Cardiac output (CO) and renal blood flow (RBF) were simultaneously evaluated (microsphere method) in awake rats, 3, 6, and 24 h after induction of acute renal failure by mercuric chloride (HgCl<sub>2</sub>; 4.7 mg/kg body weight). 3 h after injection of HgCl<sub>2</sub> CO and RBF decreased to 77 and 72% of respective control values of 32.0 ± 2.4 and 4.65 ± 0.44 ml/min/100 g. Renal vascular resistance (RVR) and total peripheral resistance (TPR) were significantly increased compared to control at this time. Similar results were observed 6 h after administration of HgCl<sub>2</sub>. Volume expansion with plasma (2% of body weight) restored CO, RBF, TPR, and RVR to normal 3 h after injection of HgCl<sub>2</sub>. Despite significantly elevated blood urea nitrogen 24 h after injection of HgCl<sub>2</sub> (103.7 mg%), all hemodynamic parameters were within control range. Plasma volume was normal 3 h after HgCl<sub>2</sub> but was significantly elevated compared to control 24 h after HgCl<sub>2</sub> (4.73 vs. 3.92 ml/l00 g, p < 0.01). These findings indicate that factors other than preferential renal vasoconstriction may be involved in the transient renal ischemia of HgCl<sub>2</sub>-induced acute renal failure.