Autoregulatory efficiency of renal blood flow (RBF) and glomerular filtration rate (GFR) was evaluated in male Sprague-Dawley rats during interference with the renin-angiotensin system by a converting enzyme inhibitor (CEI), captopril (3 mg · h^-1 · kg^-1 BW). RBF and GFR were approximately 25 (p < 0.01) and 20% (p < 0.02) higher, respectively, in rats infused with CEI than in control rats at spontaneous renal arterial pressure (RAP). A reduction of RAP to 100 mm Hg (within the autoregulatory range) resulted in effective autoregulation of GFR and RBF in control rats. In rats given CEI, however, the autoregulation of GFR was markedly impaired. GFR decreased by 35% (p < 0.001), while RBF remained relatively unchanged. This caused the filtration fraction to decrease from 0.33 ± 0.01 to 0.29 ± 0.01 (p < 0.001). RAP had a consistent effect on the urine flow rate, even though both GFR and RBF were well autoregulated in control rats. No significant decrease in electrolyte excretion was detected within the autoregulatory range in control rats, but during converting enzyme blockade this excretion decreased progressively as RAP was reduced, and the decrease correlated well to the reduction in GFR. In summary, these results suggest that the renin-angiotensin system plays an important intrarenal role in the autoregulation of GFR, probably through an efferent arteriolar mechanism. Furthermore, it is demonstrated that the contra-lateral kidney efficiently compensates in urinary electrolyte excretion for an acute unilateral reduction of RAP, both under control conditions when the perfusion pressure to the contra-lateral kidney increased and during blockade of the renin-angiotensin system when the increase in perfusion pressure was inhibited.