A67 BREAKDOWN: THE CELLULAR CONTRIBUTION TO PULMONARY HYPERTENSION: Enhanced Endothelium-Dependent Pulmonary Vasodilation And Enos Expression Limit Increased Vasoconstrictor Sensitivity In Neonatal Chronic Hypoxia

To test this hypothesis, we assessed effects of the NO synthase (NOS) inhibitor Nw-nitro-L-arginine (L-NNA) on baseline pulmonary vascular resistance (PVR) and vasoconstrictor sensitivity to the thromboxane mimetic U-46619 in saline-perfused lungs (in situ) from 2-wk-old control and CH (2 wk at 0.5...

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Bibliographic Details
Published in:	American journal of respiratory and critical care medicine Vol. 195
Main Authors:	Sheak, J R, DeKay, R J, Jernigan, N L, Walker, B R, Resta, T C
Format:	Journal Article
Language:	English
Published:	New York American Thoracic Society 01-01-2017
Subjects:	Hypotheses Hypoxia Newborn babies Nitric oxide Phosphorylation Pulmonary hypertension Rodents
Online Access:	Get full text
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Summary:	To test this hypothesis, we assessed effects of the NO synthase (NOS) inhibitor Nw-nitro-L-arginine (L-NNA) on baseline pulmonary vascular resistance (PVR) and vasoconstrictor sensitivity to the thromboxane mimetic U-46619 in saline-perfused lungs (in situ) from 2-wk-old control and CH (2 wk at 0.5 atm) rats. Exposure to CH additionally augmented NO-dependent vasodilatory responses to arginine vasopressin (AVP), pulmonary expression of NOS III (eNOS), and eNOS phosphorylation at activation residue serine-1177.
ISSN:	1073-449X 1535-4970