既往研究证明EH病人血管内皮的功能可能受损。毒蕈碱受体兴奋剂通过内皮细胞合成和释放的与一氧化氮(NO)有关的内皮舒缓因子(EDRF)导致血管扩张,而硝普钠扩张血管的机制则与内皮细胞无关。研究发现EH病人对毒蕈碱受体兴奋剂的反应受到损害,而对硝普钠的反应正常,因此认为EH病人内皮功能异常。但是作者在本 Previous studies have shown that the function of endothelial cells in EH patients may be impaired. The nitric oxide (NO) -related endothelium release factor (EDRF) that is synthesized and released by muscarinic receptor agonists leads to vasodilatation through endothelial cells, whereas the mechanism by which sodium nitroprusside dilates blood vessels is independent of endothelial cells. Study found that EH patients on muscarinic receptor agonist response was compromised, and the response to sodium nitroprusside normal, so that EH endothelial dysfunction. But the author in this