缬沙坦对高血压患者脉压及氧化应激反应的影响

The effect of valsartan on the pulse pressure and the oxidative stress in hypertension patients

目的探讨氧化应激反应变化在血管紧张素Ⅱ1型受体阻断剂（ARB）改善高血压患者脉作中的作用。方法连续65例门诊就诊的无并发症、半年内未用ARB及血管紧张素转换酶抑制剂类药的高血压患者随机分成两组：对照组32例，常规降压药物治疗；缬沙坦组33例，常规降压药物＋缬沙坦80mg／d治疗。分组治疗12个月。以动态血压观察患者治疗前、后血压变化，并以逆转录聚合链式反应（RT-PCR）方法测定血白细胞p22^phox mRNA的表达。结果治疗前两组患者性别、年龄、基础血压（包括收缩压、舒张压、脉压）及外周血白细胞p220^phox mRNA表达差异均无统计学意义（均P〉0．05）。治疗后两组患者收缩压、舒张压及脉压均较治疗前明显降低，差异有统计学意义（P〈0．05）。治疗后缬沙坦组收缩压及舒张压与对照组比较差异无统计学意义[其中收缩压（134．32±14．52）mmHg比（137．15±12．10）mmHg，舒张压（82．63±13．96）mmHg比（77．35±11．38）mmHg，P〉0．05]，但脉压下降程度明显大于对照组（27．39％比11．91％，P〈0．05）。治疗后两组患者白细胞p22^phox mRNA表达均较治疗前降低，其中对照组白细胞p22^phox mRNA表达较治疗前减少18％．但差异无统计学意义（P=O．0732），缬沙坦组白细胞p22^phox mRNA表达较治疗前减少76％（P〈0．01）。结论缬沙坦治疗12个月，能降低高血压患者的脉压，抑制高血压患者外周血白细胞NAD（P）H氧化酶亚基p22^phox mRNA的表达。缬沙坦改善动脉弹性、抗动脉硬化的效应可能归因于其具有的抗氧化作用。

Objective To investigate the possible mechanism of angiotensin 11 type 1 receptor blocker（ARB） in improving artery elasticity through observing the effect of valsartan on pulse pressure and leukocyte p22^phox expression of hypertension patients. Methods 65 consecutive hypertension patients（documented by systolic pressure〉140 mm Hg and/or diastolic pressure〉90 mm Hg）, who had not applied ARB or angiotensin conversion enzyme inhibitor for at least 6 months, were assigned equally to 2 groups according to age, sex, and blood pressure ： control （n=32, routine treatment alone）, and valsartan （n=33, routine treatment＋valsartan 80 mg/d）. Patients were treated for 12 months. At baseline and after 12 months, the pulse pressure was determined by ambula2 tory blood pressure monitoring and the leukocyte p22^phox expression was measured by reverse transcription-polymerase chain reaction （RT-PCR）. Results There were no significant differences between control and valsartan groups in age, sex, baseline blood pressure （include systolic pressure, diastolic pressure, and pulse pressure） and leukocyte p22^phox expression. After 12 months of treatment, blood pressure showed significantly improvement in both groups： in control group from （167.40±12.10）/（98.95±14.12）mm Hg to （137.15±12.10）/（77.35±11.38）mm Hg （P〈0.05）, and in valsartan group from （169.43±9.69）/（96.12±18.72）mm Hg to （134.32±14.52）/（82.63± 13.96）mm Hg （P〈0.05）. There were no significant differences between control and treatment groups in systolicpressure [（ 134.32±14.52）mm Hg VS （137.15±12.10）mm Hg, P〉0.05], and diastolic pressure [（82.63±13.96） mm Hg VS （77.35±11.38）mm Hg, P〉0.05] after treatment. The decrements of pulse pressure in the valsartan group was significantly larger than in the control group （27.39% vs 11.91%, P〈0.05）. The leukocyte p22^phox expression was decreased 18%（P〉0.05） in control group, and 76%（P〈0.0001 ） in valsartan group during the 12 months follow-up period. Conclusion Valsartan can significantly lower pulse pressure and leukocyte p22^phox expression in hypertension patients. Valsartan may play its role in improving vaseular elasticity through restraining the oxidative stress.