Investigations in which a variety of experimental approaches were used, i.e., micropuncture techniques, analysis of intrarenal hormonal receptor, and electron microscopic analysis of renal morphology, have substantiated a major role for angiotensin II (AII) within the kidney in the regulation of vascular resistances, glomerular function, and even tubular reabsorption. It is also clear that AII exerts a significant influence on glomerular hemodynamics in a variety of altered physiological and pathophysiological states. Recent studies suggest a rather complex interaction between AII and hormonal and adrenergic effects at the glomerular level. AII may also play an important functional role in the pathogenesis of certain forms of acute renal failure. The specific mechanism whereby AII decreases the glomerular ultrafiltration coefficient, however, remains to be fully elucidated. Although in vitro and in vivo studies have suggested that the glomerular effects of AII may be associated with contraction of glomerular mesangial cells, recent in vivo quantitative evaluation has suggested that a uniform vasoconstriction of glomerular capillaries with proportional reductions in glomerular surface area is probably not the sole mechanism for the AII-induced reductions in glomerular ultrafiltration coefficient.