Previous experiments from our laboratory have shown that longer lasting reductions in renal perfusion pressure (RPP) are associated with a gradual decrease in renal blood flow (RBF) that can be abolished by clamping plasma angiotensin II concentration ([Ang II]). The aim of the present study was to investigate the mechanisms behind the RBF downregulation in halothane-anaesthetized Sprague Dawley rats during a 30 min reduction in RPP to 88 mm Hg. During the 30 min of reduced RPP we also measured glomerular filtration rate (GFR), proximal tubular pressure (P_prox) and proximal tubular flow rate (Q_LP). Early distal tubular fluid conductivity was measured as an estimate of early distal [NaCl] ([NaCl]_ED) and changes in plasma renin concentration (PRC) over time were measured. During 30 min of reduced RPP, RBF decreased gradually from 6.5 ± 0.3 ml/min to 6.0 ± 0.3 ml/min after 5 min (NS) to 5.2 ± 0.2 ml/min after 30 min (P < 0.05). This decrease occurred in parallel with a gradual increase in plasma renin concentration from 38.2 ±11.0 x 10^-5 GU/ml to 87.1 ± 25.1 x 10^-5 GU/ml after 5 min (P < 0.05) to 158.5 ± 42.9 x 10^-5 GU/ml after 30 min (P < 0.01). GFR, P_prox, and [NaCl]_ED all decreased significantly after 5 min and remained low. Estimates of pre- and postglomerular resistances showed that the autoregulatory mechanisms initially dilated preglomerular vessels to maintain RBF and GFR. However, after 30 min of reduced RPP both pre- and postglomerular resistance had increased. We conclude that the decrease in RBF over time is caused by increases in both pre- and postglomerular resistance due to rising plasma renin and Ang II concentrations.