Williams S P, Adams R D, Mustafa S J
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858.
Alcohol. 1990 Mar-Apr;7(2):121-7. doi: 10.1016/0741-8329(90)90072-k.
The purpose of this study was to investigate the effects of chronic ethanol consumption on blood pressure and vascular responses, specifically, the possible alterations in endothelium-dependent relaxation which are associated with ethanol-induced hypertension in the rat model. Male rats received ethanol in drinking water for 13 weeks. Systolic pressure was recorded weekly. Following treatment, segments of thoracic aorta with and without intact endothelium were used to generate relaxation-response curves to the endothelium-dependent agents, acetylcholine, ATP and bradykinin, as well as the endothelium-independent agents, adenosine and sodium nitroprusside. Mean systolic pressures at the end of the treatment period were: 127.8 +/- 1.2 and 151.1 +/- 1.3 mmHg for controls and ethanol-treated rats, respectively. Ethanol treatment did not affect the relaxation produced by either acetylcholine, ATP or sodium nitroprusside in aorta with or without endothelium. In contrast, ring segments with intact endothelium from ethanol-treated rats exhibited augmented relaxation in response to both adenosine and bradykinin compared to controls. Removal of the endothelium abolished the relaxation produced by bradykinin in both groups. Although removal of the endothelium had no effect on the relaxation produced by adenosine in the control group, it attenuated the adenosine-induced relaxation in the ethanol-treated group back to control levels. These data suggest that chronic ingestion of ethanol causes elevated blood pressure and augments the endothelium-dependent relaxation to bradykinin. These findings also suggest that chronic ethanol treatment can cause the appearance of an endothelium-dependent component in the relaxation produced by adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究的目的是调查长期摄入乙醇对血压和血管反应的影响，具体而言，是研究在大鼠模型中与乙醇诱导的高血压相关的内皮依赖性舒张功能可能发生的改变。雄性大鼠饮用含乙醇的水13周。每周记录收缩压。处理后，使用有无完整内皮的胸主动脉节段来生成对内皮依赖性介质乙酰胆碱、ATP和缓激肽以及内皮非依赖性介质腺苷和硝普钠的舒张反应曲线。处理期末对照组和乙醇处理组的平均收缩压分别为：127.8±1.2和151.1±1.3 mmHg。乙醇处理对有无内皮的主动脉中乙酰胆碱、ATP或硝普钠产生的舒张功能没有影响。相比之下，与对照组相比，乙醇处理大鼠的有完整内皮的环段对腺苷和缓激肽的舒张反应增强。去除内皮消除了两组中缓激肽产生的舒张反应。虽然去除内皮对对照组中腺苷产生的舒张反应没有影响，但它使乙醇处理组中腺苷诱导的舒张反应减弱至对照水平。这些数据表明，长期摄入乙醇会导致血压升高，并增强对缓激肽的内皮依赖性舒张反应。这些发现还表明，长期乙醇处理可使腺苷产生的舒张反应中出现内皮依赖性成分。（摘要截短至250字）
