Ultrastructural immunocytochemical localization of renin and angiotensin II in the juxtaglomerular cells of the ischemic kidney in experimental renal hypertension.
Ultrastructural immunocytochemical localization of renin and angiotensin II in the juxtaglomerular cells of the ischemic kidney in experimental renal hypertension.
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实验性肾性高血压中缺血肾肾小球旁细胞中肾素和血管紧张素 II 的超微结构免疫细胞化学定位。
DOI：
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发表时间：
1984
影响因子：
6
通讯作者：
J. Genest
中科院分区：
文献类型：
--
作者：
M. Cantin;J. Gutkowska;J. Lacasse;M. Ballak;S. Ledoux;T. Inagami;J. Beuzeron;J. Genest
部分结扎大鼠主动脉之间的肾动脉诱导急性高血压与左（缺血）肾萎缩，强烈刺激肾小球细胞（JGC）分泌活动，并显着增加肾皮质肾素活性，血浆肾素活性，血管紧张素I（AI）和血管紧张素II（AII）的血浆水平。在光学显微镜水平和各种稀释度的肾素抗血清的未标记抗体技术，免疫反应性的肾素可以可视化在假手术对照与高稀释度的抗血清，不显示在缺血肾的JGC中的肾素JGC。AII抗血清的情况正好相反;即，高稀释度的AII抗血清免疫染色缺血肾的JGC，但不染色对照肾的JGC。用蛋白A-金技术在电子显微镜水平上，使用大小不同的金颗粒和免疫反应的两个面的一个罚款部分，肾素和AII可以定位在同一JGC分泌颗粒。用同样的技术（免疫反应只有一个小的金颗粒的精细部分的一面），定量分析揭示了一个较低浓度的肾素和较高浓度的AII的分泌颗粒的缺血肾JGC，这些颗粒也比那些控制肾JGC的尺寸较小。AI在这些细胞中无法在光学或电子显微镜水平上可视化。这些结果表明，AII与肾素共同定位在JGC分泌颗粒，并可能共同分泌，是不是由这些细胞合成，但在受体结合后内化。
Partial ligation of the rat aorta between the renal arteries induces acute hypertension with atrophy of the left (ischemic) kidney, intense stimulation of juxtaglomerular cell (JGC) secretory activity, and significant increases in renal cortical renin activity, in plasma renin activity, and in the plasma levels of angiotensin I (AI) and angiotensin II (AII). With the unlabeled antibody technique at the light-microscopic level and various dilutions of renin antiserum, immunoreactive renin can be visualized in the JGC of sham-operated controls with high dilutions of antiserum that do not reveal renin in the JGC of ischemic kidney. The reverse is true with AII antisera; ie, high dilutions of AII antisera immunostain the JGCs of ischemic kidney but not those of control kidney. With the protein A-gold technique at the electron-microscopic level, using gold particles of small and large size and immunoreacting the two faces of a fine section, renin and AII can be localized in the same JGC secretory granules. With the same technique (immunoreacting only one face of a fine section with small gold particles), quantitative analysis reveals a lower concentration of renin and a higher concentration of AII in the secretory granules of the ischemic kidney JGCs; these granules are also of smaller size than those of control kidney JGCs. AI cannot be visualized in these cells at either the light- or electron-microscopic level. These results indicate that AII co-localized with renin in JGC secretory granules and probably co-secreted, is not synthetized by these cells but is internalized following receptor binding.