Prolactin status in experimentally induced acute renal failure in the rat.
Serum prolactin levels were elevated in male Sprague-Dawley rats with acute renal failure induced by glycerol administration. Specific prolactin binding to kidney membrane preparations was reduced in glycerol and antirat glomerular basement membrane serum-treated rats, after morphological and biochemical acute renal failure was evident. Extensive tubular damage after glycerol administration may account for loss of renal binding, since prolactin receptors are mainly tubular in localization. However, the predominant glomerulopathy, with less severe tubular lesions, after antirat glomerular basement membrane serum suggests that reduced renal prolactin binding in these animals is unlikely to be due to tubular destruction alone. Thus, alterations in prolactin status occur with development of experimentally induced acute renal failure and suggest altered renal responsiveness to prolactin in uraemia.
D058186:Acute Kidney Injury / Q000097:blood* / Q000209:etiology / Q000378:metabolism; D000818:Animals; D001485:Basement Membrane / Q000276:immunology; D005990:Glycerol; D007106:Immune Sera; D007668:Kidney / Q000378:metabolism; D007678:Kidney Glomerulus / Q000276:immunology; D008297:Male; D011388:Prolactin / Q000097:blood* / Q000378:metabolism; D051381:Rats; D011956:Receptors, Cell Surface / Q000378:metabolism; D011981:Receptors, Prolactin
D007106:Immune Sera; D011956:Receptors, Cell Surface; D011981:Receptors, Prolactin; D011388:Prolactin; D005990:Glycerol