Evidence has accumulated that angiotensin II (AII) exerts multiple influences upon renal function through effects on vascular, glomerular, and tubular structures. Infusion of AII alters glomerular ultrafiltration by decreasing nephron plasma flow, increasing glomerular capillary hydrostatic pressure (PG) and the hydrostatic pressure gradient (delta P) due to increases in both afferent and efferent arteriolar vascular resistance, and effecting a reduction in the glomerular ultrafiltration coefficient (LpA), the product of glomerular membrane hydraulic conductivity and effective surface area for ultrafiltration. Spontaneous increases in intrarenal AII generation, such as observed in chronic NaCl depletion, also produce reductions in nephron plasma flow, increases in delta P, and major reductions in LpA. Angiotensin-converting enzyme inhibitor and saralasin administration prevent these alterations in plasma flow, delta P, and LpA. These AII-induced alterations in LpA may be mediated by AII effects upon the glomerular mesangial cell since AII receptors are expressed and this cell contracts in vitro in the presence of AII. Multiple studies have shown a positive effect of AII (approximately 10(-11) mol/L) on proximal tubular reabsorption, an effect independent of AII effects on peritubular physical factors. These AII effects upon the proximal tubule are clearly independent of interaction with adrenergic influences. AII also influences other mesangial cell functions such as uptake of macromolecules from the circulation. AII also exerts effects by influencing the functional expression of renal adrenergic activity, as demonstrated by studies with renal nerve stimulation in the presence and absence of angiotensin-converting enzyme inhibitor and saralasin. Inhibition of AII activity also clearly suppresses tubuloglomerular activity and the PG response to alterations in distal tubular flow rates.(ABSTRACT TRUNCATED AT 250 WORDS)