Endothelin‐1‐induced contraction in isolated aortae from normotensive and DOCA‐salt hypertensive rats: effect of magnesium

Laurant, Pascal; Berthelot, Alain

doi:10.1111/j.1476-5381.1996.tb16048.x

Cited by 41 publications

(31 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mg removal may induce changes in calcium utilization and conformational changes of receptors, or potentiate the activities of catecholamines by acting at sites in vascular smooth muscle other than the receptors (2, 35). A reduction of external Mg concentration below physiological level increases maximal responses, whereas, in agreement with this study, total Mg removal seems to decrease maximal responses of vascular smooth muscle to contractile agonists (2, 19,37,38). Although it is unclear why the absence of Mg attenuates maximal contraction in arteries without endothelium, the finding might be partly explained by the fact that Mg removal inhibits intracellular calcium release (38).…”

Section: Discussionsupporting

confidence: 87%

Magnesium Removal Impairs the Regulatory Role of Rat Endothelium.

et al. 2000

View full text Add to dashboard Cite

endothelium has been shown to play an important role in the regulation of vascular tone and, hence, impairment of the endothelium may induce hypertension. Although magnesium (Mg) deficiency could induce hypertension, the role of Mg on the endothelium is unclear. We examined the effects of Mg removal on endothelium-dependent and -independent responses using ring preparations of femoral arteries obtained from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Norepinephrine (10-9-10-4 M) evoked concentration-dependent contractions in arteries with endothelium. The maximal response was greater in SHR than in WKY. Removal of external Mg augmented the contraction in WKY but not in SHR. As a result, the contraction obtained in arteries with endothelium was identical in the two groups. Removal of the endothelium enhanced the contraction in both strains, with a greater response occurring in WKY than in SHR in Krebs, but not in Mg-free, solution. As a result, in arteries without endothelium, the contractions were identical in WKY and SHR both in Krebs and Mg-free solutions. Acetyl-

show abstract

Section: Discussionsupporting

confidence: 87%

Magnesium Removal Impairs the Regulatory Role of Rat Endothelium.

et al. 2000

View full text Add to dashboard Cite

show abstract

“…101 Furthermore, in magnesium-deficient rats, plasma ET-1 levels are elevated, whereas in magnesium-supplemented rats, plasma ET-1 levels are reduced. 94, 101 Another possible mechanism whereby Mg 2+ could have an impact on vascular function is via its antioxidant, anti- Figure 2. TRPM7 have been implicated in a number of vascular pathologies, including hypertension.…”

Section: Trpm7 Mg 2+ and Hypertensionmentioning

confidence: 99%

“…These effects might be related to altered binding of agonists to their specific cell membrane receptors and/or to production of vasoactive agents. 99, 101 Magnesium infusion also inhibits endothelin-1-induced vasoconstriction and high extracellular Mg 2+ concentration reduces the affinity of endothelin-1 for its specific receptors. 101 Furthermore, in magnesium-deficient rats, plasma ET-1 levels are elevated, whereas in magnesium-supplemented rats, plasma ET-1 levels are reduced.…”

Section: Trpm7 Mg 2+ and Hypertensionmentioning

confidence: 99%

“…99, 101 Magnesium infusion also inhibits endothelin-1-induced vasoconstriction and high extracellular Mg 2+ concentration reduces the affinity of endothelin-1 for its specific receptors. 101 Furthermore, in magnesium-deficient rats, plasma ET-1 levels are elevated, whereas in magnesium-supplemented rats, plasma ET-1 levels are reduced. 94, 101 Another possible mechanism whereby Mg 2+ could have an impact on vascular function is via its antioxidant, anti- Figure 2.…”

Section: Trpm7 Mg 2+ and Hypertensionmentioning

confidence: 99%

See 1 more Smart Citation

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

Yogi

Callera

Antunes

et al. 2011

Circ J

View full text Add to dashboard Cite

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.

show abstract

“…Magnesium reduces vascular tone and increases blood flow by modulating production of vasoactive agents such as endothelin-1 (ET-1) and nitric oxide (NO) and respon-siveness to these agents [6]. Elevated magnesium levels prevents ET-1 induced contractile responses by inhibition of ET-1's production and its hypertrophic effect [7,8]. Endothelium-dependent vasodilation mediated by NO is induced with magnesium by modifying formation and release of NO [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Magnesium: Effect on ocular health as a calcium channel antagonist

Korkmaz

Ekici²,

Tufan³

et al. 2013

J Clin Exp Invest

View full text Add to dashboard Cite

ÖZETMagnezyum hücre zar fonksiyonlarını, düz kas kontraksiyonlarını ve enzimatik reaksiyonları etkileyerek pek çok metabolik sürece katılan fizyolojik bir kalsiyum kanal blokörüdür. Magnezyumun Endothelin-1 (ET-1) ve Nitrik Oksit (NO) yolakları vasıtasıyla endotel fonksiyonları-nı modifiye ederek dokulara kan akımında artışa neden olduğu gösterilmiştir. Magnezyum aynı zamanda N-metil-D-aspartat (NMDA) reseptör ilişkili kalsiyum içe akımı-nı bloke ederek ve glutamat serbestleşmesini önleyerek nöroprotektif rol oynamakta ve hücreleri oksidatif stres ve apoptoza karşı korumaktadır. Hem kan akımında artışa neden olması hem de nöroprotektif etkileri magnezyumu glokom çalışmaları için iyi bir hedef molekül yapmaktadır. Magnezyumun retinada oksidatif stresi ve apoptozu azalttığı ve ganglion koruyucu etkileri olduğu gösterilmiştir. Bir takım çalışmalarda aynı zamanda magnezyumun diabetik hastalarda insulin resistansını azalttığı, glisemik kontrolü kolaylaştırdığı ve retinopatiyi önlediği gösterilmiştir. Magnezyumun lensteki iyon dengesinin sağlanmasında kritik önemi belirlenmiştir. Magnezyum eksikliğinin lentiküler oksidatif stresi arttırdığı ve iyon dengesini bozarak katarakt oluşumuna neden olduğu gösterilmiştir.Anahtar kelimeler: Magnezyum, kalsiyum kanal blokajı, glokom, nöroproteksiyon, diabetik retinopati, katarakt ABSTRACTMagnesium is the physiologic calcium channel blocker, involving in many different metabolic processes by maintaining cell membrane function, modulating smooth muscle contraction and influencing enzymatic activities. Magnesium has been shown to increase blood flow to tissues by modifying endothelial function via endothelin-1 (ET-1) and nitric Oxide (NO) pathways. Magnesium also exhibits neuroprotective role by blocking N-methyl-D-aspartate (NMDA) receptor related calcium influx and by inhibiting the release of glutamate, hence protects the cell against oxidative stress and apoptosis. Both increase in blood flow and its neuroprotective effect make magnesium a good candidate for glaucoma studies. Magnesium has been shown to decrease oxidative stress and apoptosis in retinal tissue and to have retinal ganglion cell sparing effect. A series of studies has been conducted about magnesium could decrease insulin resistance in diabetic patients, ease glycemia control and prevent diabetic retinopathy. Magnesium is found to be critically important in maintaining normal ionic homeostasis of lens. Magnesium deficiency has been shown to cause increased lenticular oxidative stress and ionic imbalance in the lens so trigger cataractogenesis. J Clin Exp Invest 2013; 4 (2): 244-251

show abstract

Endothelin‐1‐induced contraction in isolated aortae from normotensive and DOCA‐salt hypertensive rats: effect of magnesium

Cited by 41 publications

References 56 publications

Magnesium Removal Impairs the Regulatory Role of Rat Endothelium.

Magnesium Removal Impairs the Regulatory Role of Rat Endothelium.

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

Magnesium: Effect on ocular health as a calcium channel antagonist

Contact Info

Product

Resources

About