Mechanism Research on Captopril Regressing Left Ventricular Remodeling In Rat with Pressure Overload
Hu Wan
Abstract
Hu Wan
Abstract
Objective To observe the effect of captopril regressing left ventricular remodeling in rats with pressure overload and to elucidate its possible mechanism.Methods36Wistar male rats were ranˉdomly divided into sham operation group,model group and captopril group.Observe left ventricular mass inˉdex(LVMI),cardiac tissue collagen typeⅠandⅢ,mRNA expression of collagen typeⅠandⅢ,plasˉma angiotensinⅡ(AngⅡ)and left ventricular tissue AngⅡ,plasma atrial natriuretic factor(ANF),serum aldosterone(ALD)level in rat with left ventricular remodeling of CHF by abdominal aortic constriction.Colˉlagen typeⅠandⅢwere measured by immunohistochemistry.mRNA expression of collagen typeⅠandⅢwas measured by RT-PCR.AngⅡ,ANF and ALD were measured by radioimmunoassay.Results LVˉMI,Collagen typeⅠ,Collagen typeⅢ,Expression of collagen typeⅠmRNA of model group were increased(P0.001,P0.01,P0.05,),while those of captopril group were decreased(P0.05).Expression of collagen typeⅢmRMA of the model group was increased(P0.05,),while that of the captopril group was not decreased(P0.05).The plasma and myocardial AngⅡ,plasma ANF, serum aldosterone of the model group were increased (P0.001,P0.01),while those of the captopril group were decreased(P0.01and P0.001).Conclusions Myocardial collagen typeⅠand typeⅢand the mRNA expression in rat with pressure overload are increased.There was change of regressing left ventricular remodeling.Myocardial collagen typeⅠand typeⅢand their mRNA expression in rat with pressure overload are decreased by captopril.There was effect of regressingleft ventricular remodeling.Captopril is effective in regressing myocardial fibrosis.The effect may be related to the decrease of circulating or local AngⅡlevel,plasma ANF,serum aldosterone and affectting expression of collagen typeⅠand typeⅢmRNA.
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Objective To observe the effect of captopril regressing left ventricular remodeling in rats with pressure overload and to elucidate its possible mechanism.Methods36Wistar male rats were ranˉdomly divided into sham operation group,model group and captopril group.Observe left ventricular mass inˉdex(LVMI),cardiac tissue collagen typeⅠandⅢ,mRNA expression of collagen typeⅠandⅢ,plasˉma angiotensinⅡ(AngⅡ)and left ventricular tissue AngⅡ,plasma atrial natriuretic factor(ANF),serum aldosterone(ALD)level in rat with left ventricular remodeling of CHF by abdominal aortic constriction.Colˉlagen typeⅠandⅢwere measured by immunohistochemistry.mRNA expression of collagen typeⅠandⅢwas measured by RT-PCR.AngⅡ,ANF and ALD were measured by radioimmunoassay.Results LVˉMI,Collagen typeⅠ,Collagen typeⅢ,Expression of collagen typeⅠmRNA of model group were increased(P0.001,P0.01,P0.05,),while those of captopril group were decreased(P0.05).Expression of collagen typeⅢmRMA of the model group was increased(P0.05,),while that of the captopril group was not decreased(P0.05).The plasma and myocardial AngⅡ,plasma ANF, serum aldosterone of the model group were increased (P0.001,P0.01),while those of the captopril group were decreased(P0.01and P0.001).Conclusions Myocardial collagen typeⅠand typeⅢand the mRNA expression in rat with pressure overload are increased.There was change of regressing left ventricular remodeling.Myocardial collagen typeⅠand typeⅢand their mRNA expression in rat with pressure overload are decreased by captopril.There was effect of regressingleft ventricular remodeling.Captopril is effective in regressing myocardial fibrosis.The effect may be related to the decrease of circulating or local AngⅡlevel,plasma ANF,serum aldosterone and affectting expression of collagen typeⅠand typeⅢmRNA.
Key concepts: Captopril, Internal medicine, Ventricular remodeling, Pressure overload, Endocrinology, Aldosterone, Ventricular pressure, Type I collagen