Inhibitors of Na+/Mg2+ exchange activity attenuate the development of hypertension in angiotensin II-induced hypertensive rats

Touyz, Rhian M.; Yao, Guoying

doi:10.1097/00004872-200302000-00025

Cited by 27 publications

(25 citation statements)

References 43 publications

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“…Although not statistically significant, magnesium supplementation decreased blood pressure levels, urine protein levels, and eGFR. These results may imply that magnesium supplementation alleviates glomerular hyperfiltration via the relationship between magnesium and the renin–angiotensin system [51]. …”

Section: Discussionmentioning

confidence: 99%

Magnesium Replacement Improves the Metabolic Profile in Obese and Pre-Diabetic Patients with Mild-to-Moderate Chronic Kidney Disease: A 3-Month, Randomised, Double-Blind, Placebo-Controlled Study

Toprak

Kurt

Sarı

et al. 2017

Kidney Blood Press Res

20,429

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Background/Aims: Magnesium is an essential mineral for many metabolic functions. There is very little information on the effect of magnesium supplementation on metabolic profiles of chronic kidney disease (CKD) patients. The aim of this study was to assess the influence of magnesium supplementation on metabolic profiles of pre-diabetic, obese and mild-to-moderate CKD patients with hypomagnesemia. Methods: A total of 128 hypomagnesemic, pre-diabetic and obese patients with an estimated glomerular filtration rate between 90 and 30 ml/min/1.73m² were enrolled in a randomised, double-blind, placebo-controlled trial. Patients in the magnesium group received 365 mg of oral magnesium (n = 57) once daily for 3 months, while patients in the control group received a placebo (n = 61), also once daily for 3 months. Hypomagnesemia is defined by a serum magnesium level <1.8 mg/dl in males and <1.9 mg/dl in females; obesity is defined as a body mass index ≥30 kg/m²; and pre-diabetes is defined as fasting plasma glucose ≥100 but <126 mg/dl. The primary end point of the study was the change in insulin resistance measured by the homeostastic model assessment for insulin resistance (HOMA-IR). Results: At the end of follow-up, insulin resistance (-24.5 vs. -8.2%, P = 0.007), HOMA-IR index (-31.9 vs. -3.3%, P < 0.001), hemoglobin A1c (-6.6 vs. -0.16%, P < 0.001), insulin (-29.6 vs. -2.66%, P < 0.001), waist circumference (-4.8 vs. 0.55%, P < 0.001) and uric acid (-0.8 vs. 2.2%, P = 0.004) were significantly decreased in terms of mean changes; albumin (0.91 vs. -2.91%, P = 0.007) and magnesium (0.21 ± 0.18 vs. -0.04 ± 0.05 mg/dl, P < 0.001) were significantly increased in those taking magnesium compared with a placebo. The decrease in metabolic syndrome (-10.5 vs. -4.9%, P = 0.183), obesity (-15.7 vs. -8.2%, P = 0.131), pre-diabetes (-17.5 vs. -9.8%, P = 0.140), and systolic (-5.0 ± 14.8 vs. 0.22 ± 14.9 mm Hg, P = 0.053) and diastolic (-3.07 ± 9.7 vs. 0.07 ± 9.6 mm Hg, P = 0.071) blood pressure did not achieve to a significant level after study. Conclusion: Our data support the argument that magnesium supplementation improves the metabolic status in hypomagnesemic CKD patients with pre-diabetes and obesity.

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Section: Discussionmentioning

confidence: 99%

Magnesium Replacement Improves the Metabolic Profile in Obese and Pre-Diabetic Patients with Mild-to-Moderate Chronic Kidney Disease: A 3-Month, Randomised, Double-Blind, Placebo-Controlled Study

Toprak

Kurt

Sarı

et al. 2017

Kidney Blood Press Res

20,429

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“…Considering that TRPM7 is a Mg 2ϩ -permeant channel responsible for transcellular Mg 2ϩ transport (28) and an important mediator of cell growth (7,39), it is possible that altered cellular Mg 2ϩ homeostasis and abnormal VSMC function in hypertension may be related to defective TRPM7 expression/ activity. We previously demonstrated that TRPM7 knockdown by siRNA in VSMCs was associated with reduced [Mg 2ϩ ] i and altered cellular growth, which was reversible when Mg 2ϩ was normalized (9).…”

Section: Discussionmentioning

confidence: 99%

Differential regulation of transient receptor potential melastatin 6 and 7 cation channels by ANG II in vascular smooth muscle cells from spontaneously hypertensive rats

Touyz¹,

He²,

Montezano³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…104-111 Also, in Ang II-induced hypertension in rats, inhibition of the Na + /Mg 2+ antiport resulted in reduced blood pressure, normalization of vascular and renal MAP kinase activity and improved vascular structure. [104][105][106][107][108][109][110][111] TRPM6 and TRPM7 have been implicated in a number of vascular pathologies, including endothelial dysfunction and hypertension. 112, 113 We and others demonstrated that VSMC from mouse, rat and human resistance arteries possess TRPM6 and TRPM7 cation channels and that TRPM7 is critically involved in regulating Mg 2+ influx, cell viability, proliferation and contraction/dilation.…”

Section: Trpm7 Mg 2+ and Hypertensionmentioning

confidence: 99%

Transient Receptor Potential Melastatin 7 (TRPM7) Cation Channels, Magnesium and the Vascular System in Hypertension

Yogi

Callera

Antunes

et al. 2011

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp ypertension is the most common chronic disease in developed and developing societies and a major risk factor for morbidity and mortality. 1, 2 The most common form of hypertension is 'essential hypertension' the causes of which remain unknown. Among the many factors implicated in the pathophysiology of hypertension are neurohumoral, renal, metabolic, race, genetic, environmental factors and alterations in cellular cations, such as sodium (Na + ), calcium (Ca 2+ ), potassium (K + ) and magnesium (Mg 2+ ) have been shown to be related to the increase in systolic blood pressure. 3-7Mg 2+ , an abundant intracellular divalent cation, functions as an allosteric modulator of several proteins, controls nucleotide and protein synthesis, regulates Na + , K + , and Ca 2+ channels and is critical for myriad enzymatic reactions, particularly those involving kinases. 8,9 Mg 2+ is stored primarily in bone and the intracellular compartments of muscle and soft tissues, with less than 1% of total body Mg 2+ circulating in the blood. 9,10 Mg 2+ homeostasis depends primarily on the balance between intestinal uptake and renal excretion. Mg 2+ deficiency results from reduced dietary intake, intestinal malabsorption or renal loss. Mammalian cells tightly control magnesium levels within a narrow range (0.70-1.1 mmol/L) by specific regulatory mechanisms operating at the level of intraorganelle compartmentalization, intracellular magnesium buffering and at regulating magnesium entry and efflux across the cell membrane.Epidemiological studies indicate that low Mg 2+ status is associated with many diseases including diabetes, metabolic syndrome, dyslipidemia and hypertension.

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Inhibitors of Na+/Mg2+ exchange activity attenuate the development of hypertension in angiotensin II-induced hypertensive rats

Abstract: Our data demonstrate that inhibitors of Na -dependent Mg transport attenuate development of hypertension in rats infused with Ang II. These findings suggest a possible role for Na /Mg exchange activity in the pathogenesis of Ang II-dependent hypertension.

Cited by 27 publications

References 43 publications

Magnesium Replacement Improves the Metabolic Profile in Obese and Pre-Diabetic Patients with Mild-to-Moderate Chronic Kidney Disease: A 3-Month, Randomised, Double-Blind, Placebo-Controlled Study

Magnesium Replacement Improves the Metabolic Profile in Obese and Pre-Diabetic Patients with Mild-to-Moderate Chronic Kidney Disease: A 3-Month, Randomised, Double-Blind, Placebo-Controlled Study

Differential regulation of transient receptor potential melastatin 6 and 7 cation channels by ANG II in vascular smooth muscle cells from spontaneously hypertensive rats

Transient Receptor Potential Melastatin 7 (TRPM7) Cation Channels, Magnesium and the Vascular System in Hypertension

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