[Objective]To explore the effect of C-type natriuretic peptide (CNP ) on antagonizing 5-hydroxytryptamine(5-HT)-induced aortic smooth muscle cell contraction and its mechanism .[Methods]CNP stimulated A10 aortic smooth muscle cells in vitro by different concentrations (10-5M-10-9M ,respectively ) at different time points(0 ,5 ,10 ,15 ,20 and 30 minutes) .Then enzyme-linked immunosorbent assay(ELISA) was used to detect the changes of cGMP concentration .The expressions of PKGIα and PKGIβ in cells after CNP stimulation were detected by Western blot .The effect of CNP on 5-HT-induced cell contraction was ob-served by confocal microscopy .[Results] The generation of cGMP in smooth muscle cells after CNP treatment was obviously increased in a dose dependent manner ,and markedly increased in the beginning (5min) and reached to the peak around 10min .Meanwhile ,the expression of cGMP downstream molecule ,cGMP-depend-ent protein kinase (PKG ) after CNP treatment was activated which presented the increased expression of PKGIα.After PKG specific inhibitor interfered ,the antagonistic effect of CNP on 5-HT-induced aortic vascu-lar smooth muscle cell contraction was decreased .[Conclusion]CNP can activate cGMP-PKGIa signal against 5-HT-induced aortic vascular smooth muscle cell contraction .It indicates that CNP can be used as an effective target for the prevention and treatment of atherosclerosis .%【目的】探讨C-型利钠肽（C-type natriuretic peptide ，CNP）对5-羟色胺（5-hydroxytryptamine ，5-H T ）诱导的主动脉血管平滑肌细胞收缩的拮抗作用及其机制。【方法】主动脉血管平滑肌A10细胞，采用不同的CNP浓度（10-5～10-9 M ）分别作用不同的时间（0 min ，5 min ，10 min ，15 min ，20 min ，30 min）后，采用酶联免疫吸附法（Elisa方法）检测环磷酸鸟苷（cGMP）的含量变化；Western blot 检测CNP刺激后，细胞中蛋白激酶α（PKGIα）和 PKGIβ的蛋白表达变化；共聚焦显微镜观察 CNP拮抗5-HT 诱导的细胞收缩情况。【结果】经过不同浓度的CNP刺激后，平滑肌细胞中cGMP的生成量明显增加，呈浓度依赖性，且在刺激一开始时（5 min） cGMP浓度即开始明显增加，到10 min左右达到高峰。另外，经CNP作用后，cGMP的下游分子cGM P依赖性蛋白激酶（GM P-PKG ）被活化，主要表现为PKGIα表达增加；采用PKG特异抑制剂干扰后， CNP对5-HT诱导的主动脉血管平滑肌细胞收缩的拮抗作用减弱。【结论】CNP可活化cGMP-PKGIa信号拮抗5-HT诱导的主动脉血管平滑肌细胞收缩，表明CNP可作为预防治疗动脉粥样硬化治疗的有效靶点。
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