[Pulmonary hypertension in endothelial NO synthase knockout mice].
Inhalation of nitric oxide (NO) effectively reduces pulmonary arterial pressure in patients with pulmonary hypertension. However, it is controversial as to the role of endothelium-derived NO in pulmonary hypertension. Disruption of endothelial NO synthase (eNOS) gene causes systemic hypertension and diminishes endothelium-dependent vasodilatation. Even at normoxia eNOS knockout mice showed slightly increased right ventricular systolic pressure, but normal right ventricular weight. Hypoxia increased right ventricular systolic pressure, hematocrit, right ventricular weight in a concentration-dependent manner. The hypoxic condition induced pulmonary vascular remodeling; increases in the ratio of fully muscular vessels. Thus, pulmonary hypertension in eNOS knockout mice may be due to exaggerated vasoconstriction in response to hypoxia. In contrast, eNOS gene transduction reduces pulmonary vascular resistance.
Hirata
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Department of Cardiovascular Medicine, Faculty of Medicine, University of Tokyo.
D000818:Animals; D006976:Hypertension, Pulmonary / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000502:physiology*; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III
D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496315:Nos3 protein, mouse