Effects of Lorsartan, Fosinopril on myocardial fibrosis, angiotensin Ⅱ and cardiac remolding in hypertensive rats
- VernacularTitle:氯沙坦、福辛普利对高血压大鼠心肌纤维化、血管紧张素Ⅱ及左室重构的影响
- Author:
Bixiu HE
;
Guolong YU
;
Xiaoqiu LIANG
- Publication Type:Journal Article
- From:
Journal of Central South University(Medical Sciences)
2001;26(2):118-120
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate effects of lorsartan, fosinopril on myocardial fibrosis, angiotensin Ⅱ and cardiac remolding in the spontaneously hypertensive rats (SHR). Methods: 16-week-old SHRs were divided randomly into 3 groups: SHR-L (treated with lorsartan), SHR-F (treated with fosinopril) and SHR-C (untreated), each group consisting of 10 rats. After 8 weeks' and 16 weeks' therapeutic period, collagen volume fraction (CVF), perivascular circuferential area (PVCA), plasma and myocardium angiotensin Ⅱ concentrations were examined by pathological examination with computed processing and radioimmunoassay respectively. Results: (1) Compared with SHR-C after 8 weeks' and 16 weeks' therapeutic period, the systolic blood pressure (SBP) was decreased similarly in both treatment groups. Heart and left ventricular weights, heart weight and eft ventricular mass indexes were lower significantly in both treatment groups than in SHR-C. Left ventricular mass index was reduced to a lower extent in SHR-F group than in SHR-L group after 16 weeks. (2) Compared with SHR-C, CVF, PVCA after 8 weeks and 16 weeks were reduced significantly in SHR-F and SHR-L. Meanwhile, CVF after 16 weeks in SHR-F than in SHR-L. (3) Compared with SHR-C after both therapeutic periods, plasma and myocardium angiotensin Ⅱ concentrations were increased Significantly in SHR-L, but plasma angiotensin Ⅱ concentrations were not altered significantly in SHR-F. However, myocardium angiotensin Ⅱ concentrations were reduced significantly in SHR-F after 8 weeks and 16 weeks in SHR-F. Conclusion: Lorsartan, fosinopril inhibit myocardial fibrosis and reverse heart hypertrophy. Fosinopril may be more effective in these above effects than Lorsartan. The mechanism of the both drug's cardioprotective effects was related to inhibition of myocardium rennin-angiotension-aldsteron system.
