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American Journal of Pathology, Vol 115, 212-224, Copyright © 1984 by American Society for Investigative Pathology

REGULAR ARTICLES

Ultrastructural immunocytochemical localization of renin and angiotensin II in the juxtaglomerular cells of the ischemic kidney in experimental renal hypertension

M Cantin, J Gutkowska, J Lacasse, M Ballak, S Ledoux, T Inagami, J Beuzeron and J Genest

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.

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