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

Fibrosis in hypertensive heart disease: role of the renin-angiotensin-aldosterone system
Autor(es) : Gonzalez, A. (Arantxa)
Lopez, B. (Begoña)
Diez, J. (Javier)
Palabras clave : Angiotensin II/physiology
Collagen/biosynthesis
Collagen/metabolism
Collagen/physiology
Hypertension/pathology
Renin-Angiotensin System/physiology
Fecha incorporación: 2004
Editorial : WB Saunders
Versión del editor: http://www.medical.theclinics.com/issues
ISSN: 1557-9859
Cita: Gonzalez A, Lopez B, Diez J. Fibrosis in hypertensive heart disease: role of the renin-angiotensin-aldosterone system. Med Clin North Am 2004 Jan;88(1):83-97.
Resumen
Structural homogeneity of cardiac tissue is governed by mechanical and humoral factors that regulate cell growth, apoptosis, phenotype, and extracellular matrix turnover. ANGII has endocrine, autocrine, and paracrine properties that influence the behavior of cardiac cells and matrix by AT1 receptor binding. Various paradigms have been suggested, including ANGII-mediated up-regulation of collagen types I and III formation and deposition in cardiac conditions, such as HHD. A growing body of evidence, however, deals with the potential role of aldosterone, either local or systemic, in inducing cardiac fibrosis. Aldosterone might also mediate the profibrotic actions of ANGII. To reduce the risk of heart failure that accompanies HHD, its adverse structural remodeling (eg, myocardial hypertrophy and fibrosis) must be targeted for pharmacologic intervention. Cardioprotective agents must reverse not only the exaggerated growth of cardiac cells, but also regress existing abnormalities in fibrillar collagen. Available experimental and clinical data suggest that agents interfering with ACE, the AT1 receptor, or the mineralocorticoid receptor may provide such a cardioprotective effect.
Enlace permanente: http://hdl.handle.net/10171/21896
Aparece en las colecciones: DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista

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Fichero:  MedClinNAm2004_8883.pdf
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