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Objective: Chronic pressure overload such as hypertension commonly leads to left ventricular (LV) hypertrophy, which is a major risk factor for the development of heart failure and death.Because T lymphocytes have been implicated in the vascular dysfunction and blood pressure elevation associated with increased angiotensin Ⅱ (Ang Ⅱ) levels, we evaluated the role of the adaptive immune system in pressure overloaded mice implanted with an Ang Ⅱ-loaded pump for 4 weeks which induced the hypertension and hypertrophic cardiomyopathy.Materials and Methods: Eight-to 10-week-old female C57BL/6 mice were cared for in this study.Osmotic mini-pumps (Alzet, model 2004) containing Ang Ⅱ (1000 ng/kg per day for 4 weeks) were implanted subcutaneously in experimentalgroup.The pumps loaded with saline also implanted in control group.Thirty days after mini-pump implantation, blood pressure and heart ratewere measured noninvasively in conscious animals by the tail-cuff method.Transthoracic echocardiography was performed under light sedation with 1.0% isoflurane.LV mass, ejection fraction, fractional shortening, interventricular septum diastolic and systolic diameter, LV end diastolic volume and LV end systolic volume were examined for every week.We analyzed immunologic markers on T cells from micetreated with Ang Ⅱ or not by multicolor flow cytometry (Canto Ⅱ,BD).Whole heparinized blood were stained for 15 min at room tempereturewith antibodies and washed twice with FACS buffer.After immunostaining, cells were resuspended in FACS buffer and analyzed immediately on flow cytometer with DIVA software.Results: Infusion of Ang Ⅱ (1000 ng/kg per day) induced hypertension and hypertrophic cardiomyopathy in 90% of the animals (n=20).Pressure overload significantly increased LV mass, ejection fraction, fractional shortening, interventricular septum diastolic and systolic diameter (p < 0.05).LV end diastolic volume and LV end systolic volume decreased.Mice treated with Ang Ⅱ have an greatly increased fraction of circulating CD8+cytotoxic T cells after two weeks and the ratio of CD4+and CD8+ reversed notably (p < 0.01).The fraction of total T lymphocytes was higher than control group but was not statistically significant.Conclusion: Chronic Ang Ⅱ infusion enhanced arterial blood pressure and interventricular septum diastolic and systolic diameter and resulted in hypertrophic cardiomyopathy.The total T-cell population from micewith hypertension showed an increased fraction of proinflammatory, cytotoxic CD8+ T cells.Our studies showed that T cells are important in Ang Ⅱ induced hypertrophic cardiomyopathy.This study identify a previously undefined role for T cells in the genesis of hypertension and hypertrophic cardiomyopathy and support a role of inflammation in the basis of this prevalent disease.T cells might represent a novel therapeutic target for the treatment of high blood pressure and hypertrophic cardiomyopathy.