Sphingosine‐1‐phosphate (S1P) potently constricts cerebral arteries and plays key functions in the immune, inflammatory, and cardiovascular systems. Inflammation has an important function in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). S1P is generated and stored in erytrocytes, leukocytes, endothelial cells and platelets and released by platelets during blood clotting. We investigated the functional effect of S1P in basilar artery in a rat subarachnoid hemorrhage model. Using an infusion pump 400μl blood or saline was given with intracysternal injection to young (200–300g) Sprague‐Dawley male rats. After 48 hours brain was removed and basilar artery was isolated and mounted into a wire myograph. Vasoconstricton to KCl, S1P, serotonin (5‐HT), endothelin‐1 (ET‐1), U46619 (a tromboxane A2 agonist) and vasodilatation to acetylcholine (Ach) and sodium nitroprusside (SNP) responses were measured. Compared to saline group, 5‐HT‐, S1P‐ and ET‐1‐induced vasoconstrictions were significantly increased in blood given group whereas KCl and U46619 did not show a difference. There was no difference in Ach‐ and SNP‐induced vasodilations between saline and blood group. In summary, our results suggest that basilar artery constriction to S1P, 5‐HT and ET‐1 are increased in a rat model of SAH and can be a new target for the treatment of vasospasm after SAH.