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一氧化氮抑制内皮素促血管平滑肌细胞增殖作用的信号转导途径

摘要

培养的家兔胸主动脉血管平滑肌细胞(VSMC)分别以内皮素(ET-1)、一氧化氮(NO)前体-L-Arg和NO供体SIN-1刺激,或用ET-1+L-Arg、ET-1+SIN-1联合刺激,测VSMC~(3)H-TdR掺入、丝裂素活化蛋白激酶(MAPK)活性及蛋白激酶C(PKC)活性的改变,以研究NO抑制ET-1促VSMC增殖作用的信号转导途径。结果提示:NO抑制ET-1促VSMC增殖的作用,此 作用与NO抑制ET-1激活PKC、MAPK活性终止ET-1的细胞内信号转导途径有关。

关键词： 一氧化氮; 内皮素; 丝裂素活化蛋白激酶; 蛋白激酶C; 血管平滑肌细胞; 细胞增殖

Inhibition of signal transduction pathways of endothelin-1-induced proliferation of vascular smooth muscle cells by nitric oxide

Abstract

The signal transduction pathways of the inhibitory effect of nitric oxide (NO) on endothelin (ET)-induced proliferation of vascular smooth muscle cells (VSMCs) were studied. ~(3)H-thymidine (TdR) incorporation, mitogen-activated protein kinase (MAPK) activity and protein kinase C (PKC) activity of cultured VSMCs of rabbits thoracic aorta were measured in the presence of either NO precursor L-arginine (L-Arg) or NO donor 3-morpholino sydnonimine-hydrochloride (SIN-1), or ET-1 alone or with L-Arg or SIN-1.

Key words: Nitric oxide;Endothelin mitogen-activated;Protein kinase;Protein kinase C; Vascular smooth muscle cell;

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引用本文：

. 一氧化氮抑制内皮素促血管平滑肌细胞增殖作用的信号转导途径[J]. 生理学报 1998; 50 (4): .

. Inhibition of signal transduction pathways of endothelin-1-induced proliferation of vascular smooth muscle cells by nitric oxide. Acta Physiol Sin 1998; 50 (4): (in Chinese with English abstract).