内皮依赖性超极化因子在血管舒张中的作用

Role of endothelium-derived hyperpolarizing factor in the vasorelaxation of rats

目的 研究内皮依赖性超极化因子 (EDHF)在血管舒张中的作用及机制。方法 测定各种内皮依赖性舒张因子抑制剂、钾通道抑制因子、细胞色素P4 5 0单氧化酶抑制剂作用下的血管环张力。结果 EDHF的血管舒张作用在大鼠肠系膜微动脉明显大于胸主动脉。一氧化氮 (NO)合成受到慢性抑制时 ,胸主动脉的EDHF作用有增加趋势 ,在肠系膜微动脉投药后 3d和 1周的EDHF作用明显增加。ChTx部分抑制、TBA明显抑制EDHF在肠系膜微动脉的舒张作用。结论 EDHF在大鼠肠系膜微动脉的内皮依赖性舒张反应中起主要作用 ;在NO合成受抑制时其作用明显增加 ;其作用介导于KCa通道。

Aim To investigate the role and mechanism of endothelium-derived hyperpolarizing factor (EDHF) in the vasorelaxation of rats. Methods Isometric tension was recorded in isolated rat aorta and small mesenteric arteries to study the effect of PGI 2, NO and EDHF on endothelium-dependent relaxation. Results The contribution of EDHF to endothelium-dependent relaxation is significantly larger in small mesenteric arteries than in the aorta. In the nitric oxide synthesis inhibited rats the contribution of EDHF transiently increased. The nature and vasodilating mechanism of EDHF may not be involved the cytochrome P450 pathway, while it is partially mediated by K Ca channels. Conclusion In the small mesenteric artery of rats the endothelium-dependent relaxation was mainly caused by EDHF. When nitric oxide synthesis was inhibited, the contribution of EDHF increased in the early phase. The hyperpolarizing and vasodilating mechanism of EDHF is partially mediated by K Ca channels.