Cardiovascular Risk Factors and Magnesium JoAnn Guest

[Guest guest]

Cardiovascular Risk Factors and Magnesium

JoAnn Guest

Oct 22, 2004 20:07 PDT

 

Cardiovascular Risk Factors and Magnesium: Relationships to

Atherosclerosis, Ischemic Heart Disease and Hypertension

http://www.mgwater.com/alturacv.shtml

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B.M. Altura, B.T. Altura

 

Department of Physiology, State University of New York Health

Science

Center at Brooklyn, N.Y., USA

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Key Words. Atherogenesis - Coronary vasospasm Bioenergetics,

cellular -

Dietary Mg intake - Lipid accumulation- Modulation of Ca metabolism

in

cardiac and vascular muscle

 

Abstract. Hypertension and atherosclerosis are well-known precursors

of

ischemic heart disease, stroke and sudden cardiac death. Although

there

is general agreement that the atheroma is the hallmark of

atherosclerosis and is found in coronary obstruction, there is no

agreement as to its etiology.

 

It is now becoming clear that a lower than normal dietary intake of

Mg

can be a strong risk factor for hypertension, cardiac arrhythmias,

ischemic heart disease, atherogenesis and sudden cardiac death.

 

Deficits in serum Mg appear often to be associated with arrhythmias,

coronary vasospasm and high blood pressure. Experimental animal

studies

suggest interrelationships between atherogenesis, hypertension (both

systemic and pulmonary) and ischemic heart disease.

 

Evidence is accumulating for a role of Mg2+ in the modulation of

serum

lipids and lipid uptake in macrophages, smooth muscle cells and the

arterial wall. Shortfalls in the dietary intake of Mg clearly exist

in

Western World populations, and men over the age of 65 years, who are

at

greatest risk for development and death from ischemic heart disease,

have the greatest shortfalls in dietary Mg. It is becoming clear

that Mg

exerts multiple cellular and molecular effects on cardiac and

vascular

smooth muscle cells which explain its protective actions.

 

Introduction

 

Globally, among the leading causes of death, hypertension and

atherosclerosis rank at the top of the list. These cardiovascular

diseases, obviously, are the forerunners or precursors of ischemic

heart

disease, stroke and sudden cardiac death.

 

Among mortality and morbidity indices for man, ischemic heart

disease

ranks at the top of the list. In the industrialized world ischemic

heart

disease is the leading killer and accounts for approximately 35% of

all

deaths each year. The incidence of this disorder rises to 80% in

people

over 70 years of age. The most common cause of death results from

insufficient coronary blood flow.

 

Some deaths can occur rather suddenly, for example, sudden-death

ischemic heart disease. Possibly, as many as 40-60% of the latter

may

occur in the complete absence of any prior atherosclerosis, thrombus

formations or cardiac arrhythmias [for review, see 1].

 

These syndromes are often referred to as nonocclusive sudden-death

ischemic heart disease. Other forms of ischemic heart disease can

result

in death as a consequence of an acute coronary occlusion or

ventricular

fibrillation, whereas others are still thought to come about from

slow,

progressive occlusion of coronary vessels over a period of weeks to

years.

 

Although there is general agreement that the atheroma is the

hallmark of

atherosclerosis and is found in coronary obstruction, there is no

agreement at present as to either the characterization of the early

intimal changes or their etiology.

 

Hallmarks of Atherosclerosis

 

Irrespective of the etiology of atheromas, the lesions usually

consist

of a fibrous cap containing smooth muscle cells, macrophages, foam

cells

and lymphocytes [for reviews, see 2, 31.

 

In addition, there appears formation of dangerous necrotic centers

consisting of cholesterol crystals, cholesterol esters, calcium ions

and

dying foam cells. What produces these characteristics is not

completely

known.

 

Although vascular smooth muscle cells in atheromas change from a

contractile to a noncontractile state and become responsive to

platelet-derived growth factor and elaborate connective tissue, no

one

knows how these cells are transformed.

 

Finally, although T lymphocytes, platelets, neutrophils and

macrophages

are found in developing atherosclerotic plaques, it is not known

what

allows such cells to enter the vessel wall or be attracted to the

potential plaque site.

 

Theories on the Etiology of Hypertension

 

Although many theories have been suggested in the etiology of

hypertension, it is not known why peripheral blood vessels exhibit

increased responsiveness to pressor substances [for review, see 4].

It

is not known why peripheral blood vessels undergo vasoconstriction

either.

 

And, of course, it is not known why hypertension leads to a high

incidence of strokes and sudden cardiac death.

 

Is it possible that the atherosclerotic and hypertensive events are

related to the diet or the dietary intake of a particular food

substance, metabolite or element? Are these vascular disease

processes

related to mineral metabolism, per se?

 

Why is the incidence of hypertension, atherosclerosis, sudden-death

ischemic heart disease and stroke low, in South African Bantu

natives,

Bedouins in the Arabian desert, Aborigines in Australia and

Greenlanders?

 

And why, when these indigenous populations move to Western

civilizations, do the incidences of these cardiovascular diseases

equal

those of Western civilized populations?

 

Relation of Soil Magnesium Content and Water Hardness to Incidence

of

Cardiovascular Disease

 

If one divides the US into Eastern and Western halves, you begin to

see

several interesting phenomena. First, the soil Mg content in the

Eastern

USA is about one third that of the Western USA (table 1). Second,

the

water hardness of the Eastern USA is one half that of the Western

USA

(table 1).

 

Third, although the death rate for cardiovascular diseases in the

Eastern USA is significantly higher than that of the Western USA,

noncardiovascular death rates are equivalent (table 1). Similar

phenomena have been observed in Canada, Finland and South Africa [6-

11].

In 1983, Leary and Reves [10] published findings from 12 magisterial

districts in South Africa demonstrating that as the concentration of

Mg

in the drinking water was found to be less and less, in various

geographical regions, the death rate from ischemic heart disease was

seen to rise more and more. Studies such as these and others like

them

[6-9, 11] suggest that maybe there is an important relationship

between

dietary Mg intake and the incidence of heart disease.

 

 

Importance of Dietary Mg versus Ca Intake

 

Approximately, 12 years ago, Karppanen et al. [12] in Finland

published

interesting findings in which it was suggested that the ratio of

dietary

calcium to magnesium may be linked to ischemic heart disease.

According

to the most recent USA dietary surveys, the Ca:Mg ratio in average

American diets is rising [ 13].

 

Incidence of Hypomagnesemia in Hospitalized Patients: Possible

Relationship to Incidence of Cardiovascular Disease

 

During the past 10 years, a considerable number of studies have

appeared

which indicate that hospitalized patients have incidences of

hypomagnesemia ranging from 7 to 60%, depending upon the type of

patient

[for reviews, see [1, 14].

 

What is particularly important to note here is that many of these

patients are in acute coronary care units and intensive care units.

Many

of these patients present with numerous cardiovascular abnormalities

including cardiac arrhythmias, atrial fibrillation, hypertension,

strokes and myocardial infarctions.

 

Deficit of Myocardial Mg Content and Ischemic Heart Disease

 

Ever since the early studies of Iseri et al. [15] in 1952, there has

been an increasing number of case reports and studies which indicate

that hearts of patients who die of sudden-death ischemic heart

disease

exhibit deficits of Mg [for reviews, see 9, 11, 14]. On the average.

there appears to be about a 20% deficit in cardiac Mg content in

these

patients.

 

Mg is the only metal to be decreased to this extent consistently. It

is

important to note that we and others have found that coronary

arteries

of such victims often exhibit deficits of 30-40% in total Mg

content.

These deficits in Mg content do not appear to be a consequence of

cardiac necrosis for several reasons. First of all, nonnecrosed

cardiac

tissue areas clearly exhibit approximately the same 20% reduction in

myocardial Mg, unlike the necrotic areas which can exhibit deficits

of

almost 50% in Mg content of [9, 11, 16-181.

 

Anginal History and Myocardial Mg Content

 

It is rather interesting to note that patients with a history of

angina

on autopsy exhibit severe cardiac deficits in Mg, whereas patients

without a history of angina appear to exhibit a near-normal

myocardial

Mg content [19]. Is deficiency of myocardial Mg limited only to

angina

pectoris and sudden-death ischemic heart disease, or is Mg

deficiency

also found in other myocardial syndromes?

 

Loss of Myocardial Mg in Cardiac lschemic Syndromes

 

An examination of the literature reveals a growing body of evidence

to

indicate that loss of myocardial Mg is seen in a host of myocardial

lschemic syndromes from myocardial infarction, arrhythmias, torsades

de

pointes to experimental and iatrogenic ischemic injuries [for

reviews,

see 9, 11, 14]. Many of these are clearly associated with prior

histories of atherosclerosis and/or hypertension.

 

Hypertensive Vascular Disease and Mg Deficiency

 

Is hypertensive disease associated with Mg deficiency in blood

and/or

tissues? If so, hypertensive disease should be brought about in some

cases solely by Mg deficiency, and hypertension should be

exacerbated by

Mg deficiency. Finally, a variety of hypertensive syndromes should

be

amenable to treatment with Mg salts.

 

At this point, we would like to take the opportunity to review some

of

this evidence, including some of our own findings.

 

A number of studies in spontaneously hypertensive rats clearly

demonstrate (except for one study by Overlack et al. [20]) that the

serum content of total Mg is significantly reduced in hypertensive

animals [for review, see 21].

 

An examination of most of the clinical studies on hypertensive

patients,

so far studied, who received diuretics, where blood pressure often

continued to rise, demonstrates that serum Mg is clearly, reduced by

about 15-20% [for review, see 21].

 

A few years ago, Resnick et al. [22] examined red blood cells from

hypertensive subjects and found that the ionized Mg2+ determined by

31P

nuclear magnetic resonance (NMR) spectroscopy was inversely related

to

the diastolic blood pressure. That is. the greater the elevation in

diastolic blood pressure, the lower the ionized red blood cell Mg2+

content [22].

 

Salt-Induced Hypertension and Mg

 

If all of this is so, then even salt-induced hypertension might be

expected to be associated with Mg deficiency and should be treatable

with Mg salts.

 

We, therefore, utilized various groups of uninephrectomized male

Wistar

rats given weekly implants of deoxycorticosterone acetate in order

to

produce malignant salt-induced hypertension. Some animals were

allowed

to drink Mg aspartate HCl freely, daily, for periods up to 12 weeks.

Others were allowed to drink the Mg salt 4 weeks after salt

hypertension

for an additional 12 weeks.

 

Table 2 summarizes some of our data. By 3 weeks, mean arterial blood

pressure was elevated in all deoxycorticosterone acetate + salt

groups.

However, by 9 weeks, the groups which received Mg supplements

exhibited

significant lowering of blood pressure. Many of the untreated

animals

with malignant hypertension died at 4-7 weeks of blood pressure

levels

in excess of 245 mm Hg.

 

Figure 1 clearly shows that there is a deficit in serum Mg in

uninephrectomized rats with salt-induced hypertension and that serum

Mg

levels are restored to normal in rats allowed to drink Mg.

Interestingly, serum phosphate levels are also reduced in animals

with

malignant hypertension, whereas rats given Mg exhibit a restoration

of

phosphate to normal levels. Hypophosphatemia itself is known to

produce

high blood pressure. Whether or not this contributes to salt-induced

hypertension in these animals is under investigation.

 

 

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In view of these experiments, we wondered whether pulmonary

hypertension

is amenable to Mg therapy and whether the vascular remodeling that

normally takes place in the pulmonary circulation in this syndrome

can

be ameliorated or prevented by Mg. Rats were administered 40 mg/kg

of

monocrotaline. This plant extract is known to produce specific

pulmonary

hypertension in all mammals so far investigated, and a pulmonary,

vascular remodelling takes place within 14-21 days. We examined all

animals 21 days after monocrotaline [23].

 

Animals which received monocrotaline exhibited significant elevation

in

pulmonary blood pressure [23]. Controls and control animals which

received oral Mg aspartate HCl exhibited no alteration in pulmonary

pressure. However, monocrotaline-treated animals which received Mg

aspartate HCl for 21 days exhibited a significant amelioration of

pulmonary hypertension [23].

 

If true pulmonary hypertension is observed in human subjects or

animals,

the right ventricular to left ventricular ratio should be elevated.

Our

monocrotaline- treated animals clearly manifested a right

ventricular to

left ventricular ratio that was increased as expected [23].

 

The monocrotaline-treated animals, however, which received Mg

therapy,

clearly exhibited reduction in the elevated right ventricular to

left

ventricular ratio suggesting a reversal of the pulmonary

hypertension

[23, 24].

 

If the latter is true, then we would expect to see attenuation of

the

pulmonary hyperplasia of the arterial wall normally seen in

pulmonary

hypertension.

 

Arteriolar and arterial walls clearly underwent significant

hyperplasia,

after monocrotaline, with encroachment of the lumens [23-25]. Mg

therapy, reversed the monocrotaline-induced hyperplasia. Obviously,

elevated levels of Mg must exert significant attenuating effects on

collagen and elastin synthesis and smooth muscle cell hyperplasia

[23-25]. These actions might therefore be of value in the treatment

of

atherosclerosis.

 

Genetic Predisposition to Hypertension and Tissue Mg Levels

 

Is there any evidence to indicate that teenagers, that is children

below

the age of 20 years, may exhibit Mg deficits which could be a risk

factor for the development of hypertensive vascular disease?

 

In the past 2 years, a group in Japan (headed by Shibutani in Hyogo

Medical College) has begun to publish a number of reports which

suggest

that male children of parents with a genetic history of familial

hypertension exhibit significant deficits in red blood cell Mg

content

[26]. This may be the first study to clearly suggest that a

predilection

for high blood pressure could develop in young males if,

genetically,

they exhibit deficits in tissue Mg.

 

Dietary Mg Intake and Atherogenesis

 

If atherosclerosis is a strong risk factor for hypertension,

ischemic

heart disease and stroke, and these are truly interrelated, then Mg

should exert strong effects on atherogenesis. We, therefore, decided

to

examine rabbits given 1 or 2% cholesterol with varying Mg intake

[27].

The Mg intake was varied from 40% of normal to normal or 2.5 times

the

normal intake. The animals were followed serially for up to 10

weeks.

Aortas were excised and stained with Sudan 4 and examined

histologically

for lesions.

 

No lesions could be found from rabbits ingesting normal chow with

normal

lipid and Mg intake or normal synthetic chow [27].

 

High cholesterol intake in the presence of normal dietary Mg

resulted in

significant atherosclerotic lesions.

 

The animals receiving low dietary Mg and 2% cholesterol exhibited

lesions far in excess of those observed with normal Mg intake [27].

However, if the intake of Mg was raised to 2.5 times normal, despite

the

high cholesterol intake, the atheromas were greatly attenuated,

suggesting that Mg intake can modulate atherogenesis.

 

Overall, the data clearly indicate that the greater the lipid

intake,

the greater the number of atherosclerotic lesions [27]. In addition,

these data indicate that the lower the dietary intake of Mg, the

greater

the risk for developing atheromas.

Stating this another way, it is also clear that the higher the

intake of

Mg, the less chance for developing atheromas despite high lipid

intake.

 

Our data would seem to suggest that Mg must exert significant

effects on

smooth muscle, macrophage and monocyte accumulation of lipids and

might

affect chemotaxis and the activity of growth factors implicated in

atherogenesis.

 

If this is all true, then dietary intake of Mg would be an important

and

maybe critical factor in the prevention of atherosclerosis,

hypertension, cardiac disease, stroke and sudden cardiac death. In

addition, such a hypothesis would suggest that a suboptimal dietary

intake of Mg should put human subjects at risk for development of

cardiovascular disease.

 

Progressive Decline in Dietary Intake of Mg over the Past 90 Years

 

It is rather interesting that if one examines the intake of Mg over

the

past 90 years, we note that there is a progressive and alarming

decline

in Mg intake at the present time (table 3).

 

An examination of a recent US Department of Agriculture HANES

dietary

survey reported in 1985 indicates clear and significant shortfalls

in

dietary Mg, assuming an intake of 350 mg/day is needed for normal Mg

balance [13]. It is also clear from this survey that men over the

age of

65 years, who are known to present the greatest risk for death from

ischemic heart disease (vide supra), exhibit the greatest shortfalls

for

dietary Mg of all male age groups. This may be more than

coincidental.

 

Protective Mechanisms of Mg Action against Death from Ischemic Heart

Disease

 

If Mg can ameliorate atherosclerosis and hypertension, and promote

coronary vasodilation and unloading of the heart (8, 9, 11,14, 21],

are

these the primary mechanisms of the protective actions of magnesium

ions

against death from ischemic heart disease, or does Mg exert direct

actions on myocardial bioenergetics as well [14, 21]? We will

therefore

present and discuss some of our recent experiments on intact

perfused

hearts which may have direct bearing on this question.

 

31P NMR Spectroscopy, Myocardial Bioenergetics, [Mg2+]i and [pH]i

 

In order to get an assessment of cellular bioenergetics, we have

employed 31P NMR spectroscopy and near-infrared spectroscopy [28,

29].

When the perfusate magnesium ion concentration is elevated to

hypermagnesemic levels (2.4-4.8 mM), coronary flow, stroke volume,

cardiac output and aortic pressure are seen to rise rather

significantly, suggesting that Mg ions can exhibit inotropic-like

effects. At the same time, the heart rate and rate-pressure product

are

decreased, suggesting that Mg unloads the heart and increases its

efficiency.

 

The 31P NMR spectra for elevated magnesium indicated that elevated

[Mg2+]o results in elevated phosphocreatine levels (by 22-40%).

Second,

inorganic phosphate levels were decreased, and there were chemical

shifts in the 31P NMR spectra produced by elevated Mg [28, 29].

 

Clearly, elevated Mg resulted in spectral shifts, which suggest that

alterations in myocardial intracellular, free Mg ions and

intracellular

pH must have occurred. Elevation in [Mg2+]o (i.e. 2.4-4.8 mM)

clearly

resulted in elevation of intracellular, free Mg ions and

alkalinization

of the cytosol. Elevation of the intracellular pH in the presence of

elevation of intracellular, free Mg ions would increase the creatine

kinase reaction, resulting in more phosphocreatine, contractile

force

and stroke volume, exactly as we have observed.

 

It was clear from our data that elevation in extracellular Mg ions

to

4.8 mM resulted in a 40% rise in phosphocreatine.

 

 

Influence of [Mg2+]o on Mitochondrial Levels of Cytochrome Oxidase

and

Oxymyoglobin

 

Using a noninvasive near-infrared spectroscopic technique, we have

clearly found that the mitochondrial levels of oxidized cytochrome

aa3

and oxymyoglobin are increased by elevation in extracellular Mg ions

31P

NMR [28]. These data coupled with the data suggest that the

efficiency

of the myocardium is enhanced by Mg ions.

 

Reduction in [Mg2+]o Results in Myocardial Cellular Reduction in

[Mg2+]i, [pH]i, Oxymyoglobin and Oxidized Cytochrome aa3

 

If, however, the extracellular Mg ions are reduced below normal, the

cytosol becomes acidic and the intracellular free Mg ion level is

significantly altered [30].

 

Preliminary experiments indicate that reduction in extracellular Mg

ions

or hypomagnesemia leads to rapid falls in oxymyoglobin levels.

Finally,

our recent near-infrared experiments indicate that subjection of

intact

rat hearts to hypomagnesemia clearly, results in increased

mitochondrial

levels of reduced cytochrome oxidase aa3.

 

Conclusions

 

It is becoming clear that a large body of epidemiologic data

supports

the idea that lower than normal dietary intake of Mg can be a strong

risk factor for hypertension, cardiac arrhythmias, ischemic heart

disease and sudden cardiac death. Lower than normal myocardial and

coronary vascular Mg content seems to pose serious risks for angina,

coronary vasospasm, ischemic heart disease and sudden cardiac death.

 

Deficits in serum Mg appear often to be associated with arrhythmias,

coronary vasospasm and high blood pressure.

 

Experimental animal studies seem to suggest interrelationships

between

atherogenesis, hypertension and ischemic heart disease. Evidence is

clearly accumulating to implicate a role for Mg in the modulation of

serum lipids, lipid uptake in macrophages, smooth muscle cells and

the

arterial wall.

 

There clearly appear to be considerable shortfalls in dietary intake

of

Mg in Western world populations, and that men over the age of 65

years,

who are at greatest risk for death from ischemic heart disease, have

the

greatest shortfalls in dietary Mg.

 

Although Mg clearly influences calcium uptake and distribution in

vascular smooth muscle cells which can modulate vasomotor tone [3,

9,

14, 21, 28, 31-33], it is now becoming clear that Mg ions can

directly

alter myocardial cellular bioenergetics and influence (possibly

dictate)

efficiency of the myocardium. Noninvasive techniques such as 31P NMR

spectroscopy, near-infrared spectroscopy and image analysis should

aid

in the clarification of the role of Mg as an important risk factor

in

cardiovascular disease.

 

Acknowledgement

 

The original work received herein was supported in part by NIAAA

research grant AA-08674.

 

References

 

1 Altura BM: Ischemic heart disease and magnesium. Magnesium

1988;7:57-67.

 

2 Ross R: The pathogenesis of atherosclerosis. N Engl J Med

1986;314:488-500.

 

3 Lee KT, Onodera K. Tanaka K (eds): Atherosclerosis II. Recent

Progress

in Atherosclerosis Research. Ann NY Acad Sci 1990;598:1-589.

 

4 Laragh J, Brenner BM: Hypertension: Pathophysiology, Diagnosis and

Management. New York, Raven Press, 1990, vol 1 and 11.

 

5 Masironi R: Geochemistry and cardiovascular diseases. Philos Trans

R

Soc Lond 1979;288:193-203.

 

6 Marier J, Neri LC, Anderson TW: Water hardness, human health and

importance of magnesium, rep No 17581. Ottawa, Natl Res Council

Canada,1979.

 

7 Marier J, Neri LC: Quantifying the role of magnesium in the

interrelationship between human mortality/morbidity and water

hardness.

Magnesium 1985;4:53-59.

 

8 Altura BM: Magnesium and regulation of contractility: in Altura BM

(ed): Advances in Microcirculation: Regulation of the

Microcirculation.

Basel, Karger. 1982, pp 77-113.

 

9 Altura BM, Altura BT: Magnesium-calcium interaction and

contraction of

arterial smooth muscle in ischemic heart diseases, hypertension and

vasospastic disorders. in Wester P (ed): Electrolytes and the Heart.

New

York, Transmedica, 1983, pp 41-56.

 

10 Leary, WP, Reyes AJ: Magnesium and sudden death. S Afr Med J

1983;64:697-698.

 

11 Altura BM, Altura BT: New perspectives on the role of magnesium

in

the pathophysiology of the cardiovascular system. I. Clinical

aspects.

Magnesium 1985;4:226-244.

 

12 Karppanen HR. Pennanen R. Passinen L: Minerals, coronary heart

disease and sudden coronary death. Adv Cardiol 1978;25:9-24.

 

13 Morgan KJ, Stampley GE, Zabik ME, Fischer DR: Magnesium and

calcium

intakes in the US population. J Am Coll Nutr 1985;4:195-206.

 

14 Altura BM, Altura BT: Magnesium and the cardiovascular system:

Experimental and clinical aspects updated: in Sigel H, Sigel A

(eds):

Metal Ions in Biological Systems. New York, Dekker, 1990, vol 26:

Compendium on Magnesium: Its Physiology, Biochemistry, and

Nutrition. pp

359-416.

 

15 lseri LC, Alexander EC, MacCaughey RS, Boyle AJ, Meyers G: Water

and

electrolyte content of cardiac and skeletal muscle in heart failure

and

myocardial infarction. Am Heart J 1952;43:215-227.

 

16 Heggtveit MA, Tanser P, Hunt B: Magnesium content of normal and

ischemic hearts. Proc 7th Int Congr Clin Pathol, Montreal, 1969, p

53.

 

17 Speich M, Bousquet B, Nicholas G, Delajartre AY: Incidences de

l'infarctus du myocarde sur les teneurs en magnesium plasmatique

erythrocytaire et cardiaque. Rev Fr Endocrinol Clin 1979;20:159-163.

 

18 Speich M, Bousquet B, Nicholas G: Concentrations of magnesium,

calcium, potassium and sodium in human heart muscle after acute

myocardial infarction. Clin Chem 1980;26:1662-1665.

 

19 Johnson CJ, Peterson DR, Smith EK: Myocardial tissue

concentration of

magnesium and potassium in men dying suddenly from ischemic heart

diease. Am J Clin Nutr 1979;32:967-970.

 

20 Overlack A, Zenzen JG, Ressel C, Muller HM, Stumpe KO: Influence

of

magnesium on blood pressure and the effect of nifedipine in rats.

Hypertension 1987;9:139-143.

 

21 Altura BM, Altura BT: Role of magnesium in pathogenesis of

hypertension. Relationship to its actions on cardiac and vascular

smooth

muscle: in Laragh JH, Brenner BM (eds): Hypertension:

Pathophysiology.

Diagnosis and Management. New York, Raven Press, vol 1, 1990, pp

1003-1025.

 

22 Resnick LM, Gupta RK, Laragh JH: lntracellular magnesium in

erythrocytes of essential hypertension relation to blood pressure

and

serum divalent cations. Proc Natl Acad Sci USA 1984;81:6511-6515.

 

23 Mathew R, Gloster ES, Altura BT, Altura BM: Magnesium aspartate

hydrochloride attenuates monocrotaline pulmonary artery hypertension

in

rats. Clin Sci 1988;75:661-667.

 

24 Mathew R, Altura BM: Magnesium and the lungs. Magnesium

1988:7:173-187.

 

25 Mathew R, Altura BT, Altura BM: Strain differences in pulmonary

hypertensive response to monocrotaline alkaloid and the beneficial

effect of oral magnesium treatment. Magnesium 1989;8:110-116.

 

26 Shibutani Y, Sakamoto MK, Katsuno S, Yoshimoto S, Matsura T:

Serum

and erythrocyte magnesium levels in junior high school students:

Relation to blood pressure and a family history of hypertension.

Magnesium 1988;7:188-194.

 

27 Altura BT, Brost M, Bloom S, Barbour RL, Stempak JK, Altura BM:

Magnesium dietary intake modulates blood lipid levels. Proc Natl

Acad

Set USA 1990;87:1840-1844.

 

28 Altura BM, Barbour RL, Reiner SD, Zhang A, Cheng TP, Down JL,

Gupta

RK, Wu F, Altura BT: Influence of Mg2+ on distribution of ionized

Ca2+

in vascular smooth muscle and on cellular bioenergetics and

intracellular free Mg2+ and pH in perfused hearts probed by digital

imaging microscopy, 31P NMR and reflectance spectroscopy: in Zhakari

S,

Witt E (eds): Imaging Techniques in Alcohol Research. Monograph 21,

Washington, NIAAA, pp 235-272.

 

29 Barbour RL, Altura BM, Reiner SD, Dowd TL, Gupta RK, Wu F, Altura

BT:

Influence of Mg2+ on cardiac performance, intracellular free Mg2+

and pH

in perfused hearts as assessed with 31P-NMR spectroscopy. Magnes

Trace

Elem 1992;10:99-116.

 

30 Barbour RL, Gupta RK, Dowd TL, Reiner SD, Wu F, Altura BT, Altura

BM:

Response of cardiac energetics to elevated and low magnesium in

perfused

rat hearts. J Magn Reson Imaging, in press.

 

31 Altura BM, Altura BT: Magnesium and vascular tone and reactivity.

Blood Vessels 1978;15:5-16.

 

32 Altura BM, Altura BT: Magnesium, electrolyte transport and

coronary

vascular tone. Drugs 1984; 28(suppl 1): 120-142.

 

33 Altura BM, Altura BT, Carella A, Turlapaty PDMV: Ca2+ coupling in

vascular smooth muscle: Mg2+ and buffer effects on contractility and

membrane Ca2+ movements. Can J Physiol Pharmacol 1982;60:459-482.

 

Prof. Dr. B.M. Altura

Box 31

SUNY Health Science Center 450 Clarkson Avenue

Brooklyn, NY 11203 (USA)

 

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THE MAGNESIUM WEB SITE

 

From the 1996 FDA Science Forum. Abstract.

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http://www.mgwater.com/mgrda.shtml

 

Is the RDA for Magnesium Too Low?

N.A. Littlefield and B.S. Hass, NCTR, FDA, Jefferson AR 72079

 

Since magnesium (Mg), an essential nutrient, is abundant in the

environment and food supply, it is generally assumed that Mg

deficiency

is not a problem.

 

However, the literature indicates that deficiencies may exist in

both

thirdworld and industrialized nations and may influence cardiac and

vascular diseases, diabetes, bone deterioration, renal failure,

hypothyroidism, and stress.

 

Because Mg in certain forms is not easily absorbed and no classical

symptoms exist, the problem of Mg deficiency is readily masked,

especially in high risk groups such as diabetics, alcoholics, those

taking hypertension medication, and some athletes.

 

The current Recommended Daily Allowance (RDA) for the US is 6

mg/Kg/day,

which translates to 420 mg for a 70 Kg man. The estimated intake in

the

US is 300 mg/day.

 

Studies show that as much as 3 times this amount may be needed by

the

general population and especially by those predisposed to cardiac

disease states. This report summarizes recent research on Mg in

human

diets and the results of Mg deficiencies.

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JoAnn Guest

mrsjo-

www.geocities.com/mrsjoguest/Genes