title: [Effects of lorsartan, fosinopril on myocardial fibrosis, angiotensin II and cardiac remolding in hypertensive rats].
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 circumferential 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Geriatric Cardiology, Xiangya Hospital, Central South University, Changsha 410008, China.
authors.forename: B X
authors.initials: BX
authors.lastname: He
authors.forename: G L
authors.initials: GL
authors.lastname: Yu
authors.forename: X Q
authors.initials: XQ
authors.lastname: Liang
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D005355:Fibrosis; D017328:Fosinopril / Q000494:pharmacology*; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology; D019808:Losartan / Q000494:pharmacology*; D008297:Male; D009206:Myocardium / Q000473:pathology*; D011897:Random Allocation; D051381:Rats; D011918:Rats, Inbred SHR; D020257:Ventricular Remodeling
chemical_list: D000959:Antihypertensive Agents; D000804:Angiotensin II; D019808:Losartan; D017328:Fosinopril