摘要
本工作从整体和细胞水平探讨一氧化氮 (NO)在防止心肌肥厚反应中的作用及其机制。压力超负荷心肌肥厚大鼠左心室肌NO含量减少。内源性NO可能通过非cGMP依赖机制减轻压力超负荷引起的心肌肥厚。在培养的新生大鼠心肌细胞中血管紧张素Ⅱ (AⅡ )、内皮素 1 (ET 1 )和去甲肾上腺素 (NE)通过各自的受体和偶连的G蛋白 ,一方面引起心肌细胞肥大 ;另一方面抑制一氧化氮合酶 (NOS)活性和NO生成。心肌细胞和非心肌细胞均有内皮型NOS(eNOS)基因表达 ,AⅡ、ET 1和NE可抑制心肌细胞eNOS基因表达。外源性NO可防止AⅡ、ET 1和NE诱导的心肌细胞肥大反应。内源性和外源性NO均可抑制AⅡ和ET 1诱导的心肌细胞原癌基因c fos的表达 。
This study investigated the role of nitric oxide(NO) in the prevention of myocardial hypertrophic response and its mechanisms. Left ventricular NO content decreases in the pathophysiogenesis of myocardial hypertrophy induced by pressure overload. Endogenous NO may attenuate cardiac hypertrophy induced by pressure overload, independent of cGMP mechanism. Angiotensin Ⅱ(AⅡ), endothelin 1(ET 1) and norepinephrine(NE) can inhibit NOS activity and NO production, and induce hypertrophic response in cultured neonatal rat cardiomyocytes; these effects of AⅡ, ET 1 and NE are mediated respectively by AⅡ receptor, ETA receptor and α1 adrenergic receptor; these effects of AII and ET 1 are mediated by PTX sensitive G protein, while the effects of NE are mediated by PTX insensitive G protein. eNOS gene is expressed in cultured neonatal rat cardiac myocytes and nonmyocytes. AⅡ, ET 1 and NE can inhibit eNOS gene expression in cardiomyocytes. Exogenous NO can prevent hypertrophic response induced by AⅡ, ET 1 and NE in cardiomyocytes. Both endogenous and exogenous NO can inhibit the expression of proto oncogene c fos induced by AⅡ and ET 1, which may be involved in protein kinase C.
出处
《生理科学进展》
CAS
CSCD
北大核心
2000年第4期322-324,共3页
Progress in Physiological Sciences
基金
广东省自然科学基金资助课题!(960124)
关键词
一氧化氮
心肌肥厚
压力超负荷
AⅡ
ET-1
NE
NOS
Nitric oxide
Cardiac hypertrophy
Pressure overload
Angiotensin Ⅱ
Endothelin-1
Norepinephrine
