氯沙坦对血管紧张素Ⅱ诱导的心肌细胞核酸、蛋白质及c-fos基因表达抑制作用的研究

Inhibitory effects of losartan on myocardial cellular hypertrophy induced by angiotensin Ⅱ

目的 观察氯沙坦（ｌｏｓａｒｔａｎ，ＬＴ）对血管紧张素Ⅱ诱导的心肌细胞核酸、蛋白质及ｃｆｏｓ基因表达的抑制作用。方法 应用培养乳鼠心肌细胞，观察血管紧张素Ⅱ亚型受体拮抗剂ＬＴ对血管紧张素Ⅱ（ＡｎｇⅡ）诱导的心肌细胞肥大的抑制作用。结果 ＬＴ２×１０－６ｍｏｌ·Ｌ－１能明显抑制ＡｎｇⅡ对心肌细胞核酸及蛋白质合成的促进作用及ｃｆｏｓｍＲＮＡ表达。结论 心肌细胞膜表面的ＡＴ受体亚型介导了ＡｎｇⅡ促心肌细胞肥大作用。ｃｆｏｓ基因激活是ＡｎｇⅡ诱导心肌细胞肥大的重要机制之一。ＬＴ从受体水平阻断了ＡｎｇⅡ的作用，此类药物应是更具选择性的肾素血管紧张素系统拮抗剂。

AIM To study the inhibitory effects fo losartan(LT) on myocarcial cellular hypertrophy induced by angiotensin Ⅱ. METHODS Cultured neonatal rat cardiomyocytes were used to observe the effects of LT on myocardial cellular hypertrophy induced by angiotensin Ⅱ. RESULTS The synthesis of nuclear acid、 protein and c fos mRNA expression promoted by angiotensin Ⅱ were significantly inhibited by LT 2×10 -6 mol·L -1 . CONCLUSION Angiotensin Ⅱ 1 receptor subsytes on myocardial cellular surface madiated the promoting effect of myocardial hypertrophy by Angiotersin Ⅱ. The exitation of c fos gene is one of the most mechanisms on myocardial cellular hypertrophy induced by Angiotensin Ⅱ.Losartan mey be a more specific RAAS inhibitor because the effects of Angiotensin Ⅱ are obstructed from recceptor level.