Alcoholic liver disease is frequently accompanied by portal hypertension. We have previously shown that alcohol intake in awake, unrestrained rats is followed by an increase in portal tributary blood flow. In this study, the effect of ethanol on splanchnic hemodynamics in rats with portal hypertension was analyzed. Portal hypertension was induced by partial ligation of the portal vein. This procedure resulted in an increase in portal tributary and hepatic arterial blood flows compared to sham-operated animals. Ethanol (2 gm per kg, oral) increased portal tributary blood flow in both sham-operated and portal vein-ligated rats (sham + water = 37.6 ± 1.4; sham + ethanol = 63.1 ± 1.9; p < 0.01; partial portal vein stenosis + water = 53.2 ± 3.3; partial portal vein stenosis + ethanol = 69.5 ± 2.2 ml · kg−1. min−1; p < 0.01). In sham-operated rats, hepatic artery blood flow was unchanged following ethanol (sham + water = 6.6 ± 0.7; sham + ethanol = 7.1 ± 1.0 ml · kg−1. min−1), whereas in portal vein-ligated rats, flow was increased (partial portal vein stenosis + water = 13.7 ± 1.4; partial portal vein stenosis + ethanol = 19.8 ± 1.1 ml · kg−1 · min−1; p < 0.025). The adenosine receptor blocker 8-phenyltheophylline suppressed only the ethanol-induced increase in both portal tributary and hepatic artery blood flows in portal vein-ligated rats. The increases in hepatic artery and portal tributary blood flows observed in portal vein-ligated rats without ethanol were not influenced by 8-phenyltheophylline. In conclusion, the increase in portal tributary and hepatic artery blood flow following partial portal vein ligation is not adenosine mediated. We have now shown that, in portal hypertension, ethanol further increases portal tributary blood flow. Contrary to what is seen in normal and sham-operated rats, in portal hypertension, ethanol also increases hepatic arterial blood flow. Both the portal and arterial blood flow effects of ethanol appear to be adenosine mediated.