Under normal conditions glomerular blood flow and glomerular capillary hydrostatic pressure and hydrostatic pressure gradient are regulated within a narrow range in spite of variations in volume status and blood pressure. Glomerular ultrafiltration rate is normally regulated by the hydrostatic pressure gradient, the systemic oncotic pressure, the rate of nephron plasma flow and the glomerular ultrafiltration coefficient. Although the process of glomerular ultrafiltration is driven by the hydrostatic pressure gradient (delta P), regulation of nephron filtration rate (SNGFR) is not mediated by changes in hydrostatic pressure and the correlation between SNGFR and delta P is very poor. There are certain clinical experimental models in which the glomerular capillary hydrostatic pressure gradient is elevated. These models have been: (1) subtotal nephrectomy model, a model of reduced renal mass, (2) glomerular immune induced injury or glomerulonephritis, (3) most models of systemic hypertension, and (4) certain stages of experimental diabetes mellitus, but the mechanisms vary among the conditions. In most of these clinical models the increase in delta P is associated with a reduction in the glomerular ultrafiltration coefficient. It is also clear that superimposition of hypertension upon models of glomerular immune injury and radical subtotal nephrectomy cause progression of renal dysfunction and glomerulosclerosis. One of the contributing factors to this progression appears to be the elevation in glomerular capillary hydrostatic pressure and pressure gradient. However, other factors have been suggested to play a significant role, such as compensatory hypertrophy and possibly the neurohumoral environment. Therapy of systemic hypertension and administration of cardiovascular drugs which alter glomerular capillary hydrostatic pressure may then modify the rate of progresswion of these disorders.(ABSTRACT TRUNCATED AT 250 WORDS)