Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Angiotensin II-induced cardiomyocyte hypertrophy and cardiac fibrosis in stroke-prone spontaneously hypertensive rats
Autore:
Ikeda, Y; Nakamura, T; Takano, H; Kimura, H; Obata, JE; Takeda, S; Hata, A; Shido, K; Mochizuki, S; Yoshida, Y;
Indirizzi:
Yamanashi Med Univ, Div Blood Transfus, Yamanashi 4093898, Japan YamanashiMed Univ Yamanashi Japan 4093898 fus, Yamanashi 4093898, Japan Yamanashi Med Univ, Dept Internal Med, Yamanashi 4093898, Japan Yamanashi Med Univ Yamanashi Japan 4093898 Med, Yamanashi 4093898, Japan Yamanashi Med Univ, Dept Pathol, Yamanashi 4093898, Japan Yamanashi Med Univ Yamanashi Japan 4093898 hol, Yamanashi 4093898, Japan Hokkaido Univ, Sch Med, Dept Publ Hlth, Sapporo, Hokkaido 060, Japan Hokkaido Univ Sapporo Hokkaido Japan 060 th, Sapporo, Hokkaido 060, Japan Jikei Univ, Sch Med, Aoto Hosp, Dept Med, Tokyo, Japan Jikei Univ Tokyo Japan Univ, Sch Med, Aoto Hosp, Dept Med, Tokyo, Japan
Titolo Testata:
JOURNAL OF LABORATORY AND CLINICAL MEDICINE
fascicolo: 4, volume: 135, anno: 2000,
pagine: 353 - 359
SICI:
0022-2143(200004)135:4<353:AICHAC>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
CORONARY VASODILATOR RESERVE; LEFT-VENTRICULAR MASS; CONVERTING ENZYME; PRESSURE-OVERLOAD; IN-VIVO; HEART; INTERSTITIUM; CONTRACTILE; HYPERPLASIA; REGRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Nakamura, T Yamanashi Med Univ, Div Blood Transfus, Yamanashi 4093898, Japan Yamanashi Med Univ Yamanashi Japan 4093898 hi 4093898, Japan
Citazione:
Y. Ikeda et al., "Angiotensin II-induced cardiomyocyte hypertrophy and cardiac fibrosis in stroke-prone spontaneously hypertensive rats", J LA CL MED, 135(4), 2000, pp. 353-359

Abstract

Angiotensin-converting enzyme inhibitors (ACEIs) cause regression of hypertensive left ventricular hypertrophy (LVH) by reducing angiotensin II, increasing bradykinin, or both. The mechanisms of these cardioprotective effects remain controversial. The aims of this study were to determine whether the cardioprotective effects of ACEIs are mediated by reducing angiotensin IIand whether ACEIs ameliorate the morphologic, physiologic, and biochemicalchanges in the hearts of stroke-prone spontaneously hypertensive rats (SHRSPs). Male SHRSPs were treated with hydralazine, captopril, or candesartan,an angiotensin II type 1 receptor(AT1R) antagonist, from age 12 to 24 weeks. We measured systolic blood pressure (SBP), left ventricular weight (LVW), left ventricular (LV) myocyte cross-sectional area (myocyte size), LV interstitial collagen volume fraction (ICVF), perivascular collagen area/luminal area ratio (PVCA/LA), the medial area to luminal area ratio (MA/LA), therelative amount of V3 myosin heavy chain (MHCV3), and coronary reserve maximum (coronary flow max/ventricular weight (CFmax/VW)). These parameters were compared with those of untreated SHRSPs and Wistar-Kyoto mts (WKYs). SHRSPs exhibited decreased coronary reserve and LVH with an increase in myocyte size, PVCA/LA, MA/LA, and MHCV3 at 12 weeks of age. In addition to these changes, 24-week-old SHRSPs showed an increase in ICVF. The LVW coronary reserve, myocyte size, PVCA/LA, ICVF, and MHCV3 of SHRSPs treated with captopril or candesartan all approached control values. In contrast, hydralazine decreased only ICVF. These results suggest that ACEIs regress LVH and normalize coronary reserve by modulating the effects of angiotensin II via AT1R on the induction of cardiomyocyte hypertrophy, perivascular fibrosis, and medial thickening of intramyocardial coronary arteries in SHRSPs. We concluded that these effects, in addition to the reduction of SEP, are important in causing the regression of LVH.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 17/01/21 alle ore 17:09:36