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dc.contributor.authorKrause B.J.
dc.contributor.authorDel Rio R.
dc.contributor.authorMoya E.A.
dc.contributor.authorMarquez-Gutierrez M.
dc.contributor.authorCasanello P.
dc.contributor.authorIturriaga R.
dc.date.accessioned2020-09-02T22:21:09Z
dc.date.available2020-09-02T22:21:09Z
dc.date.issued2015
dc.identifier10.1097/HJH.0000000000000453
dc.identifier.citation33, 3, 515-524
dc.identifier.issn02636352
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5009
dc.descriptionOBJECTIVE:: Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnoea, is associated with impaired vascular function despite unaltered response to nitric oxide donors. This study addressed whether arginase contributes to the endothelial dysfunction in CIH rats. METHODS:: Adult male Sprague-Dawley rats were exposed for 21 days to CIH (5% oxygen, 12 times/h, 8h/day). The internal carotid arteries were isolated to study endothelial nitric oxide synthase (eNOS) and arginase-1 levels by western blot and immunohistochemistry, and their vasoactive responses using wire myography. Relaxation to sodium nitroprusside (SNP; nitric oxide donor) in the presence or absence of soluble guanylyl cyclase inhibitor, and acetylcholine with and without a NOS inhibitor [N-nitro-L-arginine (L-NA)] and the arginase inhibitor BEC were determined. RESULTS:: Arteries from the CIH rats presented higher active contraction induced by KCl (3.5±0.4 vs. 2.3±0.2N/m), augmented media-to-lumen ratio (∼40%), decreased relaxation to acetylcholine (12.8±1.5 vs. 30.5±4.6%) and increased sensitivity to SNP (pD2 7.3±0.1 vs. 6.7±0.1). Arginase inhibition reversed the impaired acetylcholine-induced relaxation in CIH arteries (49.5±7.4%), an effect completely blocked by L-NA. In the carotid arteries, arginase-1 protein level was increased, whereas eNOS levels decreased in the CIH arteries. CONCLUSION:: The current results suggest that endothelial dysfunction in CIH-induced hypertension may result from imbalanced arginase-1 to eNOS expression, vascular remodelling and increased contractile capacity, rather than decreased vascular response to nitric oxide. © 2015 Wolters Kluwer Health, Inc.
dc.language.isoen
dc.publisherLippincott Williams and Wilkins
dc.subjectarginase
dc.subjectchronic intermittent hypoxia
dc.subjectendothelial dysfunction
dc.subjectnitric oxide
dc.subjectvascular reactivity
dc.subjectacetylcholine
dc.subjectarginase 1
dc.subjectendothelial nitric oxide synthase
dc.subjectenzyme inhibitor
dc.subjectguanylate cyclase inhibitor
dc.subjectn(g) nitroarginine
dc.subjectnitric oxide donor
dc.subjectnitroprusside sodium
dc.subjectoxygen
dc.subjectpotassium chloride
dc.subjectacetylcholine
dc.subjectarginase
dc.subjectarginase I, human
dc.subjectendothelial nitric oxide synthase
dc.subjectnitric oxide
dc.subjectnitric oxide donor
dc.subjectnitroprusside sodium
dc.subjectadult
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectartery endothelium
dc.subjectArticle
dc.subjectblood pressure
dc.subjectblood vessel tone
dc.subjectchronic intermittent hypoxia
dc.subjectcontrolled study
dc.subjectendothelial dysfunction
dc.subjectenzyme inhibition
dc.subjectexternal carotid artery
dc.subjecthypertension
dc.subjectimmunohistochemistry
dc.subjectinternal carotid artery
dc.subjectisolation procedure
dc.subjectmale
dc.subjectmorphology
dc.subjectmyography
dc.subjectnonhuman
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectrat
dc.subjectsensitivity analysis
dc.subjectvasodilatation
dc.subjectWestern blotting
dc.subjectanimal
dc.subjectanoxia
dc.subjectartery
dc.subjectdrug effects
dc.subjectmetabolism
dc.subjectpathophysiology
dc.subjectphysiology
dc.subjectSprague Dawley rat
dc.subjectvascular endothelium
dc.subjectAcetylcholine
dc.subjectAnimals
dc.subjectAnoxia
dc.subjectArginase
dc.subjectArteries
dc.subjectEndothelium, Vascular
dc.subjectMale
dc.subjectNitric Oxide
dc.subjectNitric Oxide Donors
dc.subjectNitric Oxide Synthase Type III
dc.subjectNitroprusside
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectVasodilation
dc.titleArginase-endothelial nitric oxide synthase imbalance contributes to endothelial dysfunction during chronic intermittent hypoxia
dc.typeArticle


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