(Institución)/></a>
				</td>
				<td class= (Institución)
   (Nuevo usuario)
Ayuda  | Contacto  |  Castellano English  
 

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

Angiotensin converting enzyme inhibition prevents polyploidization of cardiomyocytes in spontaneously hypertensive rats with left ventricular hypertrophy
Autor(es) : Panizo-Santos, A. (Ángel)
Sola, J.J. (Jesús J.)
Pardo-Mindan, F.J. (Francisco Javier)
Hernandez, M. (M.)
Cenarruzabeitia, E. (Edurne)
Diez, J. (Javier)
Palabras clave : Heart
Polyploidization
Myocardial hypertrophy
Angiotensin converting enzyme
Spontaneously hypertensive rats
Flow cytometry
Arterial hypertension
Fecha incorporación: 1995
Editorial : John Wiley and Sons
Versión del editor: http://onlinelibrary.wiley.com/doi/10.1002/path.1711770415/abstract
ISSN: 1096-9896
Cita: Panizo-Santos A, Sola JJ, Pardo-Mindan FJ, Hernandez M, Cenarruzabeitia E, Diez J. Angiotensin converting enzyme inhibition prevents polyploidization of cardiomyocytes in spontaneously hypertensive rats with left ventricular hypertrophy. J Pathol 1995 Dec;177(4):431-437.
Resumen
Polyploidization of cardiomyocyte nuclei is a physiological phenomenon that increases in pathological conditions such as myocardial hypertrophy. The purpose of this study was to evaluate the potential benefit of the angiotensin converting enzyme (ACE) inhibitor quinapril in reversing the polyploidization of cardiomyocyte nuclei in spontaneously hypertensive rats (SHR) with established left ventricular hypertrophy (LVH). Sixteen week-old male SHR were treated with oral quinapril (average dose 10 mg/kg per day) for 20 weeks. Sixteen- and 36-week-old untreated SHR and 16- and 36-week-old normotensive Wistar-Kyoto (WKY) rats were used as controls. Nuclear polyploidization was determined by DNA flow cytometry of frozen tissues from the left ventricle, at least 20 000 nuclei being measured in each sample. The rates of tetraploidy in the 16- and 36-week-old SHR groups were 2·8 per cent (range 2·16-3 per cent) and 5·4 per cent (range 4·9–5·9 per cent), respectively. Treated SHR had a similar rate of DNA tetraploidy to the 16- and 36-week-old WKY rat groups: 1·8 per cent (range 1·5–2·3 per cent), 1·55 per cent (range 1·5–1·6 per cent), and 1·5 per cent (range 1·4–1·6 per cent), respectively. The differences in the percentage of tetraploid cardiomyocytes between the SHR untreated groups and the SHR treated group were statistically significant (P<0·05). Regression of LVH and normalization of blood pressure were observed in treated rats. These results indicate that DNA tetraploidy in the myocardium of SHR increases with hypertrophy and decreases on quinapril treatment. It is suggested that ACE inhibition modifies nuclear processes involved in myocyte growth in arterial hypertension.
Enlace permanente: http://hdl.handle.net/10171/22020
Aparece en las colecciones: DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista

Ficheros en este registro:

No hay ficheros asociados a este ítem.

Los ítems de Dadun están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.