No abstract

The effect of chronic alcohol administration on blood pressure was investigated in 7-week-old Wistar rats. Tail-cuff blood pressure was significantly higher in rats who received 15% ethanol in drinking water than in control rats. Intracellular free calcium concentration of lymphocytes was increased, while magnesium concentration of erythrocyte, aorta, and skeletal muscle and erythrocyte ouabain-sensitive u Na efflux rate constant (K m ) were decreased in alcohol-induced hypertensive rats but not in control rats. Extracellular fluid volume was also increased in alcohol-administered rats. Oral magnesium supplementation (1% MgO in rat chow) attenuated the development of alcohol-induced hypertension accompanied by increased magnesium concentration of erythrocyte, aorta, skeletal muscle, and K a and decreased intraerythrocyte sodium concentration. Norepinephrine half-life time of the heart and spleen was also increased in magnesium-supplemented rats. Blood pressure significantly correlated positively with intracellular calcium concentration and extracellular fluid volume, negatively with magnesium concentration of erythrocyte, aorta, skeletal muscle, and K n . These results suggest that increased intracellular calcium, which was partly due to magnesium depletion and suppressed sodium pump activity, and expanded body fluid volume had a possible role in the development of alcohol-induced hypertension. It is also suggested that oral magnesium supplementation had a hypotensive effect on alcohol-induced hypertension possibly through decreased intracellular sodium concentration caused by an activation of sodium pump and decreased sympathetic nervous activity. {Hypertension 1992;19:175-182)

A 77-year-old woman with type II diabetes mellitus was admitted to our hospital in August/ 1995 with severe hyperlipidemia. She had taken feedings through a nasogastric tube with 1,000 ml (1,000 kcal) of Ensureliquid  daily since 1993 because of the muscle weakness after rhabdomyolysis. Her serum total cholesterol was 515 mg/dl and triglyceride was 3,378 mg/dl despite administration of 10 mg of simvastatin daily. After substitution of a standard diet starting August 21, we found significant decreases of total cholesterol from 725 mg/dl to 194 mg/dl and triglyceride from 4,680 mg/dl to 550 mg/dl within 37 days. We also found a severe decrease in her serum total carnitine level of 22 µ µ µ µ µmol/l (normal range 45-91 µ µ µ µ µmol/l) before changing the diet, suggesting secondary carnitine deficiency. Severe hyperlipidemia was reversed by changing the carnitine deficient diet (Ensureliquid  ) to a carnitine-containing diet. We suggested that the development of hyperlipidemia was related to the carnitine deficiency. J Atheroscler Thromb, 2003; 10: 321-324.

Intracellular free magnesium and calcium concentrations of platelets from 21 mild essential hypertensive patients and 8 normotensive individuals were measured using mag-fura2, a recently developed fluorescent indicator, and fura2, respectively. Compared with normotensives, intracellular free magnesium concentration was significantly decreased (0.32 ± 0.10 vs. 0.50 ± 0.15 mmol/1, mean ± SD, p < 0.001) and intracellular free calcium concentration was significantly increased (40.2 ± 9.0 vs. 21.7 ± 11.8 nmol/1, p < 0.001) in the hypertensives. In all subjects, mean blood pressure correlated negatively with intracellular free magnesium (r = -0.57, p < 0.001) and positively with intracellular free calcium (r = 0.48, p < 0.02). Furthermore, intracellular free magnesium correlated negatively with intracellular free calcium. In contrast, serum and intraerythrocyte magnesium concentrations did not differ between the two groups. These results suggest that the decreased intracellular free magnesium of platelets concomitant with the increased intracellular free calcium may participate in the pathophysiology of essential hypertension. (Hypertens Res 1992; 15: 105-110)

It is known that moderation of alcohol intake reduces blood pressure, although the exact mechanism has not yet been established. To clarify the hypotensive mechanism of alcohol reduction, we evaluated the change in cellular magnesium and sodium metabolism during alcohol reduction in mild hypertensive patients. We measured intraerythrocyte sodium and magnesium, intraplatelet free magnesium concentrations, and erythrocyte ouabain-sensitive 22Na efflux rate constant (Kos) in 17 mild essential hypertensive patients regularly consuming more than 40 g/day of alcohol, before and after 4 weeks of alcohol reduction, and 12 age-matched nondrinking hypertensives. Intraerythrocyte magnesium (P < .01) and intraplatelet free magnesium (P < .05) concentrations were significantly lower in drinkers than in nondrinkers. In drinkers, advice to reduce alcohol intake for 4 weeks resulted in a reduction in self-reported alcohol consumption from 461.7 to 71.6 g/week, a significant fall in both supine systolic blood pressure (136.3 +/- 10.8 to 130.8 +/- 11.3 mm Hg, P < .001) and supine diastolic blood pressure (85.1 +/- 8.6 to 82.6 +/- 8.7 mm Hg, P < .05). The fall in mean blood pressure correlated positively with the reduction in weekly alcohol consumption. Intraerythrocyte magnesium and Kos were increased (P < .05, P < .01, respectively), while intraerythrocyte sodium was decreased (P < .01). The increase in intraerythrocyte magnesium correlated negatively with the fall in mean blood pressure and positively with the increase in Kos, which correlated negatively with the decrease in intraerythrocyte sodium.(ABSTRACT TRUNCATED AT 250 WORDS)