摘要
通过3H-Leu掺入量的测定与RNA狭线杂交技术，初步探讨血管紧张素正受体、Ca2+在血管紧张素Ⅱ刺激乳鼠心肌细胞蛋白质合成中的作用，并观察血管紧张素Ⅱ对原癌基因c-fos表达的影响。结果发现培养液中加入钙通道阻断剂（vera-pamil）、细胞外钙螯合剂（EGTA）、肌浆网钙释放抑制剂（dantrolene）和细胞内钙螯合剂（Fura-2／AM），可使血管紧张素对Ⅱ导的3H-Leu掺入量较单独加血管紧张素Ⅱ组分别降低17％、19％、22％和27％。另外，AugⅡ还可诱导c-fos基因的表达。以上结果提示:血管紧张素Ⅱ促进心肌细胞蛋白质合成作用是通过其受体介导的，有赖于[Ca2+]i升高的信息传递途径并可能与c-fos基因表达增强有关。
In this study,the role of angiotensin Ⅱ (Ang Ⅱ) receptor,Ca2+ in the Ang Ⅱ -stimulated neoeatal myocytes protein synthesis were investigated and the effect of Ang Ⅱ on expression of c-fos gene was observed. The results showed that the stimulatory effect of Ang Ⅱ on protein synthesis was blocked by the Ang Ⅱ antagonist-[Sar1 Ile8] Ang Ⅱ. When verapamil,EGTA, dantrolene, and Fura-2/AM, were added to the medium, the 3H-leucine incorporations stimulated by Ang Ⅱ were reduced by 17%, 19%, 22%,and 27%. Using calcium ionophore-A23187 did not stimulate protein synthesis, but enhanced Ang Ⅱ -induced 3H-leucine incorporation. In addition, Ang Ⅱ could induce expression of c-fos gene. These results indicated that the hypertrophic effect of Ang Ⅱ on the myocytes was mediated by Ang Ⅱ receptor and depended on increase in [Ca2+]i, and may be asociated with enhanced expression of c-fos.
出处
《中国医学科学院学报》
CAS
CSCD
北大核心
1997年第1期35-40,共6页
Acta Academiae Medicinae Sinicae
基金
国家八.五攻关基金!85-915-03-01
