The underlying mechanism responsible for the cardiovascular response to Hemorrhage (HEM) is still unknown; however, several brain areas, such as the Cuneiform nucleus (CnF) have shown to be involved. In this study, the cardiovascular effect of the CnF during HEM was evaluated. Methods: The animals were divided into the following groups: 1. Vehicle; 2. HEM; 3. Cobalt chloride (CoCl 2); 4. CoCl 2 +saline; and 5. CoCl 2 +HEM. Catheterization of the left and right femoral artery was performed to record blood pressure and blood withdrawal, respectively. Saline and CoCl 2 were microinjected into the CnF nucleus, and then blood withdrawal was done for HEM induction. Cardiovascular regulation throughout the experiments was recorded and changes (∆) in the Systolic Blood Pressure (SBP), Mean Arterial Pressure (MAP) and Heart Rate (HR) were calculated over time and compared with those treated with saline and HEM, using repeated-measures ANOVA. Results: HEM significantly reduced ∆SBP and ∆MAP and augmented ∆HR than the vehicle group. CoCl 2 did not significantly affect basic ∆SBP, ∆MAP, and ∆HR compared with the vehicle group. However, injection of CoCl 2 into the CnF before HEM (CoCl 2 +HEM group) significantly decreased ∆SBP, ∆MAP, and tachycardia, induced by HEM. Conclusion: Our results indicated that blockade of the CnF by CoCl 2 significantly reduced the hypotension and tachycardia, induced by HEM indicating the involvement of CnF in cardiovascular regulation during HEM.