The airpuff startle paradigm, a stress paradigm, elicits greater pressor and tachycardia responses in SHRLJ than WKYLJ which, unlike SHRLJ, also show bradycardia. CRF has been implicated in coordinating autonomic responses to stressors. The present studies explored the role of CRF, CRF antagonist D-PheCRF12-41 and chronic hydralazine in stress-induced cardiovascular responses. In SHRLJ CRF unmasked a bradycardia response, equal to WKYLJ receiving either aCSF or CRF, which was blocked by D-PheCRF12-41. CRF given to hydralazine-treated SHRLJ did not unmask a bradycardia. In WKYLJ CRF specifically lowered the pressor response on trial 1 compared to control, an effect abolished by the antagonist. WKYLJ receiving D-PheCRF12-41 prior to testing showed greater pressor and bradycardia responses when compared to control. In the WKYLJ CRF appears to exert an inhibitory role on the pressor and bradycardia responses while in the SHRLJ CRF exerts a permissive role on the bradycardia response which is lost when blood pressure is normalized with chronic hydralazine. CRF and D-PheCRF12-41 modify stress-induced cardiovascular responses in a strain-dependent dissimilar fashion. We conclude CRF has cardiovascular importance in the genetic hypertensive rat.