Hypertension and progression of experimental nephritis. Interaction between immunological and haemodynamic factors.
Hypertension has been shown to accelerate the course of experimental nephritis. On the other hand, Heymann nephritic rats undergoing long-term DOCA-NaCl treatment develop hypertension with a malignant course. The present study examined the effect of a short-term DOCA-NaCl load on the development of hypertension and progression of nephritis. Heymann nephritic rats were treated with DOCA-NaCl between weeks 2 and 6 after the first immunization with brush border antigen. Within six weeks, hypertension developed in Heymann nephritis-DOCA-NaCl rats but not in Heymann nephritic rats without DOCA-NaCl treatment whereas DOCA-NaCl-treated rats developed a moderate elevation of blood pressure. During that time, anti-brush border antibodies and immune deposits typical of membranous nephropathy ensued, preceding appearance of proteinuria or histopathologically detectable renal changes in the immunized rats. After discontinuation of DOCA-NaCl treatments at week 6, blood pressure nearly normalized in DOCA-NaCl-treated rats. Within one year, however, blood pressure rose most markedly in nephritic rats treated initially with DOCA-NaCl. The rise in blood pressure at that time correlated with glomerular sclerosis, tubulo-interstitial changes and proteinuria. It is concluded that, during acute nephritis, immunological and hypertensinogenic mechanisms interact, leading to hypertension and aggravated course of nephritis. These experimental observations on nephritis-associated hypertension may have important bearings on human hypertension as well.
D000818:Animals; D000936:Antigen-Antibody Complex / Q000032:analysis; D001323:Autoantibodies / Q000032:analysis; D001794:Blood Pressure; D003900:Desoxycorticosterone; D005260:Female; D005455:Fluorescent Antibody Technique; D005921:Glomerulonephritis / Q000150:complications / Q000276:immunology / Q000503:physiopathology; D006973:Hypertension / Q000139:chemically induced / Q000209:etiology* / Q000503:physiopathology; D008871:Microvilli / Q000276:immunology; D009393:Nephritis / Q000150:complications* / Q000276:immunology / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D012965:Sodium Chloride
D000936:Antigen-Antibody Complex; D001323:Autoantibodies; D003900:Desoxycorticosterone; D012965:Sodium Chloride