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)
|Issue Date: ||2010|
|Publisher: ||Hindawi Publishing Corporation|
|Publisher version: ||http://www.hindawi.com/journals/mi/2010/105489/|
|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|
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).
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.
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.
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.