Clark L T
State University of New York Health Science Center, Brooklyn.
Magnesium. 1989;8(3-4):124-31.
Alcohol use is associated with an increased prevalence of hypertension although the responsible mechanisms and hemodynamic correlates have not been well-defined. Disorders of electrolyte and water metabolism with resultant retention of sodium and water are common in alcoholics. However, although volume relates to cardiac output, and cardiac output to blood pressure, plasma volume expansion does not appear to be important in the development of the hypertension associated with chronic alcoholic use. Most available evidence suggests that the primary underlying mechanism is increased vascular resistance. Chronic alcohol administration may produce an increased accumulation of cytoplasmic calcium in vascular smooth muscle with vascular hyperreactivity, vasoconstriction, and increased peripheral resistance. Although precise mechanisms have not been elucidated, this may result from (1) a direct effect of alcohol on plasma membrane permeability, sodium transport, and Na+/Ca2+ exchange, and/or (2) impaired calcium transport due to a secondary abnormality such as magnesium depletion, which is present in alcoholics.
饮酒与高血压患病率增加有关,尽管其相关机制和血流动力学关联尚未明确界定。酒精性肝病患者常见电解质和水代谢紊乱,进而导致钠和水潴留。然而,尽管血容量与心输出量相关,心输出量与血压相关,但血浆容量扩张似乎在慢性酒精使用相关高血压的发生发展中并不重要。现有多数证据表明,其主要潜在机制是血管阻力增加。长期饮酒可能导致血管平滑肌细胞质钙蓄积增加,伴有血管反应性增强、血管收缩和外周阻力增加。尽管确切机制尚未阐明,但这可能是由于:(1)酒精对质膜通透性、钠转运及Na+/Ca2+交换的直接作用,和/或(2)继发异常(如酒精性肝病患者存在的镁缺乏)导致钙转运受损。