| Nebivolol treatment reduces serum levels of asymmetric dimethylarginine and improves endothelial dysfunction in essential hypertensive patients. | |
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MedLine Citation:
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PMID: 18772860 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: This study was conducted to evaluate (i) the effect of nebivolol, a selective beta1-adrenergic receptor antagonist, on plasma concentration of asymmetric dimethylarginine (ADMA) and on flow-mediated dilation (FMD) in essential hypertensive patients; (ii) the effect of serum derived from the treated hypertensive patients on ADMA and on dimethylarginine dimethylaminohydrolase 2 (DDAH2), the enzyme that selectively degrades ADMA, in human umbilical vein endothelial cells (HUVECs). METHODS: Forty healthy subjects and 40 matched essential hypertensive patients treated with atenolol and nebivolol according to a double-blind, randomized design participated in the study. Evaluation of brachial artery (BA) reactivity was performed by a longitudinal B-mode scan of the right BA. ADMA and L-arginine were measured by high-performance liquid chromatography. DDAH2 expression and endothelial nitric oxide synthase activity (eNOS) were also evaluated in HUVECs. RESULTS: ADMA levels were significantly decreased and FMD increased only in patients receiving nebivolol (P < 0.01). Furthermore, in nebivolol group, we found a significant correlation between changes in ADMA levels and changes in FMD (P < 0.01). Sera derived from patients treated with nebivolol but not with atenolol decreased ADMA and increased DDAH2 expression and eNOS activity (P < 0.001) in HUVECs. CONCLUSIONS: The results of this study demonstrate that the improvement of endothelial dysfunction induced by nebivolol in hypertensive patients may be related to its effect on circulating ADMA levels. Although the mechanism by which nebivolol reduces circulating ADMA in hypertensive patients remains unclear, our ex vivo results suggest that the upregulation of DDAH2 expression may have a role. |
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Authors:
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Anna Fratta Pasini; Ulisse Garbin; Chiara Stranieri; Veronica Boccioletti; Chiara Mozzini; Stefania Manfro; Andrea Pasini; Mattia Cominacini; Luciano Cominacini |
Publication Detail:
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Type: Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't Date: 2008-09-04 |
Journal Detail:
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Title: American journal of hypertension Volume: 21 ISSN: 1941-7225 ISO Abbreviation: Am. J. Hypertens. Publication Date: 2008 Nov |
Date Detail:
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Created Date: 2008-10-22 Completed Date: 2009-01-30 Revised Date: 2011-06-30 |
Medline Journal Info:
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Nlm Unique ID: 8803676 Medline TA: Am J Hypertens Country: United States |
Other Details:
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Languages: eng Pagination: 1251-7 Citation Subset: IM |
Affiliation:
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Department of Biomedical and Surgical Sciences, Section of Internal Medicine, University of Verona, Italy. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adrenergic beta-Antagonists
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pharmacology*,
therapeutic use Aged Amidohydrolases / metabolism Antihypertensive Agents / pharmacology, therapeutic use Arginine / analogs & derivatives*, blood Atenolol / pharmacology, therapeutic use Benzopyrans / pharmacology*, therapeutic use Double-Blind Method Endothelium, Vascular / drug effects, physiopathology* Ethanolamines / pharmacology*, therapeutic use Female Humans Hypertension / blood*, drug therapy, physiopathology* Male Middle Aged Nitric Oxide Synthase Type III / metabolism Vasodilation / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Adrenergic beta-Antagonists; 0/Antihypertensive Agents; 0/Benzopyrans; 0/Ethanolamines; 29122-68-7/Atenolol; 30315-93-6/N,N-dimethylarginine; 74-79-3/Arginine; 99200-09-6/nebivolol; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 3.5.-/Amidohydrolases; EC 3.5.3.18/dimethylargininase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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