Cited by 82Cardiac Ischemia and ReperfusionNitric Oxide and Endothelin EffectsNeurological Disorders and Treatments

Myocardial protection by nitrite

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Calvert, J. W., Lefer, D. J.·2009·Cardiovascular Research

Abstract

Nitrite has long been considered to be an inert oxidative metabolite of nitric oxide (NO). Recent work, however, has demonstrated that nitrite represents an important tissue storage form of NO that can be reduced to NO during ischaemic or hypoxic events. This exciting series of discoveries has created an entirely new field of research that involves the investigation of the molecular, biochemical, and physiological activities of nitrite under a variety of physiological and pathophysiological states. This has also led to a re-evaluation of the role that nitrite plays in health and disease. As a result there has been an interest in the use of nitrite as a therapeutic strategy for the treatment of acute myocardial infarction. Nitrite therapy has now been studied in several animal models and has proven to be an effective means to reduce myocardial ischaemia-reperfusion injury. This review article will provide a brief summary of the key findings that have led to the re-evaluation of nitrite and highlight the evidence supporting the cardioprotective actions of nitrite and also highlight the potential clinical application of nitrite therapy to cardiovascular diseases.

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  • Another possible cytoprotective effect of nitrite may be mediated by S-nitrosylation effects on intracellular Ca2+ handling, which decreases Ca2+ entry by inhibiting L-type Ca2+ channels and increases sarcoendoplasmic reticulum Ca2+ uptake by activating SERCA2a.

    “Another possible cytoprotective effects of nitrite may be mediated by the effects of S-nitrosylation on the intracellular Ca2+ handling, which decreases Ca2+ entry by inhibiting L-type Ca2+ channels and increasing the sarcoendoplasmic reticulum (SR) Ca2+ uptake by activating SR Ca2+ transport ATPase (SERCA2a) [102].”

    From NO-Rich Diet for Lifestyle-Related Diseases (2015) · cites this paper as [102]

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Research works printed but not linked: 2

  1. Becker BF, Heindl B, Kupatt C, Zahler S. Endothelial function and hemos- tasis. Z Kardiol 2000;89:160-167.
  2. Lefer DJ, Lefer AM. Nitric oxide homeostasis control as therapy for car- diovascular diseases. Cardiovasc Res 1993;27:2282.

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Authors
Calvert, J. W., & Lefer, D. J.
Affiliations
Emory University (US)
Corresponding author
Lefer, D. J.
Venue
Cardiovascular Research
Published
2009-02-27
Volume
83
Issue
2
Pages
195-203
ISSN
0008-6363 (ISSN-L)
OpenAlex
W1978288131
Cited by
82
References
119
Citations by year
2023: 1 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 9 · 2016: 5 · 2015: 6 · 2014: 7 · 2013: 9 · 2012: 7
FWCI
1.29
Type
journal article
Language
en
Open access
Locations
  • Cardiovascular Research (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Emory University
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (2R01HL-060849-09, R01HL060849)
  • National Institute of Diabetes and Digestive and Kidney Diseases (F32DK077380)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
Keywords
nitrite, cardioprotection, nitric oxide, nitrite therapy, acute myocardial infarction, myocardial ischemia-reperfusion injury, hypoxia, oxidative metabolism, cardiovascular disease
MeSH terms
Animals, Homeostasis, Humans, Myocardial Infarction, Myocardium, Nitric Oxide, Nitrites, Risk Factors, Myocardial Reperfusion Injury, Treatment Outcome, Cytoprotection

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