One day after rats were injected with 4.7 mg/kg HgCl2 subcutaneously, their surface nephrons usually were fluid filled, had a normal intratubular pressure, but formed minimal volumes of filtrate. Proximal tubule fluid flow rate was greatly diminished, material resembling cell debris obstructing the outflow of fluid. The finding of normal, rather than elevated, intratubular pressure in obstructed tubules indicates that effective filtration pressure probably was grossly reduced. Fluid absorption in the proximal tubule appeared to be greatly impaired. Despite slow flow in the undisturbed nephron, fluid could be collected from the proximal tubule at a normal rate, single nephron GFR being some 80% of control. The return of filtration on ‘venting’ the nephron during collections, and sustained normal single nephron GFR values after obstruction was relieved by washout of debris suggest a feed-back mechanism between impairment of tubular flow and intraglomerular filtration pressure. Intravenously injected lissamine green appeared promptly in distal tubule segments after release of obstruction, confirming the return of a normal proximal tubule fluid flow rate. Evidence for pathologically increased absorption of filtrate was not found. It is concluded that effective filtration pressure is significantly reduced in acute renal failure produced in the rat with low doses of HgCl2 that tubular obstruction plays a role in the maintenance of the low filtration pressure, and that the discrepancy between whole kidney and single nephron inulin clearance values is artifactual. The latter features appear to be unique to low dose mercury poisoning and differ significantly from findings in other models of experimental acute renal failure in the rat.