Effect of hypertension on experimental glomerulonephritis in rats

The effect of hypertension on the anatomy, physiology, and course of glomerulonephritis in rats was investigated by inducing deoxycorticosterone acetate-salt hypertension in animals with heterologous immune complex glomerulonephritis and vice versa. The effect of hypertension on glomerulonephritis with different degrees of intensity was also studied. Hypertension increased the proteinuria in the glomerulonephritic rat substantially (p less than 0.01), reduced the creatinine clearance (p less than 0.05), and induced an enormous thickening of the glomerular basement membrane. Furthermore, the life span was shortened (p less than 0.01) when hypertension was induced in nephritic rats, possibly due to insufficient cerebral vascular activity secondary to malnutrition. Glomerulonephritis did not influence the blood pressure in animals with severe protein loss; in rats with minor proteinuria the presence of glomerulonephritis increased the blood pressure. Hypertension lowered the antiserum dose needed to produce pathologic proteinuria (p less than 0.02). Hypertension seemed to increase the amount of glomerular immune deposits in early glomerulonephritis but lowered the amounts of glomerular rat IgG during the course of nephritis. In conclusion, hypertension increases the glomerular damage substantially in rats with heterologous immune complex glomerulonephritis, influences the glomerular deposition of immunoglobulins, and shortens the life span.