Change Of AT₁R,Cardiotrophin-1 And Glycoprotein130 In The Heart Of Rats With Left Ventricular Hypertrophy Induced By Pressure Overloaded And Effect Of Telmisartan

Objectives: To study the change of left ventricular mass index(LVMI), right ventricular mass index(RVMI), cardiotrophin-1(CT-1), glycoprotein130(gp130), angiotensionⅡ(AngⅡ), angiotensinⅡ type 1 receptor(AT1R), type Ⅰ collagen, type Ⅲ collagen and the relationship among these in the heart of rats with left ventricular hypertrophy(LVH) induced pressure overload, and to probe the effect of telmisatan on these. Methods: Partially banding abdominal aortic artery to achieve an experimental animal model of rats with LVH induced pressure overload. 30 male SD rats were randomly divided into three groups: operated group(LVH group, n=10), telmisartan group(telmisartan group, Tel., n=10), sham-operated group(control group, n=10). LVMI and RVMI were Calculated . AngⅡlevel of serum and cardiac tissue was measured by radioimmunoassay. The expression of CT-1 mRNA of cardiomyocytes was determined with in site hybridization histochemistry. The protein expressing of AT1R, type Ⅰ collagen, type Ⅲ collagen and gp130 in cardium was tested by immunohistochemical staining.Results: (1) Compared with control group, LVMI and RVMI was remarkedly increased in LVH group (P<0.05); Under optical microscope, myocyte hypertrophy, extended interstitial of cardiac tissue, and increased collagen in interstitial of cardiac tissue and around small vessels were found in LVH group with V-G staining; AngⅡlevel and the protein expressing of AT1R, type Ⅰ collage, type Ⅲ collagen and gp130 in cardiac tissue were significant enhanced, and CT-1 mRNA expression was also accelerated　in LVH　group (P<0.05). (2) The LVMI was positive correlation with AngⅡlevel, protein expressing of AT1R, type Ⅰ collagen, type Ⅲ collagen and gp130,and CT-1 mRNA expression respectively (P<0.05). There was also positive correlation of AngⅡlevel and AT1R with type Ⅰ collagen, type Ⅲ collagen, gp130 and CT-1 mRNA respectively(P<0.05). In addititn, there was signicantly positive relation gp130　to CT-1 mRNA expression (P<0.05). (3) LVMI, AngⅡlevel, protein expressing of AT1R, type Ⅰ collagen, type Ⅲ collagen an gp130, and CT-1 mRNA expression in cardiac tissue were significant reduced by the treatment of telmisartan (P<0.05).Conclusions: (1) AngⅡand AT1R play an important role in inducing LVH during overload of pressure. (2) The overexpression of CT-1 gene may be a vital risk factor of LVH. (3) AngⅡ, AT1R, gp130, CT-1 gene may anticipate in the development of LVH triggered by pressure overload through their cooperating. (4) The administration of telmisartan can reverse LVH resulting from that type Ⅰ and type Ⅲollagen were suppressed as well as the expression of CT-1 gene and its receptor, gp130, were down- regulated in transcription level.