Chronic administration of angiotensin-(1-7) attenuates pressure-overload left ventricular hypertrophy and fibrosis in rats
10.3321/j.issn:1673-4254.2005.05.001
- VernacularTitle:血管紧张素-(1-7)对腹主动脉缩窄大鼠心肌肥厚和纤维化的影响
- Author:
Li-Jun WANG
1
;
Jian-Gui HE
;
Hong MA
;
Yi-Ming CAI
;
Xin-Xue LIAO
;
Wu-Tao ZENG
;
Jun LIU
;
Li-Chun WANG
Author Information
1. 中山大学
- Keywords:
angiotensin-(l-7);
left ventricular;
hypertrophy;
fibrosis;
suprarenal aortic coarctation
- From:
Journal of Southern Medical University
2005;25(5):481-487
- CountryChina
- Language:Chinese
-
Abstract:
Background To test the hypothesis that chronic administration of angiotensin-(1-7) [Ang-(1-7)] attenuates cardiac hypertrophy in rats in vivo. Methods Coarctation of the suprarenal abdominal aorta was performed in 41 8-week-old male Sprague Dawley rats. Twenty-four hours after the operation, osmotic minipumps were surgically implanted subcutaneously in the rats, which were randomly divided into 3 groups, including a sham-operation group (n=15) receiving infusion with normal saline, a suprarenal aortic coarctation group (n=12), and a suprarenal aortic coarctation group (n=14) with Ang-(1-7) treatment at the dose of 25 μg.kg-1 .h-1. Four weeks later, the systolic and diastolic blood pressures were measured and the left ventricular mass index (LVMI, mg/g) was calculated from the ratio of left ventricular weight to body weight. The concentrations of Ang Ⅱ in the plasma and myocardium were measured by radioimmunoassay, and myocardial interstitial collagen volume fraction (ICVF) was determined by quantitative morphometry of the sections with Picrosirius red staining using an automated image analyzer. Results Suprarenal abdominal aortic coarctation induced a significant increase in carotid artery systolic and diastolic blood pressure, heart weight, LVMI, ICVF, and the concentration of Ang Ⅱ in the myocardium (P＜0.01). Chronic administration of Ang-(1-7) attenuated the increase in the heart weight, LVMI, ICVF and left ventricular diastolic end pressure (LVEDP) caused by suprarenal abdominal aortic coarctation (P＜0.05). Ang-(1-7) also increased the formerly decreased maximum left ventricular pressure reduction rate (-dP/dtmax) (P＜0.05), but had no effect on blood pressure and the concentration of Ang Ⅱ in the myocardium. No difference was noted in plasma concentration of Ang Ⅱ between the 3 groups. Conclusions Ang-(1-7) attenuates cardiac hypertrophy and fibrosis and preserved the impaired left ventricular function induced by left ventricular pressure-overload in rats. These effects are not associated with the changes in the concentrations of AngⅡin the left ventricular myocardium and plasma.
