Nitric oxide-dependent and -independent vascular hyporeactivity in mesenteric arteries of portal hypertensive rats
β Scribed by Akos Heinemann; Christof H Wachter; Peter Holzer; Peter Fickert; Rudolf E Stauber
- Book ID
- 110003007
- Publisher
- Nature Publishing Group
- Year
- 1997
- Tongue
- English
- Weight
- 325 KB
- Volume
- 121
- Category
- Article
- ISSN
- 0007-1188
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π SIMILAR VOLUMES
Systemic and especially splanchnic arterial vasodilation accompany chronic portal hypertension. Different soluble mediators causing this vasodilation have been proposed, the strongest evidence being for nitric oxide (NO). No data exist if structural vascular changes may partly account for this vasod
Increased nitric oxide (NO) release has been implicated in the pathogenesis of the hyperdynamic circulation in portal hypertension. NOS 3 (eNOS) causes NO release from the endothelium in response to physical stimuli, such as increased blood flow and shear stress. We evaluated the functional activity
This study examined whether an increased activity of the endothelium-derived relaxing factor, nitric oxide, may account for the hyporesponsiveness to vasoconstrictors in portal hypertension. W e performed dose-response curves to methoxamine, an eadrenoceptor agonist, with and without N"dtr0-Larginin