ArticleMolecular and cellular biochemistry1994
Neurogenic peptides and the cardiomyopathy of magnesium-deficiency: effects of substance P-receptor inhibition.
Article in Molecular and cellular biochemistry, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 55 citations in OpenAlex.
- Magnesium, Oxidative Stress, Inflammation, and Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Hypomagnesemia in critically ill patients.Journal of intensive care · 2018Review
- TRPM7 kinase activity regulates murine mast cell degranulation.The Journal of physiology · 2016Article
- Reverse remodeling and recovery from cachexia in rats with aldosteronism.American journal of physiology. Heart and circulatory physiology · 2012Article
- Cation dyshomeostasis and cardiomyocyte necrosis: the Fleckenstein hypothesis revisited.European heart journal · 2011Article
- Loss of neutral endopeptidase activity contributes to neutrophil activation and cardiac dysfunction during chronic hypomagnesemia: Protection by substance P receptor blockade.Experimental and clinical cardiology · 2011Article
- The role of magnesium deficiency in cardiovascular and intestinal inflammation.Magnesium research · 2010Article
- Neurogenic inflammation and cardiac dysfunction due to hypomagnesemia.The American journal of the medical sciences · 2009Review
- Causes and consequences of zinc dyshomeostasis in rats with chronic aldosteronism.Journal of cardiovascular pharmacology · 2008Article
- Inhibition of neutral endopeptidase potentiates neutrophil activation during Mg-deficiency in the rat.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2008Article
- The nerve-heart connection in the pro-oxidant response to Mg-deficiency.Heart failure reviews · 2006Review
- Efficacy of aldosterone receptor antagonism in heart failure: potential mechanisms.Current heart failure reports · 2004Review
- Aldosteronism and peripheral blood mononuclear cell activation: a neuroendocrine-immune interface.Circulation research · 2003Article
- Aldosterone-induced inflammation in the rat heart : role of oxidative stress.The American journal of pathology · 2002Article
- Activation of the neutrophil and loss of plasma glutathione during Mg-deficiency--modulation by nitric oxide synthase inhibition.Molecular and cellular biochemistry · 1997Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Dietary deficiency of magnesium (Mg) in rodents results in cardiomyopathic lesion formation. In our rat model, these lesions develop after 3 weeks on the Mg-deficient diet; significant elevation of several cytokines, IL-1, IL-6 and TNF alpha also occurs. In probing the mechanisms of lesion formation, we obtained data supporting the participation of free radicals (Freedman AM et al.: Bioch Biophys Res Commun 1990; 170: 1102). Recently, we identified an early elevation of circulating substance P and proposed a role of neurogenic peptides during Mg-deficiency (Weglicki WB, Phillips TM: AM J Phys 1992;262:R734). The present study was designed to evaluate the contribution of neurogenic peptides to the pathogenesis of Mg-deficiency. In the blood, substance-P and calcitonin gene related peptide (CGRP) are elevated during the first week on the diet. During the second week, circulating histamine, PGE2 and TBAR-materials were elevated and red cell glutathione was reduced, all prior to the elevation of the inflammatory cytokines during the third week. When the rats were treated with the substance P-receptor blocker [CP-96,345], the levels of substance P and CGRP remained elevated; however, increases in histamine, PGE2, TBAR-materials, and the decrease in red cell glutathione were inhibited; also, the development of cardiac lesions was inhibited significantly. These data support a central role for neurogenic peptides, especially substance P, in the development of cardiomyopathic lesions during Mg-deficiency.
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