GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.
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
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.
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
|Gene product||Qualifier||GO ID||GO term name||Evidence Code||with/from||Aspect||Notes||Status|
See Help:References for how to manage references in GONUTS.