Brief Reviews: Magnesium in Heart Muscle

Polimeni, Philip I.; Page, Ernest W.

doi:10.1161/01.res.33.4.367

Cited by 128 publications

(32 citation statements)

References 58 publications

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“…Past estimates suggest that free Mg ++ is in the range of 1-2 mM (Polimeni and Page, 1973), but recent studies indicate that intracellular Mg ++ of muscle cells might be as low as 0.2 mM (Maughan, 1983). Moreover, it has been reported that Mg ++ leaks from heart cells during ischemic episodes (Polimeni and Page, 1973). Our results also predict that phosphorylation of Tnl and acidic pH are additive in their effects on the Ca ++ sensitivity of myofibrillar ATPase activity.…”

Section: Discussionsupporting

confidence: 52%

“…The exact Mg ++ con-390 centration within heart cells is not known with certainty. Past estimates suggest that free Mg ++ is in the range of 1-2 mM (Polimeni and Page, 1973), but recent studies indicate that intracellular Mg ++ of muscle cells might be as low as 0.2 mM (Maughan, 1983). Moreover, it has been reported that Mg ++ leaks from heart cells during ischemic episodes (Polimeni and Page, 1973).…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of the activation and troponin calcium binding of dog cardiac myofibrils by acidic pH.

Blanchard¹,

Solaro²

1984

Circulation Research

167

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SUMMARY. The aim of experiments described here was to test whether deactivation of cardiac myofibrils in acidic pH is associated with decreases in amounts of calcium bound to myofilament troponin. We determined the amounts of myofibrillar bound calcium attributable to troponin, from measurements of calcium binding to myofibrils and to myosin and from determination of the troponin C content of the myofibrillar preparations (0.40 nmol troponin C/mg protein). In measurements done at 2 mvi free magnesium, 2 imi (magnesium-adenosine triphosphate, ionic strength 0.12, 22°C, the pCa 50 (-log of the half maximally activating molar free calcium) for myofibrillar magnesium-adenosine triphosphatase activity was 5.87 at pH 7.0, 5.49 at pH 6.5, and 5.04 at pH 6.2. This change in calcium sensitivity of myofibrillar magnesium-adenosine triphosphatase activity was present whether or not ethyleneglycol-bis(/3-aminoethyl ether)-N,N'-tetraacetic acid, was used to buffer the free calcium and whether or not myofibrillar troponin I had been phosphorylated by cyclic adenosine 3',5'-monophosphate-dependent protein kinase. However, the change in pCa 50 of myofibrillar adenosine triphosphatase activity induced by acidic pH, was greater when free magnesium was reduced from 2.0 to 0.05 HIM, and less when free magnesium was increased from 2.0 mM to 10 and 15 mM. The change in pCa 50 with acidic pH was less if the ionic strength was reduced from 0.12 to 0.035 M. The magnesium-adenosine triphosphatase activity of troponin/tropomyosin-free myofibrils was independent of pCa and unaffected by a reduction of pH from 7.0 to 6.5. The affinity of myofibrillar troponin C for calcium decreased as pH was reduced from 7.0 to 6.5 and to 6.2 with and without ethyleneglycolbis(/?-aminoethyl ether)-N,7V'-tetraacetic acid, and in a manner predicted from the effect of acidic pH on pCa 50 for myofibrillar activation. Our results are consistent with the idea that at least part of the mechanism responsible for deactivation of the adenosine triphosphatase activity of cardiac myofilaments in acidic pH is a reduction in the affinity of myofibrillar troponin C for calcium. (Circ Res 55: 382-391, 1984)

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Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Inhibition of the activation and troponin calcium binding of dog cardiac myofibrils by acidic pH.

Blanchard¹,

Solaro²

1984

Circulation Research

167

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“…6). This concentration of magnesium in the assay more closely approximated the physiological activity level of the divalent cation to which the enzyme is normally exposed (~1 iriM, Polimeni and Page, 1973). The findings indicate that adenylate cyclase may be an important point where adenosine exerts its inhibitory action on catecholamine effects in the myocardium.…”

Section: Discussionmentioning

confidence: 64%

Mechanism of adenosine inhibition of catecholamine-induced responses in heart.

Dobson¹

1983

Circulation Research

194

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SUMMARY. The properties of adenosine inhibition of catecholamine-induced responses were investigated, using an isolated rat heart preparation. Perfusion of hearts with 0.1 (IM isoproterenol increased myocardial cAMP content 2.8-fold, activation of cAMP-dependent protein kinase 4.4-fold, phosphorylase a formation 3.4-fold, left ventricular pressure 1.8-fold, rate of ventricular pressure development 2.1-fold, and rate of ventricular relaxation 2.2-fold within 1 minute. When perfused with the isoproterenol, 10 /IM adenosine reduced the catecholamine-produced increase in cAMP, cAMP-dependent protein kinase, and phosphorylase by 30-40%, and the elevation in left ventricular pressure and rate of ventricular pressure development by 40-70% within 40 seconds. More than 2 minutes were required for the nucleoside to significantly reduce the isoproterenol-elicited increase in the rate of ventricular relaxation. Perfusion of adenosine alone at concentrations from 0.1 to 10 fjM were without effect on the above parameters. Theophylline at 50 [IM had no effect alone on the above parameters but blocked the inhibitory actions of adenosine on the isoproterenol-induced responses. In the presence of 15 mM Mg ++ adenosine reduced by approximately 56% the 2-fold increase in myocardial membrane adenylate cyclase activity produced by 1 fiM isoproterenol without affecting basal or fluoride-stimulated activity. Adenosine also reduced the isoproterenol-induced increase in enzyme activity assayed at 1-2 mM Mg ++ , a level that more closely approximates the intracellular activity of the ion. The results suggest that physiological concentrations of adenosine attenuate the catecholamine-induced increase in cAMP content, cAMP-dependent protein kinase activation, phosphorylase a formation, and contractile parameters in the working heart, via reducing the /?-adrenergic activation of adenylate cyclase. (Circ Res 52:151-160, 1983)

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“…Interestingly, addition of Mg2, to platelets gelfiltered in the absence of Mg2' and Ca2+ promotes optimal aggregation and secretion responses while Ca2+ promotes disaggregation (50,51 ). It is possible that an initial burst of Mg2+ provided by damaged cells, which contain intracellular Mg2+ concentrations in excess of 15 mM (25)(26)(27)(28), and exposure to type I collagen could collectively induce the aggregation response. Macrophages and neutrophils also become activated during this phase, extravasating through the blood vessel wall, surrounding tissue and into the wound site.…”

Section: 33 34)mentioning

confidence: 99%

“…Under normal physiologic conditions the concentration of intracellular Mg2+ in the typical mammalian cell is reported to be between 15 and 30 mM and that of Ca2+ is only -1-2 mM (25)(26)(27)(28). On the other hand, extracellular levels of these two cations are about 1.0 and 2.5 mM, respectively (28,29).…”

Section: Introductionmentioning

confidence: 99%

Shifts in the concentrations of magnesium and calcium in early porcine and rat wound fluids activate the cell migratory response.

Grzesiak¹,

Pierschbacher²

1995

J. Clin. Invest.

119

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Accruing evidence indicates that the levels of extracellular Mg2+ and Ca2+ can have a distinct impact on the adhesive and migratory activities of many cell types. The physiological relevance of these observations, however, has remained largely unexplored. In the present study, wound fluids collected throughout the early stages of cutaneous wound repair were examined for possible Mg2" and Ca2+ fluctuations. Early in the process, when cell migration into the wound site is initiated, Mg2+ is elevated and Ca2+ is reduced (Mg2+ :Ca2+ = 1). As wound healing progresses, wound fluid concentrations of Mg2+ and Ca2+ begin to return to normal plasma levels (Mg2+ :Ca2+ = 0.4). When macrophages, keratinocytes, fibroblasts, and endothelial cells were exposed to dialyzed wound fluid, the migration stimulated by undialyzed wound fluid was lost. Addition back to dialyzed wound fluid of 24 h, postinjury concentrations of Mg2+ and Ca2+ restored all migratory stimulus. This observed migration is approximately twofold greater than when normal plasma Mg2+ and Ca2+ concentrations are present. Changes in the levels of Mg2+ and Ca2+ in wound fluid occur during the same period that inflammatory cells, keratinocytes, fibroblasts, and neovasculature have been shown to migrate during wound healing in vivo. Together, these data suggest that the impact of these changes on integrins and E-cadherin may play a direct role in the activation and maintenance of the migratory phenotypes of the cells involved in the wound healing process. (J. Clin. Invest. 1995. 95:227-233.)

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Brief Reviews: Magnesium in Heart Muscle

Cited by 128 publications

References 58 publications

Inhibition of the activation and troponin calcium binding of dog cardiac myofibrils by acidic pH.

Inhibition of the activation and troponin calcium binding of dog cardiac myofibrils by acidic pH.

Mechanism of adenosine inhibition of catecholamine-induced responses in heart.

Shifts in the concentrations of magnesium and calcium in early porcine and rat wound fluids activate the cell migratory response.

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