Journal article
Vasodilator mechanisms in the coronary circulation of endothelial nitric oxide synthase-deficient mice
American journal of physiology. Heart and circulatory physiology, Vol.279(4), pp.H1906-H1912
10/01/2000
DOI: 10.1152/ajpheart.2000.279.4.H1906
PMID: 11009479
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.
Details
- Title: Subtitle
- Vasodilator mechanisms in the coronary circulation of endothelial nitric oxide synthase-deficient mice
- Creators
- Kathryn G Lamping - Departments of Internal Medicine and Pharmacology, The Cardiovascular Center, University of Iowa, and Veterans Affairs Medical Center, Iowa City, Iowa 52246Daniel W Nuno - Departments of Internal Medicine and Pharmacology, The Cardiovascular Center, University of Iowa, and Veterans Affairs Medical Center, Iowa City, Iowa 52246Edward G Shesely - Departments of Internal Medicine and Pharmacology, The Cardiovascular Center, University of Iowa, and Veterans Affairs Medical Center, Iowa City, Iowa 52246Nobuyo Maeda - Departments of Internal Medicine and Pharmacology, The Cardiovascular Center, University of Iowa, and Veterans Affairs Medical Center, Iowa City, Iowa 52246Frank M Faraci - Departments of Internal Medicine and Pharmacology, The Cardiovascular Center, University of Iowa, and Veterans Affairs Medical Center, Iowa City, Iowa 52246
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Heart and circulatory physiology, Vol.279(4), pp.H1906-H1912
- DOI
- 10.1152/ajpheart.2000.279.4.H1906
- PMID
- 11009479
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- Language
- English
- Date published
- 10/01/2000
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040203802771
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