Nitric Oxide as selective pulmonary vasodilator

内皮细胞释放的一氧化氮（NO）在调节血管张力中起重要作用。NO可从非肾上腺素能、非胆碱能神经的壁内神经末梢释放，这也导致血管舒张。在肺动脉高压中，观察到内皮变化以及中膜血管平滑肌的肥大和增生。在高血压肺动脉区，乙酰胆碱诱导的内皮依赖性舒张和NO诱导的舒张功能受损。这可能是由于肺血管平滑肌中可溶性鸟苷酸环化酶的脱敏，因为高血压肺动脉内皮细胞中一氧化氮的产生可能增加。尽管与对照相比，对NO的舒张被抑制，但NO的舒张作用并未完全消除。肺动脉高压结构重建大鼠吸入NO可引起选择性肺血管舒张。

Nitric oxide (NO) released from endothelium plays an important role in regulating vascular tone. No may be released from intramural nerve endings from nonadrenergic, noncholinergic nerve and this also leads to vasodilation. In pulmonary hypertension endothelial changes and hypertropy and hyperplasia in vascular smooth muscles in the media are observed. In hypertensive pulmonary areies, endothelium-dependent relaxation induced by acetylcholine and relaxation induced by NO were impaired. This might due to desensitization of soluble guanylate cyclase in the pulmonary vasular smooth muscle, because there may be an increase in nitric oxide production in endothelium of hypertensive pulmonary arteries. Although relaxation to NO is depressed compared to control, the relaxant effect of NO is not completely abolished. In pulmonary hypertensive rats with structural remodeling inhaled NO did induced selective pulmonary vasodilatation.