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 AR