The rat portal vein is a useful pharmacological model to study the contractions of smooth muscle cells through both receptor-dependent and receptor-independent mechanisms. We previously showed that sepsis decreases the spontaneous and agonist-induced contractile response to angiotensin II in this model. To determine whether acidosis and hyperthermia, which occur in sepsis, might contribute to this vascular failure, rat portal veins were isolated from control rats and exposed to norepinephrine and angiotensin II. During the pharmacological tests, the rat portal vein were incubated at 37 or 39.5 degrees C or infused with a solution at low pH with normal or high pCO(2). Mild and severe acidosis had minor effects on the vascular response of rat portal vein to norepinephrine and angiotensin II. In contrast, hyperthermia decreased the response of both drugs. Nitric oxide (NO), carbon monoxide (CO), and prostaglandins were not responsible for the decreased response. Thus, acidosis observed during sepsis is not responsible for the vascular dysfunction of rat portal vein. In contrast, hyperthermia participates to the vascular failure but the mediator responsible remains unknown.