ULTRASTRUCTURAL IMMUNOCYTOCHEMICAL LOCALIZATION OF RENIN AND ANGIOTENSIN-II IN THE JUXTAGLOMERULAR CELLS OF THE ISCHEMIC KIDNEY IN EXPERIMENTAL RENAL-HYPERTENSION

  • 1 January 1984
    • journal article
    • research article
    • Vol. 115  (2) , 212-224
Abstract
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: i.e., high dilutions of AII antisera immunostain the JGC of ischemic kidney but not those of control kidney. With the protein A-Au technique at the EM level, using Au particles of small and large size and immunoreacting the 2 faces of a fine section, renin and AII can be localized in the same JGC secretory granules. With the same technique (immunoreacting only 1 face of a fine section with small Au particles), quantitative analysis reveals a lower concentration of renin and a higher concentration of AII in the secretory granules of the ischemic kidney JGC; these granules are also of smaller size than those of control kidney JGC. AI could not be visualized in these cells at either the light microscopic or EM level. AII co-localized with renin in JGC secretory granules and probably co-secreted, apparently is not synthetized by these cells but is internalized following receptor binding.