Background: Impaired vascular responsiveness to vasoconstrictors is often seen in sepsis, in particular in septic shock. Nitric oxide and superoxide anion (O2(superscript -)) usually play an important role in mediating vascular hypo-responsiveness to vasoconstrictors in sepsis. The aim of this study was to determine whether terbutaline, a known cyclic-AMP agonist, can restore vascular hypo-responsiveness in cecal ligation and puncture (CLP)-induced sepsis models. Methods: Male adult Wistar rats received CLP or sham operations followed by the intravenous administration of saline or terbutaline (0.3mg/kg at 3 and 9 h after CLP). At 0, 9 and 18 h after CLP, changes of arterial blood pressure, vascular responsiveness to norepinephrine (NE) and plasma nitrite/nitrate levels were examined. At 18 h after CLP, the animals were sacrificed and their thoracic aortae were immediately exercised to analyze O2(superscript -) levels. Results: Vascular responsiveness to NE was impaired in CLP-treated rats. The administration of terbutaline did not alter vascular responsiveness to NE in sham-operated rats but significantly mitigated the vascular hypo-responsiveness to NE in CLP-treated rats. In addition, increased plasma nitrite/nitrate levels caused by CLP were suppressed by terbutaline. However, this had no significant effect on aortic O2(superscript -)levels in CLP-treated rats. Conclusion: This study demonstrates that CLP-induced vascular hyporesponsiveness to NE is partially restored by treatment of rats with terbutaline, suggesting that terbutaline could be a new therapeutic agent to treat patients with septic shock resulting from impaired vascular responsiveness to vasoconstrictors.