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 The autoantibodies against AT1 receptor (ATR-AA),behaving like an agonist were detected in patients with refractory hypertension. ATR-AA may play a role in the pathogenesis of refractory hypertension. The present study is to explore whether AT1 receptor blocker has superior anti-hypertensive effect in patients with refractory hypertension,to determine whether ATR-AA plays a role in the pathogenesis of hypertension in clinical situation. METHODS Patients with refractory hypertension were recruited and ATR-AA was assayed by ELISA. A crossover study was carried out and the efficacy of anti-hypertension was compared between losartan and ACE inhibitor enalapril. The refractory hypertensive patients with negative ATR-AA were as control. RESULTS The blood pressure decreased by (2.2 ± 1.2)/(1.0 ±0. 5) kPa,in losartan group vs (1.6 ± 1. 0)/(0. 6 + 0. 6)kPa in enalapril group; there was significant difference between there two groups, while in control group there was no significant difference. CONCLUSION The antihypertensive efficacy of losartan is superior to that of enalapril, it is perhaps due to the blockade of ATR-AA in losartan group. ATR-AA is one important factor in the pathogenesis of hypertension and losartan can block this pathological effect.