首页> 中文期刊> 《国际心血管病杂志》 >不同血管紧张素受体拮抗剂对老年高血压患者血小板活性的影响

不同血管紧张素受体拮抗剂对老年高血压患者血小板活性的影响

         

摘要

Objective:To investigate the different inhibitory effects of lorsartan,irbesartan and valsartan on platelet aggregation in elderly hypertensive patients. Methods:According to varied medication history,90 enrolled hypertensive patients over the age of 65 were divided into lorsartan (n=30),irbesartan (n=30)and valsartan (n=30)treatment group.Then,platelet aggregation rate (PAR) and plasma levels of angiotension Ⅱ (Ang Ⅱ ),COX-2 and TXB2 were determined.Human aortic endothelial cells (HAECs)were stimulated by Ang Ⅱ with or without treatment of lorsartan,irbesartan and valsartan,and the relative expression of COX-2 and TXB2 was assessed. Results:PAR was lower with the treatment of irbesartan and valsartan compared with lorsartan (12.62% ±0.74%,10.70% ± 0.70% and 17.17%±1 .44%),P <0.001 among three groups],associated with more reduced plasma levels of COX-2[(81 .04 ± 14.19)U/L,(75.00 ± 11 .14)U/L and(145.10 ±26.52)U/L,P =0.012 among three groups]and TXB2 [(1 577.00±161 .90)pg/ml,(1 324.00±121 .40)pg/ml and(2 025.00± 154.10)pg/ml,P =0.004 among three groups].Relative increased expression in HAECs of COX-2 and secretion of TXB2 stimulated by Ang Ⅱ were more significantly inhibited by irbesartan or valsartan, respectively compared with lorsartan,P < 0.01 . Conclusion:Irbesartan and valsartan may more effectively decrease platelet activity in elderly hypertensive patients by attenuating the expression of COX-2/TXB2 .%目的:探讨氯沙坦、厄贝沙坦及缬沙坦3种血管紧张素受体拮抗剂(ARB)对老年高血压患者血小板活性的影响。方法:入选年龄>65岁、长期服用 ARB 的老年高血压患者90例,根据用药情况分成氯沙坦、厄贝沙坦、缬沙坦3个治疗组。分别测定各组血小板聚集率(PAR)、血管紧张素Ⅱ(Ang Ⅱ)、环氧化酶-2(COX-2)、血栓素 B2(TXB2)水平。比较经不同 ARB 处理的内皮细胞中,由 Ang Ⅱ诱导产生的 COX-2 mRNA 及蛋白表达量、TXB2水平。结果:氯沙坦、厄贝沙坦及缬沙坦组3组的 PAR分别为12.62%±0.74%、10.70%±0.70%和17.17%±1.44%,P <0.001;COX-2分别为(81.04±14.19)、(75.00±11.14)、(145.10±26.52)U/L,P =0.012;TXB2为(1577.00±161.90)、(1324.00±121.40)、(2025.00±154.10)pg/ml,P =0.004。与氯沙坦组相比,厄贝沙坦、缬沙坦组 COX-2 mRNA 及蛋白表达、TXB2水平下降更为显著,P <0.01。结论:厄贝沙坦、缬沙坦通过抑制 COX-2/TXB2表达,能更有效地抑制老年高血压患者的血小板活性。

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