In:
Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2000-10), p. 683-683
Kurzfassung:
32 HMG-CoA reductase inhibitors have effects that extend beyond cholesterol reduction. We used an angiotensin (Ang) II-dependent model to test the hypothesis that cerivastatin ameliorates cardiac injury. We treated rats transgenic for human renin and angiotensinogen (dTGR) chronically from week 4 to 7 with cerivastatin (0.5 mg/kg/d by gavage). We used immunohistochemistry, electrophoretic mobility shift assays, and RT-PCR techniques. Compared to control dTGR, dTGR treated with cerivastatin had reduced mortality, blood pressure, cardiac hypertrophy, macrophage infiltration, and collagen I and IV deposition. Total plasma cholesterol was not different between the groups. Immunohistochemical analysis showed increased expression of basic fibroblast growth factor (b-FGF), IL-6, and the NF-κB subunit p65 in the media of dTGR, which was markedly reduced by cerivastatin. b-FGF mRNA in the left ventricle was also significantly reduced. The transcription factors NF-κB and AP-1 were substantially less activated in the left ventricle. These results suggest that statins ameliorate Ang II-induced hypertension, cardiac hypertrophy, and remodeling, independent of cholesterol reduction. They suggest that statins interfere with Ang II-induced signaling and transcription factor activation, thereby ameliorating end-organ damage.
Materialart:
Online-Ressource
ISSN:
0194-911X
,
1524-4563
DOI:
10.1161/hyp.36.suppl_1.683-c
Sprache:
Englisch
Verlag:
Ovid Technologies (Wolters Kluwer Health)
Publikationsdatum:
2000
ZDB Id:
2094210-2
