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Titolo:
Renin angiotensin system-dependent hypertrophy as a contributor to heart failure in hypertensive rats: Different characteristics from renin angiotensin system-independent hypertrophy
Autore:
Sakata, Y; Masuyama, T; Yamamoto, K; Doi, R; Mano, T; Kuzuya, T; Miwa, T; Takeda, H; Hori, M;
Indirizzi:
Osaka Univ, Grad Sch Med, Dept Internal Med & Therapeut A8, Suita, Osaka 5650871, Japan Osaka Univ Suita Osaka Japan 5650871 peut A8, Suita, Osaka 5650871, Japan Osaka Univ, Genome Informat Res Ctr, Suita, Osaka 5650871, Japan Osaka Univ Suita Osaka Japan 5650871 Res Ctr, Suita, Osaka 5650871, Japan Osaka Univ, Grad Sch Med, Dept Med Informat Sci, Suita, Osaka, Japan OsakaUniv Suita Osaka Japan Dept Med Informat Sci, Suita, Osaka, Japan
Titolo Testata:
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
fascicolo: 1, volume: 37, anno: 2001,
pagine: 293 - 299
SICI:
0735-1097(200101)37:1<293:RASHAA>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
LEFT-VENTRICULAR HYPERTROPHY; RECEPTOR KNOCKOUT MICE; PRESSURE-OVERLOAD HYPERTROPHY; ASCENDING AORTIC-STENOSIS; MYOCYTES IN-VITRO; CARDIAC MYOCYTES; MECHANICAL STRETCH; AT(1) RECEPTOR; EXPRESSION; RESPONSES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Masuyama, T Osaka Univ, Grad Sch Med, Dept Internal Med & Therapeut A8, 2-2 Yamadaoka,Suita, Osaka 5650871, Japan Osaka Univ 2-2 Yamadaoka Suita Osaka Japan 5650871 0871, Japan
Citazione:
Y. Sakata et al., "Renin angiotensin system-dependent hypertrophy as a contributor to heart failure in hypertensive rats: Different characteristics from renin angiotensin system-independent hypertrophy", J AM COL C, 37(1), 2001, pp. 293-299

Abstract

OBJECTIVES This study aimed to characterize the difference between renin angiotensin system (RAS)dependent and PAS-independent hypertrophy and their differential contribution to the transition to heart failure. BACKGROUND Hypertensive left ventricular (LV) hypertrophy develops with RAS activation in the heart; however, LV hypertrophy develops even without RAS activation. METHODS Left ventricular geometry and function were assessed in Dahl salt-sensitive rats placed on an 8% NaCl diet from seven weeks old (hypertensiverats) and in those placed on an 0.3% NaCl diet (control rats, n = 8). The hypertensive rats were randomized to no treatment (n = 8) or treatment withthe angiotensin type 1 receptor (AT(1)R) antagonist candesartan (1 mg/kg per day, n = 10) after the baseline echocardiography study. RESULTS From 7 to 13 weeks, AT(1)R blockade at a subdepressor dose did notrestrain the development of LV hypertrophy but prevented narrowing of LV diastolic dimension, leading to the normalization of abnormally decreased end-systolic wall stress in the untreated rats. Progressive development of LVhypertrophy in spite of lower than normal end-systolic wall stress (excessive hypertrophy) after 13 weeks was suppressed by the AT(1)R blockade. Elevation of LV end-diastolic pressure and prolongation of Tau were associated with histological evidence of myocyte hypertrophy and massive interstitial fibrosis in the untreated rats, and none of these was evident in the treated rats. CONCLUSIONS Renin-angiotensin system activation and AT(1)R signaling may be dispensable for the development of early adaptive LV hypertrophy and closely linked to the transition to heart failure. (J Am Cell Cardiol 2001;37:293-9) (C) 2001 by the American College of Cardiology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 21:38:35