SUMMARYWe measured mean afferent arteriolar diameter and renal blood flow with microsphere techniques in awake rats 24 hours after induction of acute renal failure by glycerol injection. Renal blood flow, mean arterial pressure, and total renal vascular resistance in rats with acute renal failure were not different from control levels, despite significantly elevated serum urea nitrogen. Mean afferent arteriolar diameter was decreased in rats with acute renal failure compared to controls (21.1 ± 0.10 vs. 22.0 ± 0.16 jun, mean ± SE, n -5, respectively, P < 0.01). The percentage of renal intravascular microspheres (mean diameter of spheres « 22.3 ± 2.1 jim) entering the glomeruli also was decreased in rats with acute renal failure compared to control (75.9 ± 1.4 vs. 85.7 ± 0.8%, n -7, respectively, P < 0.001). Blood viscosity values of rats injected with glycerol and measured at shear rates of 61.8/sec (4.36 ± 0.06 centipoise (cP, n -6) and 123.6/sec [3.78 ± 0.05 cP, n -6] were significantly higher than those of controls (3.84 ± 0.08 cP, n = 6, P < 0.005, and 3.36 ± 0.09 cP, n = 6, P < 0.005). Therefore, preglomerular resistance is increased during glycerol-induced acute renal failure due to a combination of afferent arteriolar vasoconstriction and increased blood viscosity. The increase in preglomerular resistance will cause a reduced glomerular capillary hydrostatic pressure in glycerol-induced acute renal failure. Ore Ret 45: 583-587, 1979 A SUBSTANTIAL number of studies have demonstrated that a decreased glomerular filtration rate (GFR) is not necessarily associated with impaired renal perfusion in acute renal failure (Churchill et al., 1977;Eisenbach et al, 1974; Hsu et ai, 1977;Kurtz et al., 1976; Stein et al., 1975). These studies contrast sharply with earlier reports documenting a relationship between decreased GFR and decreased renal blood flow (RBF) in acute renal failure (Ayer et al., 1971;Chedru et al., 1972;Flamenbaum et al., 1972;Flamenbaum et al., 1974). Initially, preglomerular vasoconstriction was suggested to be the hemodynamic mechanism responsible for the impaired GFR (Chedru et al., 1972; Ruiz-Guinazu et al., 1975). The recent demonstration of normal renal blood flow in acute renal failure, however, does not preclude this concept, provided that postglomerular resistance decreases simultaneously with an increase in afferent arteriolar resistance. Thus, preglomerular vasoconstriction is still a viable hemodynamic explanation for the decreased GFR of acute renal failure. To test this hypothesis, we measured afferent arteriolar diameter in glycerol-induced acute renal failure, using a recently developed microsphere method (Chenitz et al., 1976;Ishikawa and Hollenberg, 1977;Ofstad et al., 1975). MethodsMale Sprague-Dawley rats, weighing 200-240 g, were given Purina rat chow and tap water ad libitum. Acute renal failure was induced by hindlimb intramuscular injection of 50% glycerol, 1 ml/100 g, after 15 hours of dehydration. Water was freely available thereafter. Controls were injected with equ...

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