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Analytical Techniques for Assaying Nitric Oxide Bioactivity
Published on: June 18, 2012
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Complexity of inducible nitric oxide synthase: cellular source determines benefit versus toxicity
Betty Y Poon1, Eko Raharjo, Kamala D Patel
1Department of Physiology and Biophysics, Cardiovascular, University of Calgary, Alberta, Canada.
Circulation
|August 20, 2003
Summary
Inducible nitric oxide synthase (iNOS) in cardiac myocytes benefits beta-adrenergic response during sepsis. However, neutrophil-derived iNOS damages myocytes, showing source dictates iNOS effects.
Area of Science:
- Cardiovascular Physiology
- Immunology
- Molecular Biology
Background:
- Inducible nitric oxide synthase (iNOS) exhibits dual roles in sepsis.
- Focus on cardiac myocytes and neutrophils to understand iNOS effects in the heart.
Purpose of the Study:
- Investigate the distinct functional effects of iNOS from cardiac myocytes versus neutrophils in sepsis.
- Determine how cellular source modulates iNOS activity and its impact on cardiac function.
Main Methods:
- Exposed endotoxemic cardiac myocytes to wild-type and iNOS-deficient neutrophils.
- Assessed myocyte shortening, oxidative stress, and beta-adrenergic stimulation response.
- Quantified neutrophil-derived superoxide and peroxynitrite.
Main Results:
- Neutrophil-derived iNOS increased oxidative stress and impaired myocyte shortening.
- Myocyte iNOS, however, enhanced beta-adrenergic-mediated increases in myocyte shortening.
- Peroxynitrite was not detected, despite both superoxide and NO being essential for neutrophil dysfunction.
Conclusions:
- Cellular source critically influences the role of iNOS in sepsis.
- Myocyte iNOS is beneficial for cardiac response to beta-adrenergic stimulation.
- Neutrophil iNOS is detrimental to cardiac myocytes during sepsis.
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