Nitric oxide (NO) activates soluble guanylyl cyclase in smooth muscle cells to induce vasodilation in the vasculature. However, as hemoglobin (Hb) is an effective scavenger of NO and is present in high concentrations inside the red blood cell (RBC), the bioavailability of NO would be too low to elicit soluble guanylyl cyclase activation in the presence of blood. Therefore, NO bioactivity must be preserved. Here we present evidence suggesting that the RBC participates in the preservation of NO bioactivity by reducing NO influx. The NO uptake by RBCs was increased and decreased by altering the degree of band 3 binding to the cytoskeleton. Methemoglobin and denatured hemoglobin binding to the RBC membrane or cytoskeleton also were shown to contribute to reducing the NO uptake rate of the RBC. These alterations in NO uptake by the RBC, hence the NO bioavailability, were determined to correlate with the vasodilation of isolated blood vessels. Our observations suggest that RBC membrane and cytoskeleton associated NO-inert proteins provide a barrier for NO diffusion and thus account for the reduction in the NO uptake rate of RBCs.

译文

一氧化氮(NO)激活平滑肌细胞中的可溶性鸟苷酸环化酶,从而诱导脉管系统中的血管舒张。但是,由于血红蛋白(Hb)是有效的NO清除剂,并且以高浓度存在于红血球(RBC)内部,因此NO的生物利用度将太低,以至于在存在血液的情况下不会引起可溶性鸟苷酰环化酶的活化。因此,必须保留任何生物活性。在这里,我们提出的证据表明,RBC通过减少NO流入而参与了NO生物活性的保存。通过改变带3与细胞骨架的结合程度,红细胞对NO的吸收增加和减少。高铁血红蛋白和变性的血红蛋白与RBC膜或细胞骨架的结合也显示出有助于降低RBC的NO吸收率。 RBC吸收NO的这些变化(因此没有NO的生物利用度)被确定与孤立血管的血管舒张相关。我们的观察结果表明,RBC膜和细胞骨架相关的NO惰性蛋白为NO扩散提供了障碍,因此可以解释RBC的NO吸收率降低。

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