Dadun/></a>
				</td>
				<td class= Dadun
   (New user)
Help  | Contact  |  Castellano English  
 

Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Ciencias Cardiovasculares > Enfermedad vascular hipertensiva > DA - CIMA - Cardiovasculares - Enfermedad vascular - Artículos de Revista >

Leptin inhibits the proliferation of vascular smooth muscle cells induced by angiotensin II through nitric oxide-dependent mechanisms
Authors: Rodriguez, A. (Amaia)
Gomez-Ambrosi, J. (Javier)
Catalan, V. (Victoria)
Fortuño, A. (Ana)
Frühbeck, G. (Gema)
Keywords: Leptin
Angiotensin II
Nitric Oxide
Issue Date: 2010
Publisher: Hindawi Publishing Corporation
Publisher version: http://www.hindawi.com/journals/mi/2010/105489/
ISSN: 1466-1861
Citation: Rodriguez A, Gomez-Ambrosi J, Catalan V, Fortuño A, Fruhbeck G. Leptin inhibits the proliferation of vascular smooth muscle cells induced by angiotensin II through nitric oxide-dependent mechanisms. Mediators Inflamm 2010;2010:105489
Abstract
OBJECTIVE: This study was designed to investigate whether leptin modifies angiotensin (Ang) II-induced proliferation of aortic vascular smooth muscle cells (VSMCs) from 10-week-old male Wistar and spontaneously hypertensive rats (SHR), and the possible role of nitric oxide (NO). METHODS: NO and NO synthase (NOS) activity were assessed by the Griess and (3)H-arginine/citrulline conversion assays, respectively. Inducible NOS (iNOS) and NADPH oxidase subutnit Nox2 expression was determined by Western-blot. The proliferative responses to Ang II were evaluated through enzymatic methods. RESULTS: Leptin inhibited the Ang II-induced proliferative response of VSMCs from control rats. This inhibitory effect of leptin was abolished by NOS inhibitor, NMMA, and iNOS selective inhibitor, L-NIL, and was not observed in leptin receptor-deficient fa/fa rats. SHR showed increased serum leptin concentrations and lipid peroxidation. Despite a similar leptin-induced iNOS up-regulation, VSMCs from SHR showed an impaired NOS activity and NO production induced by leptin, and an increased basal Nox2 expression. The inhibitory effect of leptin on Ang II-induced VSMC proliferation was attenuated. CONCLUSION: Leptin blocks the proliferative response to Ang II through NO-dependent mechanisms. The attenuation of this inhibitory effect of leptin in spontaneous hypertension appears to be due to a reduced NO bioavailability in VSMCs.
Permanent link: http://hdl.handle.net/10171/17923
Appears in Collections:DA - Medicina - Endocrinología - Artículos de revista
DA - CUN - Endocrinología y Nutrición - Artículos de revista
DA - CIFA - Laboratorio de investigación metabólica - Artículos de Revista
DA - CIMA - Cardiovasculares - Enfermedad vascular - Artículos de Revista

Files in This Item:

There are no files associated with this item.

Items in Dadun are protected by copyright, with all rights reserved, unless otherwise indicated.