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血管紧张素Ⅱ(AngⅡ)是控制肾小球血液动力学的重要因子。在肾小球系膜和输出小动脉中都有其高亲合力的受体。本文作者纵向观察了大鼠抗基底膜性肾炎的肾小球中血管紧张素Ⅱ受体的表达。以了解有免疫诱导的肾小球损害时,肾小球血管紧张素Ⅱ受体(AngⅡR)与循环血中AngⅡ受体的异常关系。在给予单剂羊抗鼠抗体后两个月,用Scatchacd法测定纯肾小球的AngⅡR,并同时测定循环中血浆AngⅡ浓度。注入抗体后16小时,其受体密度大约下降50%,(对照组96,4±9.3×10~6,肾炎组52.6±56×10~6,受体/肾小球,P<0.001。而血浆AngⅡ相应升高3倍对照组21±2.5,肾炎组66.6±206pg/ml,
Angiotensin Ⅱ (Ang Ⅱ) is an important factor in the control of glomerular hemodynamics. In the glomerular mesangium and the output of arterioles have their high affinity receptors. The authors longitudinally observed the expression of angiotensin II receptor in the glomerulus of rat anti-basal membranous nephritis. To understand the immune-induced glomerular damage, glomerular angiotensin Ⅱ receptor (Ang Ⅱ R) and circulating blood Ang Ⅱ receptor abnormalities. Two months after the administration of a single dose of goat anti-mouse antibody, the Ang IIR of pure glomeruli was measured by the Scatchacd method and the circulating AngII concentration was also measured. At 16 hours after antibody injection, its receptor density decreased by about 50% (control group 96.4 ± 9.3 × 10 ~ 6, nephritis group 52.6 ± 56 × 10 ~ 6, receptor / glomerular, P <0.001. Plasma Ang Ⅱ increased 3 times in the control group 21 ± 2.5, nephritis group 66.6 ± 206 pg / ml,