Effect of ethanol on blood pressure—role of magnesium

We have read with interest the recent paper of Rosito et al,1 who investigated a dose-dependent biphasic effect of ethanol on 24-h blood pressure in normotensive subjects. They concluded that acute alcohol intake elicts a biphasic hemodynamic response, causing first vasodilation and later a pressor effect. In addition, they stated that a higher prevalence of hypertension in alcohol abusers seen in epidemiological surveys results from blood pressure measurements done in the period of transiently increased blood pressure during ethanol washout. Acute and chronic consumption of alcoholic beverages are recognized to be a major contributor to blood pressure elevation in human and animal subjects.2, 3, 4 Several epidemiological studies have demonstrated a link between the average alcohol intake of more than 20 g/day and the severity of hypertension.5 In addition, severe acute or, especially, chronic alcohol ingestion is known to cause hypomagnesemia.6, 7 Pathophysiological reasons for magnesium deficiency in alcoholism may be magnesium-deficient nutrition, malabsorption, increased intestinal or perspiratory excretion, hyperaldosteronism, disturbed catecholamine metabolism, liver cirrhosis, or increased urinary magnesium excretion.8, 9 Furthermore, it is known that a moderation of alcohol intake reduces blood pressure values and leads to an increase in lowered intracellular magnesium stores.6, 10 In this context we studied 35 healthy subjects, 24 patients with a steatosis, and 19 patients with a cirrhosis of liver due to chronic alcoholism.7 The average alcohol consumption was 15.4 ± 2.9 g/day in the steatosis patients and 22.5 ± 3.6 g/day in the patients with cirrhosis of liver (P < .05) (means ± SD). Blood pressure values were significantly increased in the cirrhosis group (149.7 ± 6.8/94.7 ± 9.5 mm Hg) (P < .01). Plasma Mg++ concentrations, intracellular (red blood cell) Mg++ concentrations, and membrane (red blood cell) Mg++ concentrations were significantly decreased in the hypertensive liver cirrhosis patients versus the healthy subjects (Table 1). PLASMA, INTRACELLULAR AND MEMBRANE MAGNESIUM CONCENTRATIONS IN 35 CONTROLS (C), 24 PATIENTS WITH STEATOSIS (S), AND 19 PATIENTS WITH CIRRHOSIS OF LIVER (CL) DUE TO ALCOHOLISM (MEANS ± SD) As compared with healthy subjects, P < .05. As compared with healthy subjects, P < .01. As compared with healthy subjects, P < .001. PLASMA, INTRACELLULAR AND MEMBRANE MAGNESIUM CONCENTRATIONS IN 35 CONTROLS (C), 24 PATIENTS WITH STEATOSIS (S), AND 19 PATIENTS WITH CIRRHOSIS OF LIVER (CL) DUE TO ALCOHOLISM (MEANS ± SD) As compared with healthy subjects, P < .05. As compared with healthy subjects, P < .01. As compared with healthy subjects, P < .001. We conclude that an additional effect of hypomagnesemia on blood pressure exists in alcoholism, especially in chronic disease. As there is only a small ethanol washout phase in chronic alcoholism, a biphasic hemodynamic response as described by Rosito et al seems to be of minor interest when hypertension becomes established, probably in association with a cellular magnesium deficiency.1 Furthermore, it could be speculated that a cellular and membrane magnesium deficiency in chronic alcoholism could prevent the vasodilation described as a part of the biphasic effect after acute alcohol intake.