Tubular obstruction in acute renal failure, postulated to cause the restricted excretory function, is suggested by raising intratubular pressure, to lower effective filtration pressure and diminish urine output. To examine the applicability of the obstruction hypothesis to the pathogenesis of experimental acute renal failure, proximal intratubular pressure and renal function were measured after renal insults of different origins and severity. Obstruction in acute renal failure kidneys should manifest itself as an increase in intratubular pressure for a least 12 h, for within this time period following ureteral occlusion, elevated pressures were found to reflect obstruction. The consistent existence of raised proximal intratubular pressure in acute renal failure kidneys could not be detected; ischaemic and nephrototoxic models were found in which no rise in intratubular pressure could be demonstrated. The oliguric nature of acute renal failure kidneys could not be verified; ischaemic and nephrotoxic models were found in which urine output was either normal or enhanced. Only for methaemoglobin induced renal failure were raised intratubular pressure, oliguria and casts concurrent. It is concluded that obstruction is not a consistent feature of experimental acute renal failure and that the obstruction hypothesis may be specifically applicable to only a few models, which include haeme pigment and folic acid induced renal failure.