Angiotensin II (Ang II) regulates blood volume and stimulates erythropoiesis through AT1 (ATR1) and AT2 (ATR2) receptors, found in multiple tissues, including erythrocytes. Sickle cell disease (SCD) patients present altered Ang II levels. Hemoglobin S polymerization, deformability and phosphatidylserine translocation are important features of mature erythrocytes, therefore, our hypothesis is Ang II affects these parameters and, if it does, what would be the influence of AT1R and AT2R on these effects. A polymerization assay (PA), deformability, and annexin V binding were performed in SCD erythrocytes samples adding Ang II, ATR1 antagonist (losartan or eprosartan), and ATR2 antagonist (PD123319). Through the PA test, we observed a dose-dependent polymerization inhibition effect when comparing Ang II to control. Losartan did not affect the level or the rate of Ang II inhibition, while PD123319 showed an increased level of protection against polymerization, and eprosartan brought levels back to control. Ang II was able to reduce the translocation of phosphatidylserine from the inner to the outer leaflet, a marker of eryptosis, in the presence of PD123319. Also, ATR1 showed a positive effect increasing deformability. Our data shows that ATR1 is important for maintenance of erythrocyte physiological function in SCD and for prolonging its life.

血管紧张素 II (Ang II) 通过在包括红细胞在内的多种组织中发现的 AT1 (ATR1) 和 AT2 (ATR2) 受体调节血容量并刺激红细胞生成。镰状细胞病 (SCD) 患者表现出改变的 Ang II 水平。血红蛋白 S 聚合、可变形性和磷脂酰丝氨酸易位是成熟红细胞的重要特征，因此，我们的假设是 Ang II 影响这些参数，如果确实如此，AT1R 和 AT2R 对这些影响的影响是什么。在添加 Ang II、ATR1 拮抗剂（氯沙坦或依普罗沙坦）和 ATR2 拮抗剂（PD123319）的 SCD 红细胞样品中进行聚合测定 (PA)、变形性和膜联蛋白 V 结合。通过 PA 测试，我们在将 Ang II 与对照进行比较时观察到剂量依赖性聚合抑制作用。氯沙坦不影响 Ang II 抑制的水平或速率，而 PD123319 显示出更高的聚合保护水平，而依普罗沙坦使水平恢复到控制水平。在 PD123319 存在下，Ang II 能够减少磷脂酰丝氨酸从内叶到外叶的易位，这是红斑狼疮的标志物。此外，ATR1 显示出增加可变形性的积极作用。我们的数据表明，ATR1对于维持SCD红细胞生理功能和延长其寿命很重要。ATR1 显示出增加可变形性的积极作用。我们的数据表明，ATR1对于维持SCD红细胞生理功能和延长其寿命很重要。ATR1 显示出增加可变形性的积极作用。我们的数据表明，ATR1对于维持SCD红细胞生理功能和延长其寿命很重要。