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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 >

Losartan inhibits the post-transcriptional synthesis of collagen type I and reverses left ventricular fibrosis in spontaneously hypertensive rats
Autor(es) : Varo, N. (Nerea)
Etayo, J.C. (Juan Carlos)
Zalba, G. (Guillermo)
Beaumont, J. (Javier)
Iraburu, M. (María)
Montiel-Duarte, C. (Cristina)
Gil, M.J. (María José)
Monreal, J.I. (José Ignacio)
Diez, J. (Javier)
Palabras clave : Angiotensin
Collagen
Losartan
Myocardial fibrosis
Spontaneously hypertensive rats
Fecha incorporación: 1999
Editorial : Lippincott williams and wilkins
Versión del editor: http://journals.lww.com/jhypertension/Abstract/1999/17010/Losartan_inhibits_the_post_transcriptional.16.aspx
ISSN: 0263-6352
Cita: Varo N, Etayo JC, Zalba G, Beaumont J, Iraburu MJ, Montiel C, et al. Losartan inhibits the post-transcriptional synthesis of collagen type I and reverses left ventricular fibrosis in spontaneously hypertensive rats. J Hypertens 1999 Jan;17(1):107-114.
Resumen
OBJECTIVE: Previous studies have shown that as well as left ventricular hypertrophy, myocardial fibrosis develops early in rats with spontaneous hypertension (SHR). The present study was designed to investigate whether chronic treatment with the angiotensin II type 1 (AT1) receptor antagonist losartan modifies collagen type I metabolism and reverses left ventricular fibrosis in young SHR with left ventricular hypertrophy. DESIGN: The study was performed in 30-week-old normotensive Wistar-Kyoto (WKY) rats, untreated SHR and SHR treated with losartan (20 mg/mg per day, orally) for 14 weeks before they were killed. METHODS: Ventricular pro-alpha 1 (I) collagen messenger RNA was analyzed by Northern blot. Serum levels of the carboxy-terminal propeptide of procollagen type I (PIP) and the pyridoline cross-linked telopeptide domain of collagen type I (CITP) were determined by specific radioimmunoassays as markers of collagen type I synthesis and degradation, respectively. Collagen volume fraction was determined in the left ventricle by quantitative morphometry. RESULTS: Compared with WKY rats, SHR exhibited increased (P < 0.05) mean arterial pressure, pro-alpha 1 (I) collagen messenger RNA, PIP and left ventricular collagen volume fraction, and similar CITP values. After the treatment period, mean arterial pressure was higher (P < 0.05) in losartan-treated SHR than in WKY rats. Compared with untreated SHR, treated SHR showed no left ventricular hypertrophy and diminished (P < 0.05) values of mean arterial pressure, PIP and left ventricular collagen volume fraction. No changes in pro-alpha 1 (I) collagen messenger RNA and CITP values were observed with treatment in SHR. No significant differences in the left ventricular collagen volume fraction were observed between treated SHR with normal blood pressure and treated SHR with abnormally high blood pressure at the end of the treatment period. CONCLUSIONS: These results suggest that chronic AT1 blockade with losartan decreases the post-transcriptional synthesis of fibril-forming collagen type I molecules in young SHR. This effect may be involved in the ability of this drug to reverse left ventricular fibrosis in young rats with genetic hypertension. Apart from its antihypertensive action, other mechanisms may mediate the antifibrotic effect of losartan in this animal model.
Enlace permanente: http://hdl.handle.net/10171/20253
Aparece en las colecciones: DA - CIMA - Cardiovasculares - Enfermedad vascular - Artículos de Revista
DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista

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