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Cited by 99Nitric Oxide and Endothelin EffectsCardiovascular Health and Disease PreventionEicosanoids and Hypertension Pharmacology

Vasodilator mechanisms in the coronary circulation of endothelial nitric oxide synthase-deficient mice

Lamping, Kathryn G., Nuno, Daniel W., Shesely, Edward G., Maeda, Nobuyo, Faraci, Frank M.·2000·American Journal of Physiology-Heart and Circulatory Physiology
DOI 10.1152/ajpheart.2000.279.4.h1906
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Abstract

Previous studies have demonstrated that responses to endothelium-dependent vasodilators are absent in the aortas from mice deficient in expression of endothelial nitric oxide synthase (eNOS −/− mice), whereas responses in the cerebral microcirculation are preserved. We tested the hypothesis that in the absence of eNOS, other vasodilator pathways compensate to preserve endothelium-dependent relaxation in the coronary circulation. Diameters of isolated, pressurized coronary arteries from eNOS −/−, eNOS heterozygous (+/−), and wild-type mice (eNOS +/+ and C57BL/6J) were measured by video microscopy. ACh (an endothelium-dependent agonist) produced vasodilation in wild-type mice. This response was normal in eNOS +/− mice and was largely preserved in eNOS −/− mice. Responses to nitroprusside were also similar in arteries from eNOS +/+, eNOS +/−, and eNOS −/− mice. Dilation to ACh was inhibited by N G-nitro-l-arginine, an inhibitor of NOS in control and eNOS −/− mice. In contrast, trifluoromethylphenylimidazole, an inhibitor of neuronal NOS (nNOS), decreased ACh-induced dilation in arteries from eNOS-deficient mice but had no effect on responses in wild-type mice. Indomethacin, an inhibitor of cyclooxygenase, decreased vasodilation to ACh in eNOS-deficient, but not wild-type, mice. Thus, in the absence of eNOS, dilation of coronary arteries to ACh is preserved by other vasodilator mechanisms.

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Crossref · 10.1152/ajpheart.2000.279.4.h1906

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  • NOXs are multiprotein enzyme complexes that catalyze the electron transfer to molecular oxygen to form ROS, more commonly superoxide, but also hydrogen peroxide.

    “NOXs are multiprotein enzyme complexes that catalyze the electron transfer to molecular oxygen to form ROS, more commonly superoxide, but also hydrogen peroxide (79, 252, 383, 546, 912).”

    From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [546]

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Authors
Lamping, K. G., Nuno, D. W., Shesely, E. G., Maeda, N., & Faraci, F. M.
Affiliations
University of Iowa (US)
ORCID
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Published
2000-10-01
Volume
279
Issue
4
Pages
H1906-H1912
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
DOI
10.1152/ajpheart.2000.279.4.h1906
OpenAlex
W2188466537
Cited by
99
References
41
Citations by year
2025: 1 · 2024: 6 · 2022: 3 · 2020: 1 · 2019: 5 · 2018: 3 · 2017: 3 · 2016: 5 · 2015: 2 · 2014: 4 · 2013: 2 · 2012: 2
FWCI
2.85
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Heart, Lung, and Blood Institute (HL38901, HL39050)
  • National Institute of Neurological Disorders and Stroke (NS24621, P01NS024621)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords
endothelial nitric oxide synthase, eNOS-deficient mice, coronary vasodilation, endothelium-dependent relaxation, acetylcholine, nitric oxide, neuronal nitric oxide synthase, cyclooxygenase, L-NNA, coronary arteries
MeSH terms
Acetylcholine, Animals, Coronary Circulation, Coronary Vessels, Dose-Response Relationship, Drug, Indomethacin, Mice, Inbred C57BL, Polymethacrylic Acids, Reference Values, Vasodilation, Vasodilator Agents, Cyclooxygenase Inhibitors, Nitric Oxide Synthase, Mice, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type III

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