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

Kathryn G. Lamping, Daniel W. Nuno, Edward G. Shesely, N. Maeda, Francesca Faraci
Published 2000 in
American journal of physiology. Heart and…

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… (More)

Onoue H, Katusic ZS
Brain Res
1998

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

Abstract

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Cited By

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Nitric oxide synthases in the pathogenesis of cardiovascular disease

References

How to assess endothelial function in human blood vessels.

Acetylcholine-induced relaxation in blood vessels from endothelial nitric oxide synthase knockout mice.

Agonist-specific impairment of coronary vascular function in genetically altered, hyperlipidemic mice.

Contribution of vasodilator prostanoids and nitric oxide to resting flow, metabolic vasodilation, and flow-mediated dilation in human coronary circulation.

Does potassium channel opening contribute to endothelium-dependent relaxation in human internal thoracic artery?

Enhanced release of prostaglandins contributes to flow-induced arteriolar dilation in eNOS knockout mice.

Gene transfer of endothelial nitric oxide synthase (eNOS) in eNOS-deficient mice.

Pentobarbital-sensitive EDHF comediates ACh-induced arteriolar dilation in the hamster microcirculation.

Protein expression, vascular reactivity and soluble guanylate cyclase activity in mice lacking the endothelial cell nitric oxide synthase: contributions of NOS isoforms to blood pressure and heart rate control.

1H-[1,2,4]oxadiazolo[4,3-a]qinoxalin-1-one (ODQ) and charybdotoxin (CTX) on relaxations of isolated cerebral arteries to nitric oxide

Slides referencing similar topics

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

Abstract

Topics

5 Figures and Tables

Cited By

Compensatory Vasodilator Mechanisms in the Ophthalmic Artery of Endothelial Nitric Oxide Synthase Gene Knockout Mice

Crucial roles of nitric oxide synthases in β-adrenoceptor-mediated bladder relaxation in mice.

Animal models of coronary heart disease

Partial eNOS deficiency causes spontaneous thrombotic cerebral infarction, amyloid angiopathy and cognitive impairment

Exercise training in adverse cardiac remodeling

Role of nitric oxide synthase isoforms for ophthalmic artery reactivity in mice.

Soluble epoxide hydrolase-dependent regulation of myogenic response and blood pressure.

There's more to flow-mediated dilation than nitric oxide.

Skeletal muscle arteriolar function following myocardial infarction: Analysis of branch-order effects.

Nitric oxide synthases in the pathogenesis of cardiovascular disease

References

How to assess endothelial function in human blood vessels.

Acetylcholine-induced relaxation in blood vessels from endothelial nitric oxide synthase knockout mice.

Agonist-specific impairment of coronary vascular function in genetically altered, hyperlipidemic mice.

Contribution of vasodilator prostanoids and nitric oxide to resting flow, metabolic vasodilation, and flow-mediated dilation in human coronary circulation.

Does potassium channel opening contribute to endothelium-dependent relaxation in human internal thoracic artery?

Enhanced release of prostaglandins contributes to flow-induced arteriolar dilation in eNOS knockout mice.

Gene transfer of endothelial nitric oxide synthase (eNOS) in eNOS-deficient mice.

Pentobarbital-sensitive EDHF comediates ACh-induced arteriolar dilation in the hamster microcirculation.

Protein expression, vascular reactivity and soluble guanylate cyclase activity in mice lacking the endothelial cell nitric oxide synthase: contributions of NOS isoforms to blood pressure and heart rate control.

1H-[1,2,4]oxadiazolo[4,3-a]qinoxalin-1-one (ODQ) and charybdotoxin (CTX) on relaxations of isolated cerebral arteries to nitric oxide

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