BACKGROUND AND PURPOSE: It is well recognized that vasopressin modulates the neurogenic control of the circulation. Here we report the central mechanisms by which vasopressin modulates cardiovascular response to stress induced by immobilization. EXPERIMENTAL APPROACH: Experiments were performed in conscious male Wistar rats equipped with radiotelemetric device for continuous measurement of hemodynamic parameters: systolic and diastolic blood pressure (BP) and heart rate (HR). The functioning of the spontaneous BRR was evaluated using the sequence method and the following parameters were evaluated: BRR sensitivity (BRS) and BRR effectiveness index (BEI). KEY RESULTS: Under baseline physiological conditions intracerebroventricular injection of 100ng and 500ng of selective non-peptide V1a- or V1b- or V2-receptor antagonist did not modify BP, HR and BRR. Rats exposed to 15-minutes-long stress by immobilization exhibited increase of BP, HR, reduction of BRS and no change in BEI. Pre-treatment of rats with V1a-receptor antagonist did not modulate the BP, HR, BRS and BEI response to stress. Pre-treatment of rats with V1b-receptor and V2-receptor antagonist, at both doses, prevented BRR desensitization and tachycardia but failed to modulate stress induced hypertension. CONCLUSIONS AND IMPLICATIONS: Vasopressin by the stimulation of central V1b- and V2-like receptors mediates stress-induced tachycardia and BRR desensitization. If these mechanisms are involved BRR desensitization in heart failure and hypertension associated with poor outcome, they could be considered as novel targets for cardiovascular drug development.