Magnesium supplementation prevents the development of alcohol-induced hypertension.

Hsieh, Shao-Tung; Sano, Hiroshi; Saito, Komei; Kubota, Yoshihisa; Yokoyama, Mitsuhiro

doi:10.1161/01.hyp.19.2.175

Cited by 30 publications

(15 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2), due to the fact that fluid and food intake were reduced by alcohol consumption (data not shown). However, as reported in our previous study, which was performed under the same conditions (23), body weights in ethanol-administered rats were not decreased because of calories from ethanol ( Fig. 1).…”

Section: Studysupporting

confidence: 85%

Oral Taurine Supplementation Prevents the Development of Ethanol-Induced Hypertension in Rats.

Harada¹,

Kitazaki²,

Tsujino

et al. 2000

Hypertens Res

View full text Add to dashboard Cite

YOKOYAMATaurine is known to lower blood pressure in essential hypertension and some experimental hypertensive models. Taurine has also been reported to activate aldehyde dehydrogenase and to inhibit the elevation of plasma acetaldehyde concentration after ethanol intake. Because acetaldehyde, the first metabolite of ethanol, is suspected to be responsible for many adverse effects of alcohol consumption, we examined the effect of taurine supplementation on ethanol-induced hypertension and abnormalities in the intracellular cation metabolism in Witar-Kyoto rats. In Study 1, systolic blood pressure and intraplatelet free calcium were significantly higher in rats who received 15% ethanol in drinking water than in control rats. Oral taurine supplementation (1% taurine and 15% ethanol in drinking water) completely prevented the development of ethanol-induced hypertension. Intraerythrocyte sodium and intraplatelet free calcium were significantly decreased in taurine-supplemented rats as compared with rats who received 15% ethanol only. In Study 2, hemoglobin-associated acetaldehyde (HbAA) was measured as a marker of protein-bound acetaldehyde. HbAA was significantly elevated in rats who received 5% ethanol in drinking water as compared with control rats. Taurine supplementation (1% taurine and 5% ethanol in drinking water) significantly decreased HbAA. Our findings suggest that the oral supplementation of taurine prevents ethanol-induced hypertension by decreasing protein bound acetaldehyde and altering the cation handling by the membrane. (Hypertens Res 2000; 23: 277-284)

show abstract

Section: Studysupporting

confidence: 85%

Oral Taurine Supplementation Prevents the Development of Ethanol-Induced Hypertension in Rats.

Harada¹,

Kitazaki²,

Tsujino

et al. 2000

Hypertens Res

View full text Add to dashboard Cite

show abstract

“…8,19 -22 Conversely, hypertension is ameliorated by increasing K ϩ , Ca 2ϩ , and Mg 2ϩ or by decreasing NaCl intake. [23][24][25][26] Presumably, these dietary alterations influence ionic events at the cellular level, leading to altered tissue function, but this has been difficult to determine because previous measurements of steady state cellular ion content of, eg, K ϩ , often required cell suspension in artificial media, the use of chelating agents that distribute not only into cytosol but into other cell compartments as well, or even the disruption of cell membranes. Furthermore, focusing on single ions rather than on their mutual interaction often leads to artificial controversies in which K ϩ , Na ϩ , Ca 2ϩ , and Mg 2ϩ have each been claimed as the "most" important ionic determinant of pathologic processes such as hypertension.…”

Section: Discussionmentioning

confidence: 99%

Relation of Cellular Potassium to Other Mineral Ions in Hypertension and Diabetes

et al. 2001

View full text Add to dashboard Cite

Abstract-To investigate the role of intracellular potassium (K i )and other ions in hypertension and diabetes, we utilized 39 K-, 23 Na-, 31 P-, and 19 F-nuclear magnetic resonance (NMR) spectroscopy to measure K i , intracellular sodium (Na i ), intracellular free magnesium (Mg i ), and cytosolic free calcium (Ca i ), respectively, in red blood cells of fasting normotensive nondiabetic control subjects (nϭ10), untreated (nϭ13) and treated (nϭ14) essential hypertensive subjects, and diabetic subjects (nϭ5). In 12 subjects (6 hypertensive and 6 normotensive controls), ions were also measured before and after the acute infusion of 1 L of normal saline. Compared with those in controls (K i ϭ148Ϯ2.0 mmol/L), K i levels were significantly lower in hypertensive (132.2Ϯ2.9 mmol/L, sigϭ0.05) and in type 2 diabetic subjects (121.2Ϯ6.8 mmol/L, sigϭ0.05). K i was higher in treated hypertensives than in untreated hypertensives (139Ϯ3.1 mmol/L, sigϭ0.05) but was still lower than in normals. Although no significant relation was observed between basal K i and Na i values, saline infusion elevated Na i (PϽ0.01) and reciprocally suppressed K i levels (142Ϯ2.4 to 131Ϯ2.2 mmol/L, PϽ0.01). K i was strongly and inversely related to Ca i (rϭϪ0.846, PϽ0.001), and was directly related to Mg i (rϭ0.664, PϽ0.001). We conclude that (1) K i depletion is a common feature of essential hypertension and type 2 diabetes, (2) treatment of hypertension at least partially restores K i levels toward normal, and (3)

show abstract

“…49,50,52 It is possible that magnesium and calcium are depleted in habitual drinkers, and the alcohol-induced changes in these minerals may contribute to BP elevation and arrhythmia. 3,53 ALCOHOL AND HYPERTENSION Epidemiological studies Numerous epidemiological observational studies have examined the relationship between alcohol consumption and BP or hypertension. Almost all of them have shown that habitual drinkers have a higher BP Alcohol, blood pressure and cardiovascular disease Y Kawano and higher prevalence of hypertension than nondrinkers.…”

Section: Actions Of Alcohol On Water and Electrolyte Metabolismmentioning

confidence: 99%

“…They noted increases in the concentration of platelet intracellular calcium ions and the uptake of calcium in the aorta. Hsieh et al 53 identified increases in BP and intracellular calcium ions and a decrease in intracellular magnesium ions after 4 weeks of ethanol administration (15%) to rats. They suggested a role of magnesium deficiency in ethanolinduced hypertension as the BP elevation was attenuated by magnesium supplementation.…”

Section: Experimental Studiesmentioning

confidence: 99%

Physio-pathological effects of alcohol on the cardiovascular system: its role in hypertension and cardiovascular disease

Kawano

2010

Hypertens Res

View full text Add to dashboard Cite

Alcohol has complex effects on the cardiovascular system. The purpose of this article is to review physio-pathological effects of alcohol on cardiovascular and related systems and to describe its role in hypertension and cardiovascular disease. The relationship between alcohol and hypertension is well known, and a reduction in the alcohol intake is widely recommended in the management of hypertension. Moreover, alcohol has both pressor and depressor actions. The latter actions are clear in Oriental subjects, especially in those who show alcohol flush because of the genetic variation in aldehyde dehydrogenase activity. Repeated alcohol intake in the evening causes an elevation in daytime and a reduction in nighttime blood pressure (BP), with little change in the average 24-h BP in Japanese men. Thus, the hypertensive effect of alcohol seems to be overestimated by the measurement of casual BP during the day. Heavy alcohol intake seems to increase the risk of several cardiovascular diseases, such as hemorrhagic stroke, arrhythmia and heart failure. On the other hand, alcohol may act to prevent atherosclerosis and to decrease the risk of ischemic heart disease, mainly by increasing HDL cholesterol and inhibiting thrombus formation. A J-or U-shaped relationship has been observed between the level of alcohol intake and risk of cardiovascular mortality and total mortality. It is reasonable to reduce the alcohol intake to less than 30 ml per day for men and 15 ml per day for women in the management of hypertension. As a small amount of alcohol seems to be beneficial, abstinence from alcohol is not recommended to prevent cardiovascular disease. INTRODUCTIONAlcohol has complex effects on the cardiovascular system. The relationship between alcohol and hypertension is well known, and a restriction of alcohol intake is widely recommended as a part of lifestyle modifications in the management of hypertension. 1-6 Alcohol has both pressor and depressor actions, however, and the genetic susceptibility regarding alcohol metabolism influences the cardiovascular effect of alcohol. 3,7 The effect of alcohol on blood pressure (BP) is also modified by several factors, such as the level of consumption, time period after the last drink and overall drinking behavior.Alcohol consumption is associated with several cardiovascular diseases, such as brain hemorrhage, heart failure and arrhythmia, as well as with other disorders. 3,[8][9][10][11] Heavy drinking and alcoholism not only lead to medical problems but are also serious social concerns. However, alcohol also seems to have beneficial effects, including the prevention of ischemic heart disease. It has been shown that cardiovascular and all-cause mortality is lower in light drinkers compared with nondrinkers. 3,[8][9][10][11][12] The purpose of this article is to review physio-pathological effects of alcohol on cardiovascular and related systems and to describe its role

show abstract

Magnesium supplementation prevents the development of alcohol-induced hypertension.

Cited by 30 publications

References 46 publications

Oral Taurine Supplementation Prevents the Development of Ethanol-Induced Hypertension in Rats.

Oral Taurine Supplementation Prevents the Development of Ethanol-Induced Hypertension in Rats.

Relation of Cellular Potassium to Other Mineral Ions in Hypertension and Diabetes

Physio-pathological effects of alcohol on the cardiovascular system: its role in hypertension and cardiovascular disease

Contact Info

Product

Resources

About