Effect of Telmisartan on Myocardial Remodeling in Rats with Renovascular Hypertention
10.3870/j.issn.1004-0781.2015.09.010
- VernacularTitle:替米沙坦对肾性高血压大鼠心肌重构的影响
- Author:
Xin LI
;
Yuanyuan FENG
;
Xuanxuan SUN
;
Bing LI
- Publication Type:Journal Article
- Keywords:
Telmisartan;
Hypertension,renovascular;
Myocardial remodeling;
Calcium and nerve phosphatase;
β-myosin heavy chain
- From:
Herald of Medicine
2015;(9):1161-1164
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the the molecular mechanism of telmisartan for myocardial remodeling in rats with renovascular hypertention. Methods The renovascular hypertensive myocardial hypertrophy model of rats were established by narrowing the left renal artery.The total of 45 mature male SD rats were divided into sham-operated group(n= 15),model control (n = 15 ) and telmisartan group ( n = 15 ) randomly. The rats in telmisartan group were treated with telmisartan (10 mg?kg-1?d-1 ) while those in the sham-operated and model control were reated with the same amounts of distilled water by intragastrical administration . At 8th week of administration, the myocardial structure and function were detected by ultrasonography.The blood pressure was measured by arterial catheterization and calculating the left ventricular mass index (LVMI) .The level of serum calcium and nerve phosphatase ( CaN) and the expression of β-myosin heavy chain ( β-MHC) mRNA were detected. Results The thickness of left ventricular,ejection fraction[(69.23± 1.09)% vs(73.77± 3.00)%], fractional shortening [(30.21±2.02)% vs(35.29±0.90)%],LVMI[(2.83±0.14) mg?g-1 vs(2.32±0.11) mg?g-1 ] were decreased,and the differences were statistically significant (P<0.05).The level of serum calcium and nerve phosphatase (CaN) and the expression of β-myosin heavy chain (β-MHC) mRNA were decreased in telmisartan treated rats,and the differences were statistically significant (P< 0.05) when compared with the model control group. Conclusion Telmisartan can improve the myocardial hypertrophy of renovascular hypertensive rats,and it may downregulate the expression of β-MHC by inactivating of the start signal CaN and its downstream signal pathway.
