RENAL RESPONSE TO BLOOD-PRESSURE ELEVATION IN NORMAL AND GLOMERULONEPHRITIC RATS

Concurrent renal disease appears to augment greatly the adverse effect s of systemic hypertension on renal function and the development of gl omerulosclerosis, This study examined the effects of systemic hyperten sion and treatment of hypertension in groups of normal non-nephritic r ats and rats submitted to 16 wk of glomerulonephritis induced by the a dministration of anti-glomerular basement membrane antibody, Hypertens ion was produced by application of a clip to the right renal artery an d blood pressure was treated with an angiotensin-converting enzyme (AC E) inhibitor, quinapril, Glomerulosclerosis of two types developed: a diffuse type that is characteristic of anti-glomerular basement membra ne glomerulonephritis, and a focal segmental glomerulosclerosis that i s characteristic of systemic hypertension. Glomerulonephritis signific antly reduced the capacity of ACE inhibitors to decrease systolic bloo d pressure in awake animals. In addition, glomerulonephritis produced significant effects on plasma angiotensin II concentrations, whereby A CE inhibition no longer lowered plasma angiotensin II levels and in fa ct produced an increase. Glomerular capillary hydrostatic pressure and hydrostatic pressure gradient correlated with systolic blood pressure and with the incidence of focal glomerulosclerosis in non-nephritic r ats. However, in glomerulonephritis, systolic blood pressure no longer correlated with glomerular capillary pressure, and glomerular capilla ry pressure no longer correlated with the development of glomeruloscle rosis, although systolic blood pressure did correlate with the degree of focal segmental glomerulosclerosis, Concurrent glomerulonephritis s trongly conditions the effects of superimposed hypertension by alterin g the relationship between systemic blood pressure and glomerular capi llary hydrostatic pressure and by decreasing the response of hypertens ion to therapy.