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目的:难治性高血压患者存在抗AT1受体自身抗体(ATR-AA),这一抗体具有受体激动剂样作用,可能参与了高血压的发病。本研究拟探讨AT1受体阻滞剂氯沙坦可否通过阻断ATR-AA的激动作用起到更优越的降压作用,从临床水平阐明ATR-AA是否参与高血压的发病。方法:收集难治性高血压患者,测定患者血清ATR-AA,将抗体阳性难治性高血压交叉给予氯沙坦和转化酶抑制剂伊那普利治疗各4周,观察两组血压下降差异,以抗体阴性难治性高血压作为对照。结果:最终完成试验34例,氯沙坦治疗组血压平均下降(2.2±1.2)/(1.0±0.5)kPa,伊那普利组平均下降(1.6±1.0)/(0.6±0.6)kPa,两组收缩压及舒张压下降差异均极显著(P<0.01);而对照组血压下降差异无显著性。结论:ATR-AA阳性难治性高血压氯沙坦降压疗效显著优于伊那普利,氯沙坦可能不仅阻断血管紧张素II引起的AT1受体激动,还可能通过阻断ATR-AA引起的AT1受体激动,起到额外的降压作用。ATR-AA是参与抗体阳性难治性高血压的发病的因素之一,氯沙坦可阻断其病理效应。
OBJECTIVE: Anti-AT1 receptor autoantibodies (ATR-AA) exist in patients with refractory hypertension, which have agonist-like effects and may be involved in the pathogenesis of hypertension. This study was to investigate whether AT1 receptor blocker Losartan can play a more superior antihypertensive effect by blocking the agonism of ATR-AA, and to clarify whether ATR-AA is involved in the pathogenesis of hypertension from the clinical level. Methods: ATR-AA was measured in patients with refractory hypertension, serum antibody-refractory hypertension was given to losartan and Inaspri for 4 weeks. Antihypertensive patients were divided into two groups: Antibody negative refractory hypertension as a control. Results: The final test was completed in 34 patients. Losartan decreased blood pressure (2.2 ± 1.2) / (1.0 ± 0.5) kPa in the Losartan group and decreased (1.6 ± 1.0) / (0.6 ± 0.6) kPa in the Enalapril group Systolic blood pressure and diastolic blood pressure decreased significantly (P <0.01); while the control group decreased blood pressure was no significant difference. Conclusion: ATR-AA positive refractory hypertension losartan antihypertensive effect was significantly better than that of enalapril, losartan may not only block angiotensin II-induced AT1 receptor activation, but also by blocking ATR-AA Caused by AT1 receptor activation, play an additional antihypertensive effect. ATR-AA is involved in the pathogenesis of antibody-refractory hypertension, losartan can block the pathological effects.