by vindoline, whereas gliclamide, BaCI2 or Y-27632 failed to affect this relaxant effect. Vindoline reduced the contraction evoked by CaCl2 in Ca-free 60 mmol·L-1 K+ Kreb's solution, as well as in ( - )-Bay K8644 in 15 mmol · L- 1 K + solution. In addition, vindoline caused the parallel relaxation in rings with or without endothelia. Conclusions The current results suggest that vindoline dilates renal arteries in vitro through one or more pathways including inhibition of calcium entry, TEA + - sensitive potassium channel or protein kinase pathways in vascular smooth muscle ceils.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2012年第8期1096-1100,共5页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No 30901847
30901848)
"重大新药创制"科技重大专项资助项目(No2012ZX09103101-053)
广东省珠江科技新星项目(DMZ2011JZ200045)
广东省高层次人才项目(RWJ)
关键词
文多灵
肾动脉
血管舒张
内皮细胞
钙内流
蛋白激酶C
vindoline
renal arteries
vasorelaxation
endothelial cells
calcium entry
protein kinase C