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一氧化氮 (NO)通过激活细胞内特异性受体可溶性鸟苷酸环化酶 (sGC) ,催化三磷酸鸟苷 (GTP)生成细胞内信使分子环磷酸鸟苷 (cGMP) ,产生调节血管舒缩反应、影响血管重构等多种生物学效应[1,2 ] 。以往NO体系与肺动脉高压发生机制的研究较多集中于单纯缺O2 下的NO上游通路 ,下游
Nitric oxide (NO) activates intracellular specific receptor soluble guanylate cyclase (sGC) to catalyze the formation of intracellular messenger guanosine monophosphate (cGMP) by guanosine triphosphate (GTP) Shrink reaction, affecting vascular remodeling and other biological effects [1,2]. The previous studies on the mechanism of NO and pulmonary hypertension mainly focused on the NO upstream pathway lacking O2 alone and the downstream