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...

Renal hemodynamics and renal vascular resistance (RVR) were measured in the spontaneously hypertensive rat (SHR) and in the normotensive Wistar-Kyoto rat (WKY). In addition, the autoregulatory response and segmental RVR in the SHR were studied after aortic constriction. Mean arterial pressure (MAP) and RVR were higher in the SHR than in the WKY, but renal blood flow (RBF) and glomerular filtration rate were similar in both groups. Measurement of mean afferent arteriolar diameter (AAD) by a microsphere method showed a significantly smaller AAD in SHR (17.7 +/- 0.35 micrometers) than in the WKY (19.5 +/- 0.20 micrometers). This decrease in AAD could account for a 47% increase in preglomerular resistance. Aortic constriction in the SHR, sufficient to reduce renal perfusion pressure from 152 to 115 mmHg, did not alter the AAD. Since RBF and glomerular filtration were also well maintained following aortic constriction, these autoregulatory responses suggest that vessels proximal to the afferent arteriole rather than postglomerular vasculature are primarily involved in the changes on intrarenal vascular resistance in SHR.

Results from many laboratories, including our own, support the following view of the status of renal blood flow (RBF) in acute renal failure (ARF). During the initiation phase of virtually all forms of experimental ARF, RBF appears to be substantially decreased. The mechanisms for the decrease in RBF vary depending on the model employed. However, we have shown that changes in cardiac output are involved in both HgCh and glycerol models of ARF. The degree to which the decreased RBF contributes to the impaired glomerular filtration rate (GFR) characterizing the initial phase of ARF also depends on the particular model that is studied. In terms of the maintenance phase of ARF, our studies show that total RBF is essentially normal in both glycerol and HgCU models of ARF. A general consensus exists that RBF is not related to the decreased GFR in the maintenance phase of ARF, regardless of the model of ARF employed. Results from this laboratory suggest, however, that a hemodynamic mechanism may still contribute to the decreased filtration in ARF despite the dissociation between total RBF and GFR. This mechanism may involve an increase in preglomerular resistance, either alone or in association with a decrease in postglomerular resistance. An extensive amount of research has been performed on the renal circulation in ARF over the past two decades. It appears that this research has basically confirmed Ole Munck’s impression of the role of renal blood flow in the pathophysiology of ARF.

In this report, we present the case history of a patient who developed a brief period of oliguria following acute tubular necrosis. Obstructive uropathy and renal underperfusion were ruled out as etiologic causes of oliguria. While glomerular filtration rate (GFR) returned rapidly toward normal, an unusually prolonged and massive diuresis and saluresis (as high as 45 liters/24 h and 5,700 mEq Na/24 h) ensured for almost 1 month; following this, remission was completed over a matter of days. We believe this case dramatically illustrates the importance of functional maturation of tubules in recovery from acute tubular necrosis, and the protective effect against excess fluid and salt losses afforded by decrease in GFR usually seen in this syndrome.