Jessup W
Cell Biology Unit, Heart Research Institute, Camperdown, Sydney, New South Wales, Australia.
Curr Opin Lipidol. 1996 Oct;7(5):274-80. doi: 10.1097/00041433-199610000-00003.
Nitric oxide has an important biological role as endothelium-derived relaxing factor, a key agent in the maintenance of normal vascular tone. It can also suppress lipoprotein oxidation, a potential anti-atherogenic property. However, in arteries subject to hypercholesterolemia or atherosclerosis, whereas nitric oxide synthesis is normal its biological activity is attenuated. This may be caused by its inactivation in the intima by components of oxidized lipoproteins acting both directly (by reaction with nitric oxide) and indirectly (by simulation of release of nitric oxide scavengers). Thus in hypercholesterolemia the normal balance between nitric oxide availability and lipoprotein oxidation is shifted to favour a self-reinforcing cycle of nitric oxide depletion and accelerated lipoprotein oxidation that may ultimately lead to atherosclerosis.
一氧化氮作为内皮源性舒张因子具有重要的生物学作用，是维持正常血管张力的关键因子。它还能抑制脂蛋白氧化，这是一种潜在的抗动脉粥样硬化特性。然而，在患有高胆固醇血症或动脉粥样硬化的动脉中，尽管一氧化氮合成正常，但其生物学活性却减弱了。这可能是由于氧化脂蛋白成分在内膜中使其失活，这些成分既直接作用（与一氧化氮反应）又间接作用（通过刺激一氧化氮清除剂的释放）。因此，在高胆固醇血症中，一氧化氮可用性与脂蛋白氧化之间的正常平衡发生偏移，有利于一氧化氮耗竭和脂蛋白氧化加速的自我强化循环，这最终可能导致动脉粥样硬化。
