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Measurement of vasorelaxant substance derived from endothelium and innervating nerve by biocascade system

生物级联系统测定内皮和神经支配的血管舒张物质

基本信息

批准号：
10670083
负责人：
AYAJIKI Kazuhide
金额：
$ 2.05万
依托单位：
Shiga University of Medical Science
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

项目摘要

Substances associated with endothelium-dependent or neurogenic relaxations were examined in isolated arteries and corpus cavernosum. Endothelium-derived relaxing substance other than nitric oxide (NO) and prostacyclin, and nerve-derived NO were tried to be measured by a biocascade system.(1) In isolated monkey coronary arteries, vasopressin-induced relaxation is mediated by NO released from the endothelium via stimulation of VィイD21ィエD2 receptors.(2) In isolated monkey lingual arteries, acelycholine (ACh)-induced, endothelium-dependent relaxation was partially inhibited by L-NA, a NO synthase inhibitor. The remaining relaxation was abolished by CィイD12+ィエD1-dependent KィイD1+ィエD1 channel blockers or cytochrome P450 (CYP) 3A-inhibitors. The biocascade system failed to detect the relaxant substance, possibly endothelium-dependent derived hyperpolarizing factor (EDHF), indicating that the substance may be unstable. Products of arachidonic acid incubated with human liver microsome containing C … More YP3A relaxed the artery, the relaxation was abolished by the KィイD1+ィエD1 channel blockers. Products co-incubated with CYP3A-inhibitors did not relax the artery. These findings suggest that the relaxation by ACh in this artery is mediated by NO and KィイD1+ィエD1-channel opening substance(s) from arachidonic acid produced by CYP3A in the endothelium.(3) Histological studies with isolated canine corpus cavernosum demonstrated that saponin induced degenerative changes in the endothelial cells selectivity. ACh relaxed the intact, but not the saponin-treated, cavernos strips, the relaxation was partially inhibited by L-NA and the remaining relaxation was abolished by high concentration of KィイD1+ィエD1. On the other hand, neurogenic relaxation sensitive to L-NA was not affected by saponin. The nerve-derived NO was not detected by the biocascade system. These findings suggest that ACh acts on the endothelium and liberates NO and KィイD1+ィエD1-channel opening substance which relax the smooth muscle of the cavernosum. Nitroxidergic nerve function appears to be unaffected by the damage of endothelial cells. Less

在离体动脉和阴茎海绵体中检查与内皮依赖性或神经源性舒张相关的物质。尝试通过生物级联系统测量一氧化氮（NO）和前列环素以外的内皮源性舒张物质以及神经源性NO。(1)在离体猴冠状动脉中，加压素诱导的舒张是通过刺激血管内皮细胞D21受体介导的NO释放。(2)在离体猴舌动脉中，乙酰胆碱（ACh）诱导的内皮依赖性舒张可被NO合酶抑制剂L-NA部分抑制。其余的舒张被C_（12）D_1 + C_（12）D_1依赖性K_（12）D_1 + C_（12）D_1通道阻断剂或细胞色素P450（P450）3A抑制剂消除。生物级联系统未能检测到松弛物质，可能是内皮依赖性衍生超极化因子（EDHF），表明该物质可能不稳定。花生四烯酸与含C的人肝微粒体孵育产物 ...更多信息 YP 3A使动脉舒张，这种舒张作用可被K + D1通道阻断剂阻断。与CYP 3A抑制剂共孵育的产品不会松弛动脉。这些结果表明，ACh在该动脉中的舒张作用是由NO和内皮细胞中CYP 3A产生的花生四烯酸的K-β-D1+ β-D1-通道开放物质介导的。(3)离体犬阴茎海绵体的组织学研究表明，皂苷诱导内皮细胞选择性退行性变化。ACh松弛的完整的，但不是皂苷处理，海绵条，松弛部分抑制L-NA和剩余的松弛被废除高浓度的K β D1+ β D1。另一方面，对L-NA敏感的神经源性松弛不受皂苷的影响。生物级联系统未检测到神经源性NO。提示ACh作用于血管内皮细胞，释放NO和K+通道开放物质，使海绵体平滑肌松弛。一氧化氮能神经功能似乎不受内皮细胞损伤的影响。少