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目的:观察血管紧张素Ⅱ(AngⅡ)1型受体(AT1)拮抗剂缬沙坦(Valsartan)对AngⅡ诱导的肥大心肌细胞胞内钙([Ca2+]i)变化的影响,并探讨其机制。方法:原代培养的大鼠心肌细胞,3H-亮氨酸掺入法测定心肌细胞蛋白质合成速率,利用共聚焦显微镜技术测定[Ca2+]i。结果:AngⅡ诱导心肌细胞肥大48h后[Ca2+]i明显增加,与空白对照组比较差异有统计学意义(P<0.01);缬沙坦预处理后,[Ca2+]i与肥大组相比下降,差异有统计学意义(P<0.01),与空白对照组相比,差异无统计学意义(P>0.05)。结论:AngⅡ诱导肥大心肌细胞[Ca2+]i增加,缬沙坦通过阻断AT1受体,抑制肥大心肌细胞[Ca2+]i增加。
Objective: To investigate the effect of Valsartan, an angiotensin Ⅱ type 1 receptor (AT1) antagonist, on intracellular calcium ([Ca2 +] i) induced by Ang Ⅱ in hypertrophic cardiomyocytes and its mechanism. Methods: Primary cultured rat cardiomyocytes were harvested for 3H-leucine incorporation assay of cardiomyocyte protein synthesis rate and confocal microscopy was used to measure [Ca2 +] i. Results: Compared with blank control group, [Ca2 +] i increased significantly after AngⅡ induced cardiomyocyte hypertrophy 48h (P <0.01); Compared with hypertrophic group, [Ca2 +] i decreased after valsartan pretreatment, The difference was statistically significant (P <0.01), compared with the blank control group, the difference was not statistically significant (P> 0.05). CONCLUSION: [Ca2 +] i increases in hypertrophic cardiomyocytes induced by Ang II, while valsartan inhibits the increase of [Ca2 +] i in hypertrophic cardiomyocytes by blocking AT1 receptor.