血管紧张素Ⅱ及其受体拮抗剂对心肌细胞肥大的影响

Angiotensin Ⅱ and its Antagonists on Cultured Cardiac Myocytes Hypertrophy

目的 观察血管紧张素Ⅱ (AngⅡ )、AT1受体拮抗剂氯沙坦和AT2 受体拮抗剂PD12 3177对心肌细胞蛋白质合成速率和AT1受体mRNA表达的影响。方法 采用3 H 亮氨酸掺入法测定培养的心肌细胞蛋白质合成速率 ,RT PCR方法检测心肌细胞AT1受体mRNA表达。结果 在培养的心肌细胞中加入AngⅡ可明显增加心肌细胞3 H 亮氨酸的掺入量 ,并呈剂量依赖性 ,氯沙坦可显著抑制AngⅡ引起的蛋白质合成增加 ,而PD12 3177对其无影响 ;AngⅡ上调AT1受体基因表达 ,氯沙坦抑制其上调 ,PD12 3177无影响。结论 AngⅡ可通过上调AT1受体引起心肌细胞肥大 ,氯沙坦下调AT1受体 ,抑制心肌细胞肥大。

Aim\ To investigate the effects of angiotensin Ⅱ(AngⅡ),AT 1 receptor antagonist losartan and AT 2 receptor antagonist PD123177 on protein synthesis rate and AT 1 receptor mRNA expression in cultured neonatal rat cardiac myocytes. Methods\ The protein synthesis rate in cultured cardiac myocytes was determined by the 3H leucine incorporation,AT 1 receptor mRNA expression of cardiac myocytes was assessed by reverse transcription polymerase chain reaction(RT PCR). Results\ AngⅡ increased the 3H leucine incorporation in cultured cardiac myocytes in a dose dependent manner,losartan but not PD123177 could significantly inhibit AngⅡ induced protein synthesis,;AT 1 receptor mRNA expression was upregulated after AngⅡ,and inhibited by losartan,but not PD123177. Conclusion\ AngⅡ can induce cardiac myocytes hypertrophy via upregulating AT 1 receptor,and AT 1 receptor antagonist can decrease AT 1 receptor expression,reduce cardiac myocytes hypertrophy.