Pontremoli S, Salamino F, Sparatore B, De Tullio R, Patrone M, Tizianello A, Melloni E
Institute of Biological Chemistry, University of Genoa, Italy.
Biochem Biophys Res Commun. 1989 Feb 15;158(3):966-72. doi: 10.1016/0006-291x(89)92816-7.
In neutrophils of patients with essential hypertension the NADPH-dependent O2- production elicited by stimulation with f-Met-Leu-Phe is three to four fold higher in comparison with neutrophils of normotensive control subjects. Neutrophils from hypertensive patients are less responsive to priming, by non-stimulating doses of the agonist, as compared to control cells, which following this pretreatment augment superoxide anion production up to levels close to those expressed by neutrophils from hypertensive patients. No difference in NADPH oxidase activity, between neutrophils from the two groups of subjects, was observed when the rate of O2- production was evaluated in a reconstructed cell-free system containing the membrane fraction and the cytosolic cofactors. These results are consistent with the hypothesis that differences in the functional organization of the oxidase at the membrane level in neutrophils of hypertensive are responsible for the enhanced O2- production following agonist stimulation.
与血压正常的对照受试者的中性粒细胞相比，原发性高血压患者的中性粒细胞经f-Met-Leu-Phe刺激后引发的NADPH依赖性O₂⁻生成高出三到四倍。与对照细胞相比，高血压患者的中性粒细胞对非刺激剂量激动剂引发作用的反应较弱，对照细胞在这种预处理后可将超氧阴离子生成增加至接近高血压患者中性粒细胞所表达的水平。当在含有膜组分和胞质辅因子的重构无细胞系统中评估O₂⁻生成速率时，未观察到两组受试者的中性粒细胞之间NADPH氧化酶活性存在差异。这些结果与以下假设一致，即高血压患者中性粒细胞中氧化酶在膜水平的功能组织差异是激动剂刺激后O₂⁻生成增强的原因。
