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PMID:11821712

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Citation

Kubis, N, Besnard, S, Silvestre, JS, Feletou, M, Huang, PL, Lévy, BI and Tedgui, A (2002) Decreased arteriolar density in endothelial nitric oxide synthase knockout mice is due to hypertension, not to the constitutive defect in endothelial nitric oxide synthase enzyme. J. Hypertens. 20:273-80

Abstract

Hypertension in endothelial nitric oxide synthase knockout (eNOS-/-) mice is believed to be partly due to altered vasodilatation. However, nitric oxide (NO) is also known to play an important part in angiogenesis.

Links

PubMed

Keywords

Animals; Antihypertensive Agents/therapeutic use; Arterioles/anatomy & histology; Arterioles/drug effects; Arterioles/enzymology; Blood Pressure/drug effects; Blood Pressure/physiology; Body Weight/drug effects; Body Weight/physiology; Capillaries/anatomy & histology; Capillaries/drug effects; Capillaries/enzymology; Disease Models, Animal; Endothelium, Vascular/drug effects; Endothelium, Vascular/enzymology; Heart/anatomy & histology; Heart/drug effects; Heart/physiology; Hydralazine/therapeutic use; Hypertension/complications; Hypertension/drug therapy; Hypertension/enzymology; Male; Mice; Mice, Knockout/anatomy & histology; Models, Cardiovascular; Muscle, Smooth, Vascular/blood supply; Muscle, Smooth, Vascular/drug effects; Muscle, Smooth, Vascular/enzymology; Nitric Oxide Synthase/drug effects; Nitric Oxide Synthase/metabolism; Nitric Oxide Synthase Type II; Nitric Oxide Synthase Type III; Organ Size/drug effects; Organ Size/physiology

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


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References

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