Experimental Hypomagnesemia Induces Neurogenic Inflammation and Cardiac Dysfunction
| Autor: | Christopher F. Spurney, Jay H. Kramer, I. Tong Mak, William B. Weglicki, Terry M. Phillips, Joanna J. Chmielinska |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty NMDA receptor blockade inflammatory cytokines Neuropeptide Substance P magnesium deficiency 030204 cardiovascular system & hematology medicine.disease_cause Hypomagnesemia Proinflammatory cytokine perfused rat heart model 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine medicine neutral endopeptidase inhibition Neprilysin Neurogenic inflammation cardiac dysfunction business.industry medicine.disease Blockade 030104 developmental biology Endocrinology substance P and substance P receptor blockade chemistry RBC glutathione neutrophil superoxide generation business Oxidative stress oxidative/nitrosative stress |
| Zdroj: | Hearts Volume 1 Issue 2 Pages 11-116 |
| ISSN: | 2673-3846 |
| DOI: | 10.3390/hearts1020011 |
| Popis: | Hypomagnesemia occurs clinically as a result of restricted dietary intake, Mg-wasting drug therapies, chronic disease status and may be a risk factor in patients with cardiovascular disorders. Dietary restriction of magnesium (Mg deficiency) in animal models produced a pro-inflammatory/pro-oxidant condition, involving hematopoietic, neuronal, cardiovascular, renal and other systems. In Mg-deficient rodents, early elevations in circulating levels of the neuropeptide, substance P (SP) may trigger subsequent deleterious inflammatory/oxidative/nitrosative stress events. Evidence also suggests that activity of neutral endopeptidase (NEP, neprilysin), the major SP-degrading enzyme, may be impaired during later stages of Mg deficiency, and this may sustain the neurogenic inflammatory response. In this article, experimental findings using substance P receptor blockade, NEP inhibition, and N-methyl-D-aspartate (NMDA) receptor blockade demonstrated the connection between hypomagnesemia, neurogenic inflammation, oxidative stress and enhanced cardiac dysfunction. Proof of concept concerning neurogenic inflammation is provided using an isolated perfused rat heart model exposed to acute reductions in perfusate magnesium concentrations. |
| Databáze: | OpenAIRE |
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