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Am J Physiol Heart Circ Physiol 279: H1906-H1912, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 4, H1906-H1912, October 2000

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

Kathryn G. Lamping, Daniel W. Nuno, Edward G. Shesely, Nobuyo Maeda, and Frank M. Faraci

Departments of Internal Medicine and Pharmacology, The Cardiovascular Center, University of Iowa, and Veterans Affairs Medical Center, Iowa City, Iowa 52246

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 NG-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.

nitric oxide synthase; acetylcholine; cyclooxygenase


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