钙调神经磷酸酶依赖的信号通路参与血管紧张素Ⅱ刺激的心肌细胞肥大

本研究观察了钙调神经磷酸酶依赖的信号通路在血管紧张素Ⅱ诱导的大鼠心肌细胞肥大中的作用。在ＡｎｇⅡ刺激的大鼠心肌细胞肥大模型上,应用环孢素Ａ（ＣｓＡ）阻断ＣａＮ通路,观察心肌细胞＾３Ｈ－亮氨酸掺入,ＣａＮ,ＭＡＰＫ及ＰＫＣ活性的变化。结果表明,ＡｎｇⅡ（１０＾－７ｍｏｌ／Ｌ）刺激大鼠心肌细胞＾３Ｈ－亮氨酸掺入较对照组增高４６％（Ｐ〈０．０１）,ＣｓＡ（０．５－５μｇ／ｍｌ）可以浓度依赖性方式抑制Ａｎ

Involvement of calcineurin-dependent signal pathway in the angiotensin II-induced cardiac myocyte hypertrophy

The present study was undertaken to observe the role of calcineurin (CaN)-dependent signaling pathway in the angiotensin II (Ang II)-induced cardiac myocyte hypertrophy. In cultured myocardial cells of neonatal rats, Ang II was used to stimulate hypertrophy and CaN-pathway blocked by CsA(an inhibitor of CaN). 3H-leucine incorporation, and activities of CaN, mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) were investigated. The results showed that 3H-leucine incorporation of Ang II-stimulated myocardial cells was 46% higher than control (P < 0.01), which could be inhibited by CsA (0.5-5 micrograms/ml) and PD098059(an inhibitor of MAPK). CaN and PKC activities of Ang II-stimulated myocardial cells were 39% and 280% higher than control (P < 0.001) respectively, while no significant increase in MAPK activities was observed. CsA could reverse the increase of CaN activity, but had no effect on PKC. It is concluded that the CaN-dependent signaling pathway may play an important role in the development of the Ang II-induced cardiac myocyte hypertrophy.