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Chronic exercise in dogs increases coronary vascular nitric oxide production and endothelial cell nitric oxide synthase gene expression.
Abstract
Recently, we have shown that chronic exercise increases endothelium-derived relaxing factor (EDRF)/nitric oxide (NO)-mediated epicardial coronary artery dilation in response to brief occlusion and acetylcholine. This finding suggests that exercise can provide a stimulus for the enhanced production of EDRF/NO, thus possibly contributing to the beneficial effects of exercise on the cardiovascular system. Therefore, the purpose of the present study was to examine whether chronic exercise could influence the production of NO (measured as the stable degradation product, nitrite) and endothelial cell NO synthase (ECNOS) gene expression in vessels from dogs after chronic exercise. To this end, dogs were exercised by running on a treadmill (9.5 km/h for 1 hour, twice daily) for 10 days, and nitrite production in large coronary vessels and microvessels and ECNOS gene expression in aortic endothelial extracts were assessed. Acetylcholine (10(-7) to 10(-5) mol/L) dose-dependently increased the release of nitrite (inhibited by nitro-L-arginine) from coronary arteries and microvessels in control and exercised dogs. Moreover, acetylcholine-stimulated nitrite production was markedly enhanced in large coronary arteries and microvessels prepared from hearts of dogs after chronic exercise compared with hearts from control dogs. One potential mechanism that may contribute to the enhanced production of nitrite in vessels from exercised dogs may be the induction of the calcium-dependent ECNOS gene. Steady-state mRNA levels for ECNOS were significantly higher than mRNA levels for von Willebrand's factor (vWF, a specific endothelial cell marker) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH, a constitutively expressed gene) in exercised dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
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“One important activator of production of NO in the endothelium is shear stress (43, 163).”
From Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia (2017) · cites this paper as [163]
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Metadata
- Authors
- Sessa, W. C., Pritchard, K., Seyedi, N., Wang, J., & Hintze, T. H.
- Affiliations
- New York Medical College (US)
- Venue
- Circulation Research
- Published
- 1994-02
- Volume
- 74
- Issue
- 2
- Pages
- 349-353
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2125823894
- Cited by
- 934
- References
- 0
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 11 · 2023: 8 · 2022: 10 · 2021: 14 · 2020: 17 · 2019: 15 · 2018: 11 · 2017: 11 · 2016: 18 · 2015: 29 · 2014: 18 · 2013: 16 · 2012: 27
- FWCI
- 32.87
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Heart, Lung, and Blood Institute (P01HL043023, P01 HL 43023)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Keywords
- exercise training, nitric oxide, endothelial nitric oxide synthase, coronary arteries, coronary microvessels, nitrite production, endothelium-derived relaxing factor, acetylcholine, von Willebrand factor, aortic endothelial cells, treadmill running, dogs
- MeSH terms
- Amino Acid Oxidoreductases, Animals, Coronary Vessels, Dogs, Endothelium, Vascular, Physical Exertion, Female, Male, Nitric Oxide, Nitrites, RNA, Time Factors, Gene Expression, Nitric Oxide Synthase
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