Cardiovascular and intestinal responses to oxidative and nitrosative stress during prolonged magnesium deficiency

Am J Med Sci. 2011 Aug;342(2):125-8. doi: 10.1097/MAJ.0b013e318222e88c.


In rodents with dietary magnesium deficiency (Mg deficiency), hypomagnesemia, occurs leading to a rise in circulating substance P from neuronal tissues to trigger systemic inflammatory stress in cardiac and intestinal tissues. Sustained elevations of substance P may result from impaired neutral endopeptidase (NEP) activity due to reactive oxygen and reactive nitrogen species. Associated increase in intestinal permeability includes infiltration of WBC and endotoxemia, which can further amplify the systemic inflammatory response that leads to impaired contractile function associated with up-regulation of the cardiac CD14 endotoxin receptor. The neurogenic signal transduction pathways that we have identified in the pro-oxidant/pro-inflammatory processes found with prolonged hypomagnesemia are described in this report.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiovascular System / metabolism*
  • Cardiovascular System / physiopathology
  • Humans
  • Inflammation / metabolism
  • Inflammation / physiopathology
  • Intestinal Mucosa / metabolism*
  • Intestines / physiopathology
  • Magnesium Deficiency* / metabolism
  • Magnesium Deficiency* / physiopathology
  • Neprilysin / metabolism
  • Oxidative Stress / physiology*
  • Rats
  • Reactive Nitrogen Species / metabolism
  • Receptors, Immunologic / metabolism
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Substance P / physiology


  • Reactive Nitrogen Species
  • Receptors, Immunologic
  • Receptors, N-Methyl-D-Aspartate
  • endotoxin receptor
  • Substance P
  • Neprilysin