ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2008
Inhibition of neutral endopeptidase potentiates neutrophil activation during Mg-deficiency in the rat.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- The Bidirectional Effects of Periodontal Disease and Oral Dysbiosis on Gut Inflammation in Inflammatory Bowel Disease.Journal of Crohn's & colitis · 2025Observational
- Mg supplementation attenuates ritonavir-induced hyperlipidemia, oxidative stress, and cardiac dysfunction in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- d-Propranolol protects against oxidative stress and progressive cardiac dysfunction in iron overloaded rats.Canadian journal of physiology and pharmacology · 2012Article
- 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
- Neutral endopeptidase inhibition enhances substance P mediated inflammation due to hypomagnesemia.Magnesium research · 2009Article
- AZT-induced oxidative cardiovascular toxicity: attenuation by Mg-supplementation.Cardiovascular toxicology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Neutral endopeptidase (NEP), which degrades substance P (SP), may regulate neutrophil activation during Mg-deficiency (MgD). Male Sprague-Dawley rats (180g) were fed MgD (approximately 50 mg Mg/kg) or Mg-sufficient (MgS, 608 mg Mg/kg) diets for 7 days +/- NEP inhibitor phosphoramidon (PR, 5 mg/kg/day, s.c.). MgD alone induced a 9-fold (vs. MgS, p <0.01) elevation in plasma SP; MgD+PR enhanced it further to 18-fold (p <0.001). Neutrophils from MgD+PR rats displayed a 3.9-fold higher (p <0.01) basal .O(2-) generation, but those from MgD or PR alone were not activated. Plasma PGE2-metabolite levels rose 2.67- (p <0.01) and 1.56- (p <0.05) fold, respectively, in MgD+PR and MgD groups; the corresponding red blood cell glutathione levels were decreased 21% (p <0.025) and 7% (NS). MgD+PR significantly reduced neutrophil NEP activity by 48% (p <0.02); PR or MgD alone only reduced this activity 26% and 15%, respectively. We conclude that NEP inhibition potentiates SP-mediated neutrophil .O(2-) production and may promote other inflammatory activities during MgD.
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Registered trials
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