Document Detail


Neurogenic inflammation and cardiac dysfunction due to hypomagnesemia.
MedLine Citation:
PMID:  19593099     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hypomagnesemia continues to be a significant clinical disorder that is present in patients with diabetes mellitus, alcoholism, and treatment with magnesuric drugs (diuretics, cancer chemotherapy agents, etc.). To determine the role of magnesium in cardiovascular pathophysiology, we have used dietary restriction of this cation in animal models. This review highlights some key observations that helped formulate the hypothesis that release of substance P (SP) during experimental dietary Mg deficiency (MgD) may initiate a cascade of deleterious inflammatory, oxidative, and nitrosative events, which ultimately promote cardiomyopathy, in situ cardiac dysfunction, and myocardial intolerance to secondary stresses. SP acts primarily through neurokinin-1 receptors of inflammatory and endothelial cells, and may induce production of reactive oxygen and nitrogen species (superoxide anion, NO*, peroxynitrite, hydroxyl radical), leading to enhanced consumption of tissue antioxidants; stimulate release of inflammatory mediators; promote tissue adhesion molecule expression; and enhance inflammatory cell tissue infiltration and cardiovascular lesion formation. These SP-mediated events may predispose the heart to injury if faced with subsequent oxidative stressors (ischemia/reperfusion, certain drugs) or facilitate development of in situ cardiac dysfunction, especially with prolonged dietary Mg restriction. Significant protection against most of these MgD-mediated events has been observed with interventions that modulate neuronal SP release or its bioactivity, and with several antioxidants (vitamin E, probucol, epicaptopril, d-propranolol). In view of the clinical prevalence of hypomagnesemia, new treatments, beyond magnesium repletion, may be needed to diminish deleterious neurogenic and prooxidative components described in this article.
Authors:
Jay H Kramer; Christopher Spurney; Micaela Iantorno; Constantine Tziros; I-Tong Mak; M Isabel Tejero-Taldo; Joanna J Chmielinska; Andrei M Komarov; William B Weglicki
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  The American journal of the medical sciences     Volume:  338     ISSN:  0002-9629     ISO Abbreviation:  Am. J. Med. Sci.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-07-13     Completed Date:  2009-08-17     Revised Date:  2013-08-30    
Medline Journal Info:
Nlm Unique ID:  0370506     Medline TA:  Am J Med Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  22-7     Citation Subset:  AIM; IM    
Affiliation:
Department of Biochemistry and Molecular Biology, The George Washington University Medical Center, Washington DC 20037, USA. phyjhk@gwumc.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiomyopathies* / etiology,  physiopathology
Diet
Endotoxemia / metabolism
Humans
Magnesium Deficiency / complications*
Myocardial Reperfusion Injury / metabolism
Neurogenic Inflammation* / etiology,  physiopathology
Neuropeptides / metabolism
Oxidative Stress
Rats
Receptors, N-Methyl-D-Aspartate / metabolism
Receptors, Neurokinin-1 / metabolism
Grant Support
ID/Acronym/Agency:
HL-65178/HL/NHLBI NIH HHS; R01 HL-62282/HL/NHLBI NIH HHS; R01 HL062282/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Neuropeptides; 0/Receptors, N-Methyl-D-Aspartate; 0/Receptors, Neurokinin-1
Comments/Corrections

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