Noise-induced hypertension and magnesium in rats: relationship to microcirculation and calcium

Altura, Burton M.; Altura, Bella T.; Gebrewold, Asefa; Ising, H; Gunther, Twm Tijmen

doi:10.1152/jappl.1992.72.1.194

Cited by 82 publications

(64 citation statements)

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“…Magnesium deficiency, as assessed by decreased magnesium in the blood or tissues, and cardiovascular disease are linked [27,28]. In a recent review [29], none of the various circulating spasmogenic theories could satisfactorily account for coronary vasospasm in hyperthyroidism, and Miyagi et al [30] had shown magnesium to suppress coronary spastic angina.…”

Section: Discussionmentioning

confidence: 99%

Magnesium Metabolism in Hyperthyroidism.

et al. 1996

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Section: Discussionmentioning

confidence: 99%

Magnesium Metabolism in Hyperthyroidism.

et al. 1996

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“…Antioxidant scavenging of ROS also potentially reduces vasoconstriction that occurs with ROS production [46, for review see 27]. One effect of magnesium is reduction of noise-induced vasoconstriction [67,[79][80][81].…”

mentioning

confidence: 99%

Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma

Prell

Hughes

Miller

2007

Free Radical Biology and Medicine

198

188

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Free radical formation in the cochlea plays a key role in the development of noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant formation of both reactive oxygen species and reactive nitrogen species 7-10 days following noise exposure. Reduction in cochlear blood flow as a result of free radical formation has also been described. Here we report that the antioxidant agents, vitamins A, C, and E, act in synergy with magnesium to effectively prevent noise-induced trauma. Neither the antioxidant agents nor magnesium reliably reduced NIHL or sensory cell death with the doses we used when these agents were delivered alone. In combination, however, they were highly effective in reducing both hearing loss and cell death even with treatment initiated just one hour prior to noise exposure. This study supports roles for both free radical formation and noise-induced vasoconstriction in the onset and progression of NIHL. Identification of this safe and effective antioxidant intervention that attenuates NIHL provides a compelling rationale for human trials in which free radical scavengers are used to eliminate this single major cause of acquired hearing loss. Keywords cochlea; free radical; noise; hearing; antioxidant; vasodilation Mechanical destruction of cells in the organ of Corti was once assumed to be the primary cause of noise-induced hearing loss (NIHL) [1][2][3][4][5][6][7][8], with perhaps some effect of reduced blood flow to the inner ear [9][10][11][12][13][14][15][16][17][18]. We now know that another key factor is intense metabolic activity that results in production of excess free radicals [19][20][21][22][23] and lipid peroxidation products [24]. Noise-induced production of reactive oxygen species (ROS) in the cochlea has now been well characterized, and several recent reviews are available [25][26][27]. Mitochodrial dysfunction and ROS production have been implicated in numerous neurodegenerative syndromes and diseases [28-34, see 35,36]. The use of antioxidant agents holds significant therapeutic promise for many neurodegenerative processes [32,33,[37][38][39][40][41][42], and there is some suggestion that Correspondence to: C. G. Le Prell, Kresge Hearing Research Institute, University of Michigan, 1301 East Ann Street, Ann Arbor, MI 48109-0506, USA. Tel: +1-734-763-5104; fax +1-734-764-0014. E-mail address: colleeng@umich.edu. Disclosure. Dr. Miller is a founding member and Chairman of the Board of Directors at OtoMedicine, Inc., a company that has an option to license the intellectual property described in this report. Dr. Le Prell is a paid consultant to OtoMedicine, Inc. Drs. Miller and Le Prell have disclosed these relationships to the Medical School Conflict of Interest Board at the University of Michigan; conflict management plans including semi-annual review by the Board are in place.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publicatio...

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“…Moreover, dietary deficiency of Mg, under very-controlled laboratory conditions, in rats and rabbits has been shown to cause vascular remodeling concomitant with hypertension and atherogenesis (i.e., arteriolar wall hypertrophy and alterations in arterial wall matrices) of unknown origin [4,6,[15][16][17][36][37][38][39].…”

Section: Introductionmentioning

confidence: 99%

Potential Roles of Magnesium Deficiency in Inflammation and Atherogenesis: Importance and Cross-talk of Platelet-Activating Factor and Ceramide

Bm¹

2016

J Clin Exp Cardiolog

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Epidemiologic studies in North America and Europe have shown that people consuming Western-type diets are low in magnesium (Mg) content (i.e., < 30 -65% of the RDA for Mg); most such diets in the USA show that 60 -80% of Americans are consuming only 185 -235 mg/day of Mg. Low Mg content in areas of soft-water, and Mg-poor soil, is associated with high incidences of ischemic heart disease (IHD), coronary artery disease, hypertension, and sudden cardiac death (SCD). It is clear that the leading underlying cause of death worldwide is atherosclerosis. Importantly, both animal and human studies have shown an inverse relationship between dietary intake of Mg and atherosclerosis. The myocardial level of Mg has consistently been observed to be lower in subjects dying from IHD and SCD in soft-water areas than those in hard-water areas. Over the past 20 years, our laboratories, using several types of primary cultured vascular smooth muscle (VSM) cells, and myocardial cells, demonstrated that declining levels of extracellular Mg ([Mg 2+ ] 0 ) activated several enzymatic pathways to produce increases in cellular sphingolipids, particularly ceramides which are known to exert numerous types of cardiovascular manifestations including inflammatory effects ; the latter play important roles in atherogenesis and cardiovascular diseases. Approximately 20 years ago, we reported that low [Mg 2+ ] 0 caused formation of platelet-activating factor (PAF) as well as other types of PAF-like molecules and suggested that these molecules might be causative agents in low Mg 2+ -induced IHD and SCD. Herein, we review results and data from our labs which strongly support roles for ceramides, PAF and PAF-like lipids in low [Mg 2+ ] 0 -induced IHD and SCD.

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Noise-induced hypertension and magnesium in rats: relationship to microcirculation and calcium

Cited by 82 publications

References 0 publications

Magnesium Metabolism in Hyperthyroidism.

Magnesium Metabolism in Hyperthyroidism.

Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma

Potential Roles of Magnesium Deficiency in Inflammation and Atherogenesis: Importance and Cross-talk of Platelet-Activating Factor and Ceramide

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