Magnesium Deficiency Produces Spasms of Coronary Arteries: Relationship to Etiology of Sudden Death Ischemic Heart Disease

Turlapaty, Prasad; Altura, Burton M.

doi:10.1126/science.7361117

Cited by 374 publications

(171 citation statements)

References 21 publications

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“…In a recent in vitro strudy, we demonstrated that acute withdrawal of magnesium induces contractile responses in canine coronary arteries (Turlapaty & Altura, 1980). Furthermore, we also demonstrated that magnesium withdrawal potentiated the contractile responses of coronary arteries to various vasoactive agents which have been implicated, clinically, in induction of coronary vasospasm.…”

Section: Litroductionmentioning

confidence: 82%

“…Since it is known that vasoactive agents utilize different sources of calcium (Ca) for their contractile responses (Weiss, 1978), it has been suggested that in a magnesium-deficient state, Ca2' influx might be enhanced, thereby resulting in an increased tone and contractility (Altura & Altura, 1974;1978;1981;Altura, 1979;Turlapaty & Altura, 1980). It is also possible that Mg2+-deficiency might increase the sensitivity of postsynaptic receptors, as it has been shown by several investigators that Mg2e can alter the sensitivity of non-cardiac blood vessels to several neurohumoral I©The Macmillan Press Ltd 1982 substances (Somlyo, Woo & Somlyo, 1966;Altura & Altura, 1971;1978;Altura, 1975;Turlapaty, Carrier & Jurevics, 1975;Altura, Altura & Waldemar, 1976;Goldstein & Zsoter, 1978).…”

Section: Litroductionmentioning

confidence: 99%

“…Because of possible segmental differences in coronary arterial reactivity (Altura, 1966) width), were tied at both ends with sutures and arranged isometrically, in vitro, under a resting tension of 1.0 g for large arteries (LC, CF) and 0.5 g for small arteries (LCB, RCB), respectively, as described previously (Turlapaty & Altura, 1980). These were incubated in 20 ml muscle chambers containing Krebs Ringer bicarbonate solution (composition, mmol/l: NaCl 118, KCl 4.7, CaCI2 2.5, KH2PO41.2, MgSO41.2, glucose 10, and NaHCO3 25) and maintained at 37°C through which a mixture of 02 (95%) and CO2 (5%) was bubbled.…”

Section: Animals and Coronary Artery Preparationsmentioning

confidence: 99%

See 2 more Smart Citations

Withdrawal of Magnesium Enhances Coronary Arterial Spasms Produced by Vasoactive Agents

Altura

Turlapaty

1982

British J Pharmacology

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Section: Litroductionmentioning

confidence: 82%

Section: Litroductionmentioning

confidence: 99%

Section: Animals and Coronary Artery Preparationsmentioning

confidence: 99%

See 1 more Smart Citation

Withdrawal of Magnesium Enhances Coronary Arterial Spasms Produced by Vasoactive Agents

Altura

Turlapaty

1982

British J Pharmacology

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“…98,99 Hypomagnesemia has also been shown to cause an increase in coronary vascular reactivity and could potentially accelerate plaque rupture. 100,101 Ang II can trigger most of the changes reported to be associated with magnesium deficiency, including induction of pro-oxidant and proinflammatory conditions. 102 Moreover, Ang II induces the synthesis of plasminogen activator inhibitor type 1 in endothelial cells.…”

Section: Plaque Stabilizationmentioning

confidence: 99%

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

2009

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Since their inception, angiotensin-converting enzyme (ACE) inhibitors have been used as first-line therapy for the treatment of cardiovascular and renal diseases. They restore the balance between the vasoconstrictive salt-retentive and hypertrophy-causing peptide angiotensin II (Ang II) and bradykinin, a vasodilatory and natriuretic peptide. As ACE is a promiscuous enzyme, ACE inhibitors alter the metabolism of a number of other vasoactive substances. ACE inhibitors decrease systemic vascular resistance without increasing heart rate and promote natriuresis. They have been proven effective in the treatment of hypertension, and reduce mortality in congestive heart failure and left ventricular dysfunction after myocardial infarction. They inhibit ischemic events and stabilize plaques. Furthermore, they delay the progression of diabetic nephropathy and neuropathy and act as antioxidants. Ongoing studies have elucidated protective roles for them in both memory-related disorders and cancer. INTRODUCTIONIn recent years, stressful and fiercely competitive lifestyles and food habits have compounded the problems of hypertension. Long-standing and stressful, progressively rising hypertension can lead to many disorders, including myocardial infarction (MI), cerebrovascular events, congestive heart failure, peripheral arterial insufficiency, premature mortality 1 and renal dysfunction leading to glomerulosclerosis and kidney artery aneurysm. 2 A number of therapies are available, but angiotensin-converting enzyme (ACE) inhibitors have been the preferred first-line therapy for hypertension, congestive heart failure, left ventricular (LV) systolic dysfunction and MI. 3,4 ACE inhibitors (ACEis) have been in use for the past two decades, and the interest in them is still growing. Recently, the discovery of domain-selective ACEis and new members of the renin-angiotensin system (RAS) (that is, angiotensin-converting enzyme 2) have again fueled the interest of researchers. Some new studies have expanded the already impressive clinical profile of ACEis. This review traces some already known and new facets of ACE inhibition and introduces new advances in the designing of a new generation of ACEis.

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“…Serotonin receptor activity is altered by changes in levels of ionized Mg +2 [31,32] and vasoconstriction induced by serotonin can be effectively blocked by pretreatment with Mg +2 [33]. Experimental Mg +2 deficiency leads to generation and release of substance P [34] which is thought to act on sensory fibers and cause the pain in headache [35].…”

Section: Discussionmentioning

confidence: 99%

A comparative study of magnesium, flunarizine and amitriptyline in the prophylaxis of migraine

et al. 2000

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Circumstantial evidence points to the possible role of magnesium (Mg +2 ) deficiency in the pathogenesis of migraine and has raised questions about the clinical utility of magnesium as a therapeutic regimen in migraine. This was a prospective, randomized, double-blind, placebocontrolled trial comparing the efficacy and tolerability of 1830 mg magnesium citrate (23 patients), 10 mg flunarizine (22 patients) and 10 mg amitriptyline (20 patients) with placebo (22 patients) in the prophylaxis of migraine diagnosed according to the criteria of the International Headache Society. Patients were evaluated for attack frequency, severity and drug side effects monthly for 3 months. Magnesium, flunarizine and amitriptyline were all superior to placebo (p<0.001) in reducing both attack frequency and severity after the first month. There was no significant difference between the 3 active drugs in reduction of attack frequency and severity. No serious side effects were observed and the frequencies of side effects were not significantly different in all treatment groups. Our results show that oral magnesium is an effective and well tolerated drug in the prophylaxis of migraine and compares well to established drugs like flunarizine and amitriptyline both in effectiveness and occurence of side effects. Magnesium may be an alternative drug in migraine prophylaxis, but more and larger comparative trials are needed to confirm these results.

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Magnesium Deficiency Produces Spasms of Coronary Arteries: Relationship to Etiology of Sudden Death Ischemic Heart Disease

Cited by 374 publications

References 21 publications

Withdrawal of Magnesium Enhances Coronary Arterial Spasms Produced by Vasoactive Agents

Withdrawal of Magnesium Enhances Coronary Arterial Spasms Produced by Vasoactive Agents

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

A comparative study of magnesium, flunarizine and amitriptyline in the prophylaxis of migraine

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