Lesions of the lateral parabrachial nucleus (LPBN) impair blood pressure recovery after hypotensive blood loss (Am J Physiol 280: R1141, 2001). This study tested the hypothesis that post-hemorrhage blood pressure recovery is mediated by activation of neurons located in the ventrolateral aspect of the LPBN (VL-LPBN) that initiate blood pressure recovery by restoring sympathetic vasomotor drive. Hemorrhage experiments (16 ml/kg over 22 min) were performed in unanesthetized male Sprague-Dawley rats prepared with bilateral ibotenate lesions or guide cannulas directed toward the external lateral subnucleus of the VL-LPBN. Hemorrhage initially decreased mean arterial pressure (MAP) from ~100 mmHg control to 40-50 mmHg, and also decreased heart rate. In animals with sham lesions, MAP returned to 84±4 mmHg by 40 min post-hemorrhage, and subsequent autonomic blockade with hexamethonium reduced MAP to 53±2 mmHg. In contrast, animals with VL-LPBN lesions remained hypotensive at 40 min post-hemorrhage (58±4 mmHg) and hexamethonium had no effect on MAP, implying a deficit in sympathetic tone. VL-LPBN lesions did not alter the renin response or the effect of vasopressin V1 receptor blockade after hemorrhage. Post-hemorrhage blood pressure recovery was also significantly delayed by VL-LPBN infusion of the ionotropic glutamate receptor antagonist kynurenic acid. Both VL-LPBN lesions and VL-LPBN kynurenate infusion caused post-hemorrhage bradycardia to be significantly prolonged. Bradycardia was reversed by hexamethonium or atropine, but did not contribute to post-hemorrhage hypotension. Taken together, these data support the hypothesis that stimulation of VL-LPBN glutamate receptors mediates spontaneous blood pressure recovery by initiating restoration of sympathetic vasomotor drive.