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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2002, Vol. 7 ›› Issue (4): 306-310.

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Effects of simvastatin on myocardial fibrosis in NO-deficient hypertensive rats

YI Chun-Tao, CHENG Xiao-Shu, YU Jian-Hua, YAN Ding-Hong, SU Hai, WU Qing-Hua   

  1. Department of Cardiology, The Second Affiliated Hospital of Jiangxi Medical College, Nanchang 33000
  • Received:2002-04-23 Revised:2002-05-16 Online:2002-08-26 Published:2020-11-24

Abstract: AIM: To investigate the effects of simvastatin on myocardial fibrosis in NO-deficient hypertensive rats. METHODS: Twenty-four male Wistar-Kyoto rats were divided into three groups: Control ( C) group, L-NAME ( L) group, and L-NAME plus Simvastatin ( L +S) group. The levels of ACE and Ang Ⅱ in plasma and myocardial tissue, and the contents of hydroxyproline concentration in myocardial tissue were measured after 8 weeks. The values of CVF, PVCA and the hydroproline concentration ( HC ) were studied using the methods of pathological examination combined with computed processing. RESULTS: The activity of ACE in serum in L group was lower than that in C group ( P <0. 01). Simvastatin treatment did not significantly increase the activity of ACE compared with L group ( P >0. 05). However, the activity of ACE in myocardial tissue was lower than that of C group ( P <0. 05). Although the levels of Ang Ⅱ in plasma were not altered by L-NAME ( P >0. 05), the concentrations of Ang Ⅱ in myocardial tissue ( P < 0. 01) were significantly increased in L group compared to C group. Simvastatin significantly decreased the levels of Ang Ⅱ in myocardial tissue ( P <0. 05). The hydroxyproline concentration and the value of PVCA and CVF in L group were significantly higher than that in C group ( P <0. 01), which were significantly attenuated by simvastatin tratment ( P <0. 05). CONCLUSION: Simvastatin may decrease the production of Ang Ⅱ and attenuate myocardial fibrosis via reducing the activity of ACE in NOdeficient hypertensive rats.

Key words: simvastatin, angiotensin Ⅱ, myocardial fibrosis, angiotensin-converting enzyme, hypertension, NOS inhibitor

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