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

与内皮素相关的物质-依赖性或神经遗传学关系在孤立的植物和细胞Cavernosum中进行了研究。内酯衍生的放松物质比硝酸氧化物（NO）和前列腺素，神经衍生的NO被试着通过生物级联系统进行测量。（1） In isolated monkey coronary arteries， vasopressin-induced relaxation is mediated by NO released from the endothelium via stimulation of Vy D21 y D2 receptors。（2）孤立的猴子语言植物，乙酰胆碱素（ACh）诱导的，内皮素依赖放松部分被L-NA抑制，是一种无合成酶抑制剂。Remaining relaxation was abolished by C-D12+ D-1-dependent K-D1+ D-1 channel blockers or cytochrome P450 （CYP）3 A-inhibitors。生物级联系统失败了，无法检测不稳定的物质，可能是内壳依赖性衍生的超极化因子（EDHF），并表明物质可能是不稳定的。含有人类活体微组C的甲氧烷酸孵化的产品 ... More YP3A relaxed the artery， the relaxation was abolished by the Ky D1+ Yy D1 channel blockers。与CYP 3A-抑制剂共同孵化的产品不能放松你的电池。These findings suggest that the relaxation by ACH in this artery is mediated by NO and Kyi D1+ Kyi 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 cell selectivity。ACh放松了接触，但没有被处理的肥皂泡， Cavernos条被L-NA部分地抑制了放松，而剩余的放松则被Kyi D1+ Yye D1高度集中废除。在另一方面，神经遗传学放松对L-NA的敏感性不受saponin的影响。神经衍生出的“不”并没有被生物等级系统检测到。These findings suggest that ACh？on the endothelium and liberates NO and Ky D1+イエD1-channel opening substance which relax the smManagement muscle of the cavernosum。Nitroxidergic nerve function appears to be unaffected by endothelial cells的损害。Less（低）

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