Portal hypertension initiates a splenorenal reflex, whereby increases in splenic afferent nerve activity and renal sympathetic nerve activity cause a decrease in renal blood flow. We postulated that mesenteric vascular congestion similarly compromises renal function through an intestinal-renal reflex. The portal vein was partially occluded in anesthetized rats, either rostral or caudal to the junction with the splenic vein. Portal venous pressure increased (6.8±0.3mmHg to13.0±0.3mmHg; n=65), and mesenteric venous outflow was equally obstructed in both cases. However, rostral occlusion increased splenic venous pressure, whereas caudal occlusion caused no such change. Rostral occlusion caused a fall in renal blood flow (RBF) (-1.2±0.2mL/min, n=9) which was attenuated by renal denervation (-0.5±0.1mL/min, n=6), splenic denervation (-0.2±0.1mL/min, n=11), and celiac ganglionectomy (-0.3±0.1mL/min, n=9). Caudal occlusion induced a significantly smaller fall in RBF (-0.5±0.1mL/min, n=9), which was not influenced by renal denervation (-0.2±0.2mLmin, n=6), splenic denervation (-0.1±0.1mL/min, n=7), or celiac ganglionectomy (-0.1±0.3mL/min, n=8). Renal arterial conductance fell only in the intact animals subjected to rostral occlusion (-0.007±0.002 mL min^-1 mmHg^-1). This was accompanied by increases in splenic afferent nerve activity (15.0±3.5 spikes/sec to 32.6±6.2 spikes/sec, n=7) and renal efferent nerve activity (32.7±5.2 spikes/sec to 39.3±6.0 spikes/sec, n=10). In the animals subjected to caudal occlusion, there were no such changes in renal arterial conductance or splenic afferent/renal sympathetic nerve activity. We conclude that the portal hypertension-induced fall in RBF is initiated by increased splenic, but not mesenteric, venous pressure i.e. we did not find evidence for intestinal-renal reflex control of the kidneys.