We studied the mechanical properties of canine basilar arteries subjected to experimental subarachnoid hemorrhage (SAH). Smooth muscle contractility was determined from pressure-diameter curves obtained after subjecting the basilar arteries to three different conditions: Krebs-Ringer solution (KRS), Krebs-Ringer solution containing serotonin (5HT), and saline solution. Pressure-diameter curves obtained in KRS and 5HT are biphasic and have sharp flexions that yield flexion points. The pressure level at the flexion point increases as vasospasm increases. Strong constriction is retained up to that pressure above which the constriction is released abruptly. These data suggest that increasing the intraluminal pressure dilates the spastic artery nonlinearly and that induced hypertension could relieve the cerebral ischemia caused by vasospasm if blood pressure were maintained above the flexion point. The contractile response of spastic arterial wall to serotonin remains unchanged after SAH although the spastic constriction increases progressively and becomes maximal seven days after SAH. The lesser the arterial wall stiffness, the more efficiently it constricts. This means that the diminution of arterial stiffness observed after SAH might be one of the factors promoting the development of vasospasm.