Vasopressin V_1b receptor is specifically expressed in the pituitary and mediates adrenocorticotropin release, thereby regulating stress responses via its corticotropin releasing factor-like action. In the present study we examined catecholamine release in response to two types of stress in mice lacking the V_1b receptor gene (V_1bR^-/- mice) in comparison with wild type mice. There were no significant differences in the basal plasma levels of catecholamines between the two genotypes. In response to stress induced by forced swimming, norepinephrine (NE), but not epinephrine (E) or dopamine (DA), were increased in wild type mice, while the increases in NE and DA were not observed in V_1bR^-/- mice. In wild type mice, E, but not NE or DA, was increased in response to social isolation stress, while the increase in E was not observed in V_1bR^-/- mice. These results suggest that the V1b receptor regulates stress-induced catecholamine release. As it has been suggested that AVP is related to the development of depression, we also evaluated immobility time in the forced swimming test, and we found no significant change in V_1bR^-/- mice. Taken together, these findings suggest that, in addition to the previously elucidated effect on the hypothalamic-pituitary-adrenal axis, vasopressin activity via V_1b receptors regulates stress-induced catecholamine release.