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Type: Artigo de periódico
Title: Enhanced Endothelium-dependent Relaxation Of Rat Pulmonary Artery Following Beta-adrenergic Overstimulation: Involvement Of The No/cgmp/vasp Pathway
Author: Davel
Ana P.; Victorio
Jamaira A.; Delbin
Maria A.; Fukuda
Livia E.; Rossoni
Luciana V.
Abstract: Aims: The aim of this study was to investigate whether beta-adrenoceptor (beta-AR) overstimulation induced by in vivo treatment with isoproterenol (ISO) alters vascular reactivity and nitric oxide (NO) production and signaling in pulmonary arteries. Main methods: Vehicle or ISO (0.3 mg kg(-1), day(-1)) was administered daily to male Wistar rats. After 7 days, the jugular vein was cannulated to assess right ventricular (RV) systolic pressure (SP) and end diastolic pressure (EDP). The extralobar pulmonary arteries were isolated to evaluate the relaxation responses, protein expression (Western blot), NO production (diaminofluorescein-2 fluorescence), and cyclic guanosine 3',5'-monophosphate (cGMP) levels (enzyme immunoassay kit). Key findings: ISO treatment induced RV hypertrophy; however, no differences in RV-SP and EDP were observed. The pulmonary arteries from the ISO-treated group showed enhanced relaxation to acetylcholine that was abolished by the NO synthase (NOS) inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME); whereas relaxation elicited by sodium nitroprusside, ISO, metaproterenol, mirabegron, or KCI was not affected by ISO treatment. ISO-treated rats displayed enhanced endothelial NOS (eNOS) and vasodilator-stimulated phosphoprotein (VASP) expression in the pulmonary arteries, while phosphodiesterase-5 protein expression decreased. ISO treatment increased NO and cGMP levels and did not induce eNOS uncoupling. Significance: The present data indicate that beta-AR overactivation enhances the endothelium-dependent relaxation of pulmonary arteries. This effect was linked to an increase in eNOS-derived NO production, cGMP formation and VASP content and to a decrease in phosphodiesterase-5 expression. Therefore, elevated NO bioactivity through cGMP/VASP signaling could represent a protective mechanism of beta-AR overactivation on pulmonary circulation. (C) 2015 Elsevier Inc. All rights reserved.
Subject: Nitric-oxide Synthase
Adrenoceptor-mediated Responses
Right-ventricular Hypertrophy
Sympathetic-nerve Activity
Protein Expression
Chronic Hypoxia
Country: OXFORD
Citation: Enhanced Endothelium-dependent Relaxation Of Rat Pulmonary Artery Following Beta-adrenergic Overstimulation: Involvement Of The No/cgmp/vasp Pathway. Pergamon-elsevier Science Ltd, v. 125, p. 49-56 Mar-2015.
Rights: embargo
Identifier DOI: 10.1016/j.lfs.2015.01.018
Date Issue: 2015
Appears in Collections:Unicamp - Artigos e Outros Documentos

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