Different blood pressure response to DOCA-NaCl treatment in autoimmune and N,N'- diacetylbenzidine-induced nephropathies.
In order to explore the effect of immunologically-induced nephropathy versus a non-immunological model on development of hypertension, rats with either Heymann nephritis or N,N'-diacetylbenzidine (N,N'-DAB)-induced nephropathy were subjected to DOCA-NaCl treatment. Hypertension developed during DOCA-NaCl treatment in Heymann nephritic rats but not in rats wih N, N'-DAB nephropathy, despite similar degrees of proteinuria and other features of nephrosis. There were no signs of different fluid balance, either. Azotemia did not ensue. Histology and immunohistology showed membranous glomerulonephritis in Heymann  nephritic rats whereas glomerular epithelial cell alterations without immune deposits along the glomerular capillary walls were seen in rats with N, N'-DAB nephropathy. The type of renal damage or factors mediating such damage appear to be important determinants for the hypertensive response of Heymann nephritic rats to DOCA-NaCl treatment.
D000818:Animals; D001327:Autoimmune Diseases / Q000150:complications*; D001560:Benzidines; D001794:Blood Pressure; D003900:Desoxycorticosterone / Q000494:pharmacology; D005260:Female; D006977:Hypertension, Renal / Q000209:etiology*; D007674:Kidney Diseases / Q000139:chemically induced / Q000150:complications*; D007678:Kidney Glomerulus / Q000473:pathology; D009393:Nephritis / Q000150:complications*; D011507:Proteinuria; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride / Q000494:pharmacology
D001560:Benzidines; C007291:N,N'-diacetylbenzidine; D003900:Desoxycorticosterone; D012965:Sodium Chloride