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An acth‐induced renal glomerular lesion in the mouse: Immunofluorescence microscopy
Author(s) -
Feldman David L.,
Gorfien Stephen F.,
Christian John J.
Publication year - 1983
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711390311
Subject(s) - immunofluorescence , glomerulus , endocrinology , adrenocorticotropic hormone , medicine , albumin , chemistry , macula densa , staining , lesion , kidney , antibody , pathology , biology , hormone , renin–angiotensin system , immunology , blood pressure
Abstract Mice were injected with adrenocorticotropic hormone (ACTH) and the glomerular lesion that was induced was studied by light and immunofluorescence microscopy. By light microscopy, kidneys from ACTH‐treated mice showed typical ACTH‐induced glomerular lesions. Immunofluorescence of kidneys from ACTH‐treated mice revealed intense staining for IgG and IgM in the extraglomerular mesangium (EGM), in Bowman's space, and in the ascending thick limb of Henle near the macula densa. Staining for immunoglobulins was unchanged after treatment with acid buffer. Immunoreactivity for complement (C 3 ) was confined largely to the EGM and Bowman's space. Staining for albumin was almost exclusively in Bowman's space or the peripheral glomerular tuft in discrete aggregates. The above patterns of IgG, IgM, C 3 and albumin were seen in control mice, although much less frequently. The results show that in mice, treatment with ACTH results in the increased accumulation of plasma proteins in the juxtaglomerular apparatus (JGA). This effect may reflect a role for the JGA in the normal clearing of plasma proteins from the glomerulus and/or directly from the blood.