Autoantibodies against the angiotensin receptor (AT1) in patients with hypertension

Autoantibodies against the angiotensin receptor (AT1) in patients with hypertension
复制标题

DOI:
10.1097/00004872-200018070-00017
复制
发表时间:
2000-07-01
影响因子:
4.9
通讯作者:
Hoebeke, J
Hoebeke, J
中科院分区:
医学2区
文献类型:
--
作者:
Fu, MLX;Herlitz, H;Hoebeke, J

文献摘要

被引文献

相似文献

对14例恶性高血压患者、12例以肾血管疾病为主的恶性继发性高血压患者、11例无恶性高血压的肾血管疾病患者和35例血压正常的健康献血员血清中抗G蛋白偶联心血管受体自身抗体的检测结果表明,恶性高血压患者、恶性继发性高血压患者、肾血管疾病患者和对照组分别有14、33、18和14%的患者检测到抗血管紧张素II受体(AT(1))自身抗体。酶免疫分析的敏感性为5mU g/mlIg G,患者未检测到抗缓激肽(B-2)或血管紧张素II亚型(AT(2))受体的抗体,从阳性患者中亲和纯化的自身抗体定位于中国仓鼠卵巢转基因细胞中的AT受体,并对培养的新生大鼠心肌细胞具有正性变时性作用。这些结果表明恶性高血压患者存在抗人AT1受体胞外功能区的自身抗体,提示这些自身抗体可能参与了恶性高血压的发病机制。J Hyperten 2000,18:945-953(C)Lippincott Williams&Wilkins.
Sera from patients with malignant essential hypertension (n = 14), malignant secondary hypertension mainly attributable to renovascular diseases (n = 12) and renovascular diseases without malignant hypertension (n = 11) and from normotensive healthy blood donors (n = 35) were studied for the presence of autoantibodies against G-protein-coupled cardiovascular receptors, Autoantibodies against the angiotensin II receptor (AT(1)) were detected in 14, 33, 18 and 14% of patients with malignant essential hypertension, malignant secondary hypertension, renovascular diseases and control patients, respectively. Sensitivity of the enzyme immunoassay was assessed as 5 mu g/ml IgG, Patients did not show antibodies against bradykinin (B-2) Or angiotensin II subtype 2 (AT(2)) receptors, Autoantibodies affinity-purified from positive patients localized AT receptors in Chinese hamster ovary transfected cells, and displayed a positive chronotropic effect on cultured neonatal rat cardiomyocytes, These results demonstrate the existence of autoantibodies against a functional extracellular domain of human AT1 receptors in patients with malignant hypertension, and suggest that these autoantibodies might be involved in the pathogenesis of malignant hypertension. J Hypertens 2000, 18:945-953 (C) Lippincott Williams & Wilkins.