Bates J N, Baker M T, Guerra R, Harrison D G
Cardiovascular Institute, University of Iowa College of Medicine, Iowa City 52242.
Biochem Pharmacol. 1991 Dec 11;42 Suppl:S157-65. doi: 10.1016/0006-2952(91)90406-u.
Nitric oxide (NO) was produced from sodium nitroprusside in the presence of vascular tissue but was not released spontaneously from the nitroprusside anion. In the absence of tissue in the dark nitroprusside did not release NO. When solutions of nitroprusside alone were irradiated with visible light, nitric oxide was released at rates linearly proportional to nitroprusside concentration and light intensity. Nitric oxide was produced from solutions of nitroprusside in the dark after the addition of vascular tissue, including lengths of rabbit aorta, subcellular fractions of aorta, and human plasma. NO was also released from nitroprusside after reaction with various reducing agents including cysteine and other thiols, ascorbic acid, sodium dithionite, ferrous chloride, hemoglobin, myoglobin, and partially purified cytochrome P450 with an NADPH-regenerating system. HCN was simultaneously produced in these solutions, and addition of KCN blocked NO release. Iodine oxidized intermediate cyanoferrates and blocked nitric oxide release. KCN or iodine also blocked NO production by tissue, but had no effect upon photochemical NO release. These results show that, apart from photolysis which makes no physiological contribution, release of nitric oxide from nitroprusside, in simple solutions and in biological tissue, occurs after nitroprusside has undergone reduction and lost cyanide.
一氧化氮（NO）由硝普钠在血管组织存在的情况下产生，但不会从硝普钠阴离子中自发释放。在黑暗中且无组织存在时，硝普钠不会释放NO。当单独的硝普钠溶液用可见光照射时，一氧化氮以与硝普钠浓度和光强度成线性比例的速率释放。在加入血管组织（包括兔主动脉段、主动脉亚细胞组分和人血浆）后，硝普钠溶液在黑暗中产生一氧化氮。与包括半胱氨酸和其他硫醇、抗坏血酸、连二亚硫酸钠、氯化亚铁、血红蛋白、肌红蛋白以及带有NADPH再生系统的部分纯化细胞色素P450在内的各种还原剂反应后，硝普钠也会释放NO。这些溶液中同时会产生HCN，加入KCN会阻止NO释放。碘氧化中间氰铁酸盐并阻止一氧化氮释放。KCN或碘也会阻止组织产生NO，但对光化学NO释放没有影响。这些结果表明，除了无生理作用的光解外，在简单溶液和生物组织中，硝普钠在经历还原并失去氰化物后才会释放一氧化氮。
