Our previous study showed that chronic intermittent hypobaric hypoxia (CIHH) could prevent decreases in systemic arterial blood pressure (SABP) during acute hypoxia. However, the mechanism was not clear. The purpose of the present study was to observe whether the carotid sinus baroreflex (CSB) was involved in the antagonizing effect of CIHH on SABP decrease induced by acute hypoxia and to explore the underlying mechanism using perfusion technique in rat isolated carotid sinus area. After 14-day and 28-day CIHH exposure, the CSB in rats was enhanced markedly, manifesting as increases in PS and RD, and decreases in TP and SP. This facilitation of CSB was partly abolished by Glibenclamide (Gli, 10 μM), a K ATP channel blocker, but was not influenced by L-NAME (100 μM), a nitric oxide synthase (NOS) inhibitor. The results of the study suggested that CIHH facilitated CSB through opening the K ATP channels in carotid sinus of anesthetic rats and might be one of mechanisms of CIHH keeping SABP homeostasis during acute hypoxia.