Magnesium Uptake by Intestinal Brush-Border Membranes of Spontaneously Hypertensive Rats

Gilles-Baillien, M.; Cogneau, M.

doi:10.3181/00379727-201-43489

Cited by 7 publications

(3 citation statements)

References 12 publications

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“…Underlying mechanisms for altered magnesium homeostasis in hypertension are unclear, but inborn errors of magnesium handling, decreased membrane permeability, altered Na ϩ / Mg 2ϩ exchange, defective membrane binding, and impaired cellular responsiveness have been implicated (66). My group recently suggested that dysregulation of vascular TRPM6 and/or TRPM7 also may play a role in aberrant cellular magnesium handling in hypertension (78, 206, 230).…”

Section: Magnesium and Hypertensionmentioning

confidence: 99%

Transient receptor potential melastatin 6 and 7 channels, magnesium transport, and vascular biology: implications in hypertension

Touyz¹

2008

American Journal of Physiology-Heart and Circulatory Physiology

133

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Magnesium, an essential intracellular cation, is critically involved in many biochemical reactions involved in the regulation of vascular tone and integrity. Decreased magnesium concentration has been implicated in altered vascular reactivity, endothelial dysfunction, vascular inflammation, and structural remodeling, processes important in vascular changes and target organ damage associated with hypertension. Until recently, very little was known about mechanisms regulating cellular magnesium homeostasis, and processes controlling transmembrane magnesium transport had been demonstrated only at the functional level. Two cation channels of the transient receptor potential melastatin (TRPM) cation channel family have now been identified as magnesium transporters, TRPM6 and TRPM7. These unique proteins, termed chanzymes because they possess a channel and a kinase domain, are differentially expressed, with TRPM6 being found primarily in epithelial cells and TRPM7 occurring ubiquitously. Vascular TRPM7 is modulated by vasoactive agents, pressure, stretch, and osmotic changes and may be a novel mechanotransducer. In addition to its magnesium transporter function, TRPM7 has been implicated as a signaling kinase involved in vascular smooth muscle cell growth, apoptosis, adhesion, contraction, cytoskeletal organization, and migration, important processes involved in vascular remodeling associated with hypertension and other vascular diseases. Emerging evidence suggests that vascular TRPM7 function may be altered in hypertension. This review discusses the importance of magnesium in vascular biology and implications in hypertension and highlights the transport systems, particularly TRPM6 and TRPM7, which may play a role in the control of vascular magnesium homeostasis. Since the recent identification and characterization of Mg2+-selective transporters, there has been enormous interest in the field. However, there is still a paucity of information, and much research is needed to clarify the exact mechanisms of magnesium regulation in the cardiovascular system and the implications of aberrant transmembrane magnesium transport in the pathogenesis of hypertension and other vascular diseases.

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Section: Magnesium and Hypertensionmentioning

confidence: 99%

Transient receptor potential melastatin 6 and 7 channels, magnesium transport, and vascular biology: implications in hypertension

Touyz¹

2008

American Journal of Physiology-Heart and Circulatory Physiology

133

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“…102-106 Underlying mechanisms for altered magnesium homeostasis in hypertension are unclear, but inborn errors of Mg 2+ handling, decreased membrane permeability, altered Na + /Mg 2+ exchange, defective membrane binding and impaired cellular responsiveness have been implicated. 107 We and others showed that the Na + /Mg 2+ antiport function, which plays a major role in Mg 2+ extrusion in cardiac, renal and VSMC, is altered in hypertension. 108-111 Furthermore, amiloride and quinidine-mediated inhibition of Na + /Mg 2+ antiport increased vascular [Mg 2+ ]i and attenuated the development of hypertension in SHR.…”

Section: Trpm7 Mg 2+ and Hypertensionmentioning

confidence: 99%

“…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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Role of magnesium in hypertension

Sontia¹,

Touyz²

2007

Archives of Biochemistry and Biophysics

160

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Magnesium Uptake by Intestinal Brush-Border Membranes of Spontaneously Hypertensive Rats

Cited by 7 publications

References 12 publications

Transient receptor potential melastatin 6 and 7 channels, magnesium transport, and vascular biology: implications in hypertension

Transient receptor potential melastatin 6 and 7 channels, magnesium transport, and vascular biology: implications in hypertension

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

Role of magnesium in hypertension

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