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血管内皮舒张因子(Endothelium-derived relaxing factor, EDRF)是血管内皮细胞产生释放的活性物质,它介导和决定许多舒血管活性物产生的舒张效应。已知硝基类扩血管药硝普钠(Sodium Nitroprusside,SNP)是通过形成一氧化氮(Nitric oxide, NO)而导致血管平滑肌产生舒张。有报导认为EDRF等同于NO。本文采用供受者双标本微量生物测定法,以SNP作为NO的供给源,通过比较EDRF与SNP舒张大鼠主动脉平滑肌的效应及其相互作用,以研究EDRF是否NO。结果发现:大鼠主动脉的内皮细胞在无活性物刺激时也能持续产生释放一种EDRF,即基础释放的EDRF(basal EDRF)。它可抑制NO的舒张效应,而NO作用于血管平滑肌后则可增强Ach激发的EDRF的舒张效应。可见,basal EDRF与NO的性质不相同,而激发的EDRF与NO的性质相似,EDRF与NO不能等同。为目前国际上这一争议提出了新的见解。
Endothelium-derived relaxing factor (EDRF) is an active substance released by vascular endothelial cells. It mediates and determines the relaxation effect of many vasodilators. It is known that the nitric oxide vasodilator sodium nitroprusside (SNP) causes the relaxation of vascular smooth muscle by the formation of nitric oxide (NO). There are reports that EDRF equals NO. In this study, double-labeled micro-bioassay for donors and SNPs as the source of NO were used to investigate whether EDRF is NO by comparing the effects of EDRF and SNP on aortic smooth muscle relaxation in rats. As a result, it was found that the endothelial cells of the rat aorta continuously produce and release EDRF (basal EDRF) when stimulated with no active substance. It inhibits the diastolic effect of NO, whereas NO acts on vascular smooth muscle and enhances the relaxation effect of Ach-stimulated EDRF. It can be seen that the properties of basal EDRF and NO are not the same, while the excited EDRF is similar to the properties of NO, and EDRF and NO can not be equal. For the current international controversy put forward new ideas.