Thom S A, Hughes A D, Martin G N, Sever P S
Department of Clinical Pharmacology, St Mary's Hospital Medical School, London, UK.
J Hypertens Suppl. 1985 Dec;3(3):S97-9.
Isolated human arterial segments have been used to demonstrate the presence and release of the endothelium derived relaxing factor (EDRF) in human vasculature. This has been shown in peripheral, splanchnic and coronary arteries. Agents which have been shown to promote the release of the human EDRF in these studies include acetylcholine (by a muscarinic mechanism), the calcium ionophore A23187, histamine and vasoactive intestinal peptide (VIP). Nordihydroguaretic acid (NDGA), methylene blue and haemoglobin reverse the effect of the EDRF. The EDRF effect is calcium-dependent and is not inhibited by indomethacin. Atheromatous disease in coronary arteries impairs the response to agents which release EDRF; its relative absence in this circumstance may play a role in the phenomenon of coronary artery spasm. The possibility of a specific alpha 2-adrenoceptor mechanism for the release of EDRF was investigated. This does not appear to be present in the human vasculature.
分离的人体动脉节段已被用于证明人体血管中内皮衍生舒张因子（EDRF）的存在和释放。这已在周围动脉、内脏动脉和冠状动脉中得到证实。在这些研究中已被证明能促进人体EDRF释放的物质包括乙酰胆碱（通过毒蕈碱机制）、钙离子载体A23187、组胺和血管活性肠肽（VIP）。去甲二氢愈创木酸（NDGA）、亚甲蓝和血红蛋白可逆转EDRF的作用。EDRF的作用依赖于钙，且不受消炎痛抑制。冠状动脉粥样硬化疾病会损害对释放EDRF物质的反应；在这种情况下EDRF相对缺乏可能在冠状动脉痉挛现象中起作用。研究了EDRF释放的特定α2 -肾上腺素能受体机制的可能性。在人体血管中似乎不存在这种机制。
