The nerve-heart connection in the pro-oxidant response to Mg-deficiency

Tejero-Taldo, M. I.; Kramer, Jay H.; Mak, I. Tong; Komarov, Andrei M.; Weglicki, William B.

doi:10.1007/s10741-006-9191-7

Cited by 50 publications

(33 citation statements)

References 83 publications

(129 reference statements)

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“…Mg 2ϩ -deficient mice exhibit severe cardiovascular inflammation and oxidative injury, which are normalized by Mg 2ϩ supplementation. 34,35 In our study, dietary Mg 2ϩ ameliorated aldosterone-induced damaging actions and reduced fibrosis in the kidney, heart, and aorta, similar to effects previously reported. 10 We examined expression of IL-6, a secondary cytokine, VCAM1, a proinflammatory adhesion molecule and COX2, a key enzyme involved in the inflammatory response.…”

Section: Discussionsupporting

confidence: 89%

Downregulation of Renal TRPM7 and Increased Inflammation and Fibrosis in Aldosterone-Infused Mice

et al. 2008

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Abstract-Hyperaldosteronism is associated with hypertension, cardiovascular fibrosis, and electrolyte disturbances, including hypomagnesemia. Mechanisms underlying aldosterone-mediated Mg 2ϩ changes are unclear, but the novel Mg 2ϩ transporters TRPM6 and TRPM7 may be important. We examined whether aldosterone influences renal TRPM6/7 and the TRPM7 downstream target annexin-1 and tested the hypothesis that Mg 2ϩ administration ameliorates aldosterone-induced cardiovascular and renal injury and prevents aldosterone-associated hypertension. C57B6 mice were studied (12 weeks, nϭ8 to 9/group); (1) control group (0.2% dietary Mg 2ϩ ), (2) Mg 2ϩ group (0.75% dietary Mg 2ϩ ), (3) aldosterone group (Aldo, 400 g/kg/min and 0.9% NaCl drinking water), and (4) AldoϩMg 2ϩ group. Blood pressure was unaltered by aldosterone and was similar in all groups throughout the experiment. Serum Na ϩ was increased and serum K ϩ and Mg 2ϩ decreased in the Aldo group. Aldo mice had hypomagnesuria and proteinuria, and renal, cardiac, and aortic fibrosis, which were normalized by Mg 2ϩ supplementation. Renal and cardiovascular expression of interleukin-6, VCAM1 and COX2 was increased in the Aldo group. Magnesium attenuated renal and cardiac interleukin-6 content and decreased renal VCAM1 and cardiac COX2 expression (PϽ0.05). Aldosterone decreased expression of renal TRPM7 and the downstream target annexin-1 (PϽ0.05) without effect on TRPM6. Whereas Mg 2ϩ increased mRNA expression of TRPM6 and TRPM7, it had no effect on TRPM7 and annexin-1 protein content. Our data demonstrate that aldosterone mediates blood pressure-independent renal and cardiovascular fibrosis and inflammation through Mg 2ϩ -sensitive pathways. We suggest that altered Mg 2ϩ metabolism in hyperaldosteronism may relate to TRPM7 downregulation and that Mg 2ϩ protects against cardiovascular and renal damaging actions of aldosterone. A ldosterone, classically thought to be produced by the zona glomerulosa of the adrenal cortex and implicated in the maintenance of sodium, potassium, and acid-base balance and blood pressure regulation, is now considered a hormone with pleiotropic actions, produced by multiple tissues, including the heart, vessels, kidney, and brain. 1,2 In addition to regulating renal electrolyte excretion, aldosterone contributes to vascular inflammation, oxidative stress, collagen deposition, and endothelial dysfunction. [3][4][5] As such, aldosterone has been implicated in the development of cardiovascular and renal remodeling, fibrosis, and injury. The importance of these processes in clinical medicine is being increasingly recognized by the cardiovascular and renal protective effects of the aldosterone antagonists, spironolactone and eplerenone. 6,7 The profibrotic and proinflammatory actions of aldosteronism are accompanied by disturbances in cation homeostasis including hypomagnesemia and decreased intracellular free magnesium concentration ([Mg 2ϩ ] i ). 8,9 Recent evidence suggests that aldosterone-induced cardiovascular inflammation is induced, in part...

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Section: Discussionsupporting

confidence: 89%

Downregulation of Renal TRPM7 and Increased Inflammation and Fibrosis in Aldosterone-Infused Mice

et al. 2008

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“…Clinical and animal studies have described influence of magnesium on inflammation [36][37] . In present study, hypomagnesaemia was associated with increased levels of inflammatory markers suggesting associated low grade inflammation.…”

Section: Discussionmentioning

confidence: 99%

Relation of magnesium with insulin resistance and inflammatory markers in subjects with known Coronary artery disease

Mahalle¹,

Mk²,

Kulkarni³

et al. 2014

J Cardiovasc. Dis. Res.

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INTRODUCTIONMagnesium is the second most abundant intracellular cation and is an essential element that has numerous biological functions. Magnesium is plentiful in green leafy, cereal, grain, nuts and legumes, however, refining or processing of food may deplete magnesium content by nearly 85% 1 . About 30% of ingested magnesium is absorbed by distal small intestine. Magnesium acts as a cofactor in many of enzymatic reactions in the human body. Magnesium is essential for the synthesis of nucleic acids and proteins, for intermediary metabolism particularly related to the neuromuscular and cardiovascular systems. Over 300 enzymes are dependent on magnesium. Magnesium influences the enzymatic activity by binding to legends such as ATP in ATP-requiring enzymes, enolase, pyruvate kinase, and pyrophosphatase, leading to conformational change during ABSTRACT Background: Magnesium plays an important role in regulating insulin action and secretion. Dietary magnesium deficiency and hypomagnesemia have been associated with inflammation. There is paucity of data regarding this in Indian subjects. Hence, we studied the relation of serum and dietary magnesium with insulin resistance (IR) and inflammatory markers. Methods & Results:We studied the relation of serum high sensitive C-Reactive Protein (hsCRP), interlukin-6 (IL-6) and tumor Necrosis Factor (TNF-α) with cardiovascular risk factors in three hundred coronary artery disease patients. Nutrition assessment was done at the time of recruitment. Patients were evaluated for anthropometry, cardiovascular risk factors, and blood samples were collected. Patients were divided into three groups according to serum magnesium levels; ≤1.6 (Group 1), >1.6-2.6 (Group 2) and: >2.6 mg/dl (Group 3) and into two groups according to recommended dietary allowance (RDA) for magnesium (≤350 mg/day and >350 mg/day). More than half of patients (58.6%) were having hypomagnesemia and 62% were consuming magnesium below RDA. Insulin and IR was significantly higher and insulin sensitivity was significantly lower in group 1 compared to group 2 and 3. Insulin and IR was correlated negatively; and insulin sensitivity was correlated positively with serum magnesium. Similarly inflammatory markers were significantly higher in group1 when compared with group 2 and 3 and they were correlated negatively with serum magnesium. Dietary magnesium was positively correlated with serum magnesium. Insulin and IR were significantly higher and insulin sensitivity was significantly lower in subjects with low RDA for magnesium. Insulin and IR were correlated negatively and sensitivity was correlated positively with dietary magnesium. Inflammatory markers; IL-6, TNF-α, and hs CRP were significantly high in subjects with low RDA for magnesium and were correlated negatively with dietary magnesium. Conclusion: Hypomagnesemia and low dietary magnesium is associated with IR and inflammatory markers in patients with coronary artery disease.

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“…Mg deficiency also favours the release of vaso--constrictive and platelet aggregating factors (derived from fatty acid metabolism and endothelium), increases the thromboxane B2 to prostaglandin I2 (TxB 2 /PgI 2 ) ratio and enhances intravascular blood coagulation (Ceremuzynski et al, 1978;Franz 2004;Dong et al, 2008;Sontia and Touyz, 2007). Most interestingly, Mg deficiency itself doesn't induce specific pathology but reduces the tolerance to secondary stress (Tejero--Taldo et al, 2006). The active transport systems between plasma and cerebrospinal fluid enable elevated and relatively constant Mg concentrations in the CSF (typically 1.1 mmol/l in CSF compared to 0.8 mmol/l in plasma) .…”

Section: Magnesium Interaction With Stress Pathwaysmentioning

confidence: 99%

Magnesium in the Central Nervous System

Vink

Nechifor

2011

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This book, containing chapters written by some of the foremost experts in the field of magnesium research, brings together the latest in experimental and clinical magnesium research as it relates to the central nervous system. It offers a complete and updated view of magnesium's involvement in central nervous system function and in so doing, brings together two main pillars of contemporary neuroscience research, namely providing an explanation for the molecular mechanisms involved in brain function, and emphasizing the connections between the molecular changes and behavior.

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The nerve-heart connection in the pro-oxidant response to Mg-deficiency

Cited by 50 publications

References 83 publications

Downregulation of Renal TRPM7 and Increased Inflammation and Fibrosis in Aldosterone-Infused Mice

Downregulation of Renal TRPM7 and Increased Inflammation and Fibrosis in Aldosterone-Infused Mice

Relation of magnesium with insulin resistance and inflammatory markers in subjects with known Coronary artery disease

Magnesium in the Central Nervous System

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