摘要
目的:观察增加β2-肾上腺素受体(β2-AR)的表达对心衰大鼠心肌细胞收缩功能的影响并对其机制进行初步探讨。方法:用大剂量异丙肾上腺素制作大鼠心衰模型,分离培养心衰大鼠心肌细胞,在其上增加β2-AR的表达,Western blot检测心肌细胞β2-AR的表达。测定异丙肾上腺素刺激引起的细胞收缩幅度的改变。结果:心衰组心肌细胞收缩幅度较正常对照组降低(P<0.01),增加β2-AR表达可增加心衰组心肌细胞的收缩幅度(P<0.01,心衰+Adv.β2组vs心衰组);选择性β2-AR拮抗剂ICI118,551可部分反转这种效应(P<0.5,心衰+Adv,β2+ICI组vs心衰+Adv.β2组),但不能使收缩幅度降到心衰组水平(P<0.05,心衰+Adv.β2+ICI组vs心衰组)。选择性β1-AR拮抗剂CGP20712A可完全阻断β2-AR表达增加的效应。结论:增加β2-AR表达,可使心衰的心肌细胞的收缩功能得到改善,这种作用可能与β1-AR有关。
To investigate the role of overexpression of β2-adrenoceptor on contraction in cardiac myocytes isolated from failure hearts of rats and primarily analyses its mechanisms, Methods： Primarily cultured cardiac myoeytes were infected with adenovirus containing the sequence for human β2-adrenoceptors. The expression of β2-adrenoceptors was tested by Western blot. The contraction amplitudes induced by imprenaline stimulation were measured. Results： Overexpms.sion of β2-adrenoceptor increased the content in failure cardiac myocytes. The contraction amplitudes in failure cardiac myocytes were lower than that in the control（ P〈0.01 ）. Overexpression of β2-adrenoceptor improved the contraction of failure cardiac myocytes（ P 〈 0.01, Failure ＋ Adv. β2 group vs Failure group）. Selective β2-adrenoceptor antagonist ICI 118,551 partially reversed the effects（P〈0.05, Failure＋ Adv.β2 ＋ ICI group vs Failure ＋ Adv.β2 group）, but the contraction amplitudes in this Failure ＋ Adv. β2 ＋ ICI 118,551 group were still higher than that in only heart failure group（ P 〈 0.05）. Selective β1-adren^ceptor antagonist CGP20712A completely inhibited the effects of overexpression of β2-adreno- ceptor on contraction amplitude in failure cardiac myocytes. C0nelusion： Overexpression of β2-adrenoceptors improves the contraction of cardiac myocyms isolated from failure hearts of rats. The effect is related to β1-adrenoceptor.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2007年第4期410-414,共5页
Chinese Journal of Applied Physiology
基金
徐州市社会发展项目(58号)
江苏省教育厅自然科学基金项目(02KJB310008)
