2001Zhongguo bingli shengli zazhiRequires access

Role of angiotensin II receptors in overload pressure-induced left ventricular hypertrophy

Chi Luxiang

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Abstract

AIM and METHODS: To investigate the role of angiotensin Ⅱ recepters(ATRs) in overload pressure-induced left ventricular hypertrophy. The rat abdominal aortic constraction model was adopted. At 10th week after operating, angiotensin Ⅱ in myocardium was measured by radioimmunoassay,tissue ATRs and its subtype were analysed by radioligand binding assay. RESULTS: The AngⅡ content in the operated group was significantly higher than that of the control group, LVMI was positively correlated with AngⅡ(r=0.8066,P0.01).The maximal binding capacity of ATRs in the operated group was significantly higher than that of the control group(P0.01). However,the equilibrium dissociation constant(kd) and ratio of AT 1R to AT 2R in these two groups had no significantly different. Left ventricular hypertrophy was significantly reduced by AT 1R antagonist irbesartan,and not influenced by AT 2R antagonist CGP42112A. CONCLUSION: These results suggested that left ventricular ATRs upregulate during pressure overload.The left ventricular hypertrophy induced by AngⅡis mainly mediated by AT 1R.

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AIM and METHODS: To investigate the role of angiotensin Ⅱ recepters(ATRs) in overload pressure-induced left ventricular hypertrophy. The rat abdominal aortic constraction model was adopted. At 10th week after operating, angiotensin Ⅱ in myocardium was measured by radioimmunoassay,tissue ATRs and its subtype were analysed by radioligand binding assay. RESULTS: The AngⅡ content in the operated group was significantly higher than that of the control group, LVMI was positively correlated with AngⅡ(r=0.8066,P0.01).The maximal binding capacity of ATRs in the operated group was significantly higher than that of the control group(P0.01). However,the equilibrium dissociation constant(kd) and ratio of AT 1R to AT 2R in these two groups had no significantly different. Left ventricular hypertrophy was significantly reduced by AT 1R antagonist irbesartan,and not influenced by AT 2R antagonist CGP42112A. CONCLUSION: These results suggested that left ventricular ATRs upregulate during pressure overload.The left ventricular hypertrophy induced by AngⅡis mainly mediated by AT 1R.

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Available abstract

AIM and METHODS: To investigate the role of angiotensin Ⅱ recepters(ATRs) in overload pressure-induced left ventricular hypertrophy. The rat abdominal aortic constraction model was adopted. At 10th week after operating, angiotensin Ⅱ in myocardium was measured by radioimmunoassay,tissue ATRs and its subtype were analysed by radioligand binding assay. RESULTS: The AngⅡ content in the operated group was significantly higher than that of the control group, LVMI was positively correlated with AngⅡ(r=0.8066,P0.01).The maximal binding capacity of ATRs in the operated group was significantly higher than that of the control group(P0.01). However,the equilibrium dissociation constant(kd) and ratio of AT 1R to AT 2R in these two groups had no significantly different. Left ventricular hypertrophy was significantly reduced by AT 1R antagonist irbesartan,and not influenced by AT 2R antagonist CGP42112A. CONCLUSION: These results suggested that left ventricular ATRs upregulate during pressure overload.The left ventricular hypertrophy induced by AngⅡis mainly mediated by AT 1R.

Key concepts: Internal medicine, Endocrinology, Pressure overload, Muscle hypertrophy, Angiotensin II, Medicine, Renin–angiotensin system, Left ventricular hypertrophy

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