【摘要】 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。更多还原

【Abstract】 Objective:To explore the effects of valsartan on the level of [Ca2+]i in angiotensin Ⅱ induced hypertrophic cardiocytes. Method:Primary cultured neonatal rat cardiocytes were cultured. The protein synthesis rate in cultured cardiocytes was determined by the 3H-leucine incorporation. [Ca2+]i concentration was measured with laser confocal microscopy. Result:Hypertrophic cardiocytes were induced by angiotensin Ⅱ. After a 48 hour treatment, the level of [Ca2+]i was increased significantly compared with the control (P<0.01) whereas it decreased significantly(P<0.01) with preconditioning valsartan. There was no significant difference on the level of [Ca2+]i in valsartan and control groups(P>0.05). Conclusion:Angiotensin Ⅱ induces the increase [Ca2+]i in hypertrophic cardiocytes. Valsartan may suppress the level of [Ca2+]i through blocking the AT1 receptor.更多还原