1. The innervated hepatic arterial and portal venous vascular beds of the dog were perfused simultaneously, in situ. Under control conditions, the pressures, blood flows and calculated vascular resistances in these beds were similar to those previously reported in preparations where one bed was perfused alone. 2. The pressure-flow curves in both the hepatic arterial and portal venous vascular beds were almost linear over the pressure ranges 30--200 and 2.5--12.0 mmHg respectively. There was no evidence of pressure-induced autoregulation of flow in either circuit. 3. Increases in hepatic arterial blood flow and perfusion pressure were associated with a linearly related increase in hepatic portal vascular resistance. Occlusion of the hepatic artery caused a mean fall of 21.3% in portal vascular resistance. 4. Increases in hepatic portal blood flow and perfusion pressure were associated with a linearly related incease in hepatic arterial vascular resistance. Occlusion of the hepatic portal vein caused a mean fall of 16.0% in hepatic arterial vascular resistance. 5. Intra-arterial injections of noradrenaline (0.1--50 microgram) caused biphasic changes in hepatic arterial vascular resistance, and a rise in hepatic portal vascular resistance. Both hepatic vascular effects had a significantly shorter latency than any succeeding systemic cardiovascular effects. 6. Intraportal injections of noradrenaline (0.1--50 microgram) caused hepatic portal vasoconstriction, and a biphasic change in the hepatic arterial resistance. Both of these effects had a significantly shorter latency than any succeeding systemic effects. 7. Intra-arterial injections of isoprenaline (0.1--10 microgram) caused dose-dependent hepatic arterial vasodilatation but little change in portal vascular resistance. Intraportal isoprenaline caused little change in portal resistance but elicited dose-dependent hepatic arterial vasodilatation. 8. The time courses of the responses to intra-arterial and intraportal noradrenaline and isoprenaline indicate that the responses of the liver vascular bed which does not receive the direct injection were not due to recirculation of the vasoactive material. 9. It is postulated that vasoactive material injected into one inflow circuit of the liver elicits changes in the vascular resistance of the other inflow circuit by an intrahepatic effect.