Contractile responses of the portal vein of the anesthetized rabbit were measured quantitatively by plethysmography during transmural electrical field stimulation (TES, 0.8 ms and 15 V) and during the cerebral ischemic pressor response at various volemic states. To evoke the cerebral ischemic response, the route of blood supply to the brain was surgically restricted to the right internal carotid artery, the artery was then compressed in a stepwise fashion by a micrometer device. The maximum contractile response of the portal vein segment that could be evoked by cerebral ischemia corresponded in magnitude to that produced by TES of 10-11 Hz. The contractile response began when the internal carotid blood flow was reduced to 4 ml/min from its normal value of 13.8 +/- 1.2 (mean +/- SE) ml/min and reached a maximum at 0 ml/min. The maximum contractile response was an increase of 26% from control value under normovolemic condition, 20% after hemorrhage and 31% after volume loading. It was estimated that the contractile response in normovolemia was 95% neurogenic, the rest was thought to be of humoral origin.