Elevation of blood hematocrit has been shown to result in little effect upon renal blood flow despite the resulting elevation in whole blood viscosity (L. Share, Amer. J. Physiol. 171, 159–163, 1952). Perfused rat kidneys were used to study the effects of doubling the perfusate viscosity from 0.858 to 1.768 cP. A portion of the bovine serum albumin (BSA) that was present in the low viscosity perfusate (5 g% BSA) was replaced by a high molecular weight dextran (4 g% BSA + 1.4 g% dextran) so as to double the perfusate viscosity but keep the colloid osmotic pressure constant. [14C]Inulin was used to measure glomerular filtration rate (GFR) and absolute filtrate reabsorption (TH2O). Perusion with the high viscosity perfusate reduced the arterial flow by 50% and doubled the total renal flow resistance from 4.5 ± 0.4 (SD) to 9.1 ± 0.8 mm Hg·gKw (gram kidney weight)·min·g−1. Thus, the kidney was not capable of autoregulating the perfusate flow in response to a viscosity alteration. Both GFR and TH2O were reduced with increased viscosity (GFR, 1.18 ± 0.16 (SD) to 0.96 ± 0.200 g/min/gKw (P < 0.05) and TH2O, 0.75 ± 0.07 to 0.59 ± 0.09 g/min/gKw, P < 0.005); however, these reductions were accompanied by a fall in ATP content of the kidneys from 1.43 ± 0.15 (SD) to 1.15 ± 0.11 μmoles ATP/gKw. This indicates that a reduction in metabolic rate due to lower O2 delivery (lower flow) may have been responsible for these latter results.