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

The inhibitory effect of leptin on angiotensin II-induced vasoconstriction is blunted in spontaneously hypertensive rats
Autor(es) : Rodriguez, A. (Amaia)
Frühbeck, G. (Gema)
Gomez-Ambrosi, J. (Javier)
Catalan, V. (Victoria)
Sainz, N. (Neira)
Diez, J. (Javier)
Zalba, G. (Guillermo)
Fortuño, A. (Ana)
Palabras clave : Leptin
Smooth muscle
Fecha incorporación: 2006
Editorial : Lippincott, Williams & Wilkins
Versión del editor: http://bit.ly/kNGL8G
ISSN: 1473-5598
Cita: Rodriguez A, Fruhbeck G, Gomez-Ambrosi J, Catalan V, Sainz N, Diez J, et al. The inhibitory effect of leptin on angiotensin II-induced vasoconstriction is blunted in spontaneously hypertensive rats. J Hypertens 2006 Aug;24(8):1589-1597.
OBJECTIVE: Leptin attenuates the angiotensin II-induced increase of cytosolic calcium ([Ca2+]i) and vasoconstriction in the aorta of normotensive Wistar rats. To determine whether these effects may be altered in hypertension, we assessed the effect of leptin on angiotensin II-induced vascular response in the aorta of 10-week-old spontaneously hypertensive rats (SHR). METHODS: Contractile responses to angiotensin II (100 nmol/l) in the presence of different concentrations of leptin (0.1, 1, 10, 100 nmol/l) were evaluated in isolated aortic rings by the organ bath system. [Ca2+]i was measured in vascular smooth muscle cells (VSMCs) using Fura-2 fluorescence. The expression of the short (OB-Ra) and long (OB-Rb) isoforms of the leptin receptor in VSMCs was evaluated by real-time reverse transcriptase-polymerase chain reaction and western-blot analysis. RESULTS: Circulating leptin concentrations were increased in SHR. Serum metabolic parameters, including glucose, insulin, total cholesterol and triglyceride levels, were also elevated in SHR. Leptin did not modify the angiotensin II-induced vasoconstriction in SHR either in intact or endothelium-denuded aortic rings. In addition, leptin was not able either to diminish the angiotensin II-induced the peak rise of [Ca2+]i or to accelerate the recovery rate to basal calcium levels in VSMCs from SHR. However, OB-Ra and OB-Rb mRNA and protein expression were increased in SHR VSMCs. CONCLUSIONS: The lack of effect of leptin on angiotensin II-induced contraction in the aorta of SHR is due to an impaired handling of [Ca2+]i in VSMCs. Hyperleptinemia and overexpression of OB-R in VSMCs could be compensatory mechanisms against VSMC leptin resistance in genetically hypertensive rats.
Enlace permanente: http://hdl.handle.net/10171/18589
Aparece en las colecciones: DA - Medicina - Endocrinología - Artículos de revista
DA - CUN - Endocrinología y Nutrición - Artículos de revista
DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista
DA - CIFA - Laboratorio de investigación metabólica - Artículos de Revista
DA - CIMA - Cardiovasculares - Enfermedad vascular - Artículos de Revista

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