Vascular hyporeactivity and hyperpolarization are important causes of circulatory failure in septic shock. However, there is no data regarding the differences of vascular reactivity and resting membrane potential in survivors and non-survivors of sepsis. Thus, the aim of this study was to examine and compare the changes of vascular reactivity and resting membrane potential in survivor and non-survivor rats after cecal ligation and puncture (CLP)-induced sepsis. Wistar rats were anaesthetised by sodium pentobarbital (30 mg/kg, i.p.), and then, subjected to CLP or sham operation after the carotid artery and vein were cannulated. The changes of hemodynamics, biochemical variables, aortic isometric tension, smooth muscle membrane potential, and aortic superoxide levels were monitored during the experimental period. The CLP surgery caused circulatory failure, multiple organ dysfunction syndrome (MODS), vascular hyporeactivity to norepinephrine (NE), and vascular hyperpolarization. Compared with survivors, non-survivor rats showed a more severe organ dysfunction and a less increase in aortic superoxide levels at 9 h. In addition, non-survivor rats manifested less decreases in vascular reactivity to NE and resting membrane potential in the aortas when compared with those in the survivors. These results demonstrate significant differences of vascular reactivity and resting membrane potential in survivor and non-survivor rats after CLP-induced sepsis. However, vascular hyporeactivity and hyperpolarization only partially contributed to the early death of septic animals, while this early death was most likely due to organ dysfunction (i.e. MODS) in this CLP-induced sepsis model.