Coca A, Garay R P, Aguilera M T, De la Sierra A, Urbano-Márquez A
Department of Internal Medicine, Hospital Clinico, School of Medicine, University of Barcelona, Spain.
Am J Hypertens. 1989 Oct;2(10):784-7. doi: 10.1093/ajh/2.10.784.
Several epidemiological and clinical studies have established a clear association between alcohol consumption and hypertension. The mechanism of the pressor effect of ethanol is not well understood. We studied the in vitro effects of increasing amounts of ethanol on different Na+ transport systems from human erythrocytes. Ethanol at concentrations higher than 32 mmol/L stimulated ouabain-sensitive Na+ efflux, the Na+ efflux depending on the Na+:Li+ countertransport and Na+ leak. At the same concentrations, ethanol inhibited bumetanide-sensitive Na+ efflux. We conclude that, with the exception of Na+-K+ pump, alcohol-induced alterations and those observed in erythrocytes from essential hypertensives may overlap. Therefore, alcohol consumption could potentiate those genetic abnormalities of Na+ transport and contribute to the pathogenesis of essential hypertension.
多项流行病学和临床研究已证实饮酒与高血压之间存在明确关联。乙醇升压作用的机制尚未完全明确。我们研究了不同浓度乙醇对人红细胞中不同钠转运系统的体外作用。浓度高于32 mmol/L的乙醇刺激了哇巴因敏感的钠外流，钠外流取决于钠：锂逆向转运和钠泄漏。在相同浓度下，乙醇抑制了布美他尼敏感的钠外流。我们得出结论，除钠钾泵外，酒精引起的改变与原发性高血压患者红细胞中观察到的改变可能重叠。因此，饮酒可能会增强钠转运的那些遗传异常，并导致原发性高血压的发病机制。
