The present study investigated the effect of acute hypothermia on baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) by generating baroreflex logistic function curves, using bolus doses of phenylephrine and sodium nitroprusside, in anaesthetised male Wistar rats at a core temperature (Tb) of 37oC, during acute severe hypothermia at Tb=25oC and on rewarming to 37oC. Comparisons were made between rats without (euthermic, n=6) and with (acclimated, n=7) prior exposure to lower ambient temperatures and shorter photoperiod, simulating adaptation to winter conditions. In both groups of rats, acute hypothermia to Tb=25oC shifted the baroreflex-RSNA curve slightly leftwards and downwards with decreases in the setpoint pressure and maximal gain, whereas it markedly impaired baroreflex-HR curve characterised by decreases in response range by ~90% (P<0.001), minimum response by ~10% (P<0.05) and maximum gain by ~95% (P<0.001), from that at Tb=37oC. All parameters were restored to precooling levels on rewarming. Electrical stimulation of cardiac vagal efferents induced a voltage related bradycardia, the magnitude of which was partially reduced during acute hypothermia, and there was a significant prolongation of the electrocardiogram intervals indicating a delay in cardiac conduction. Mild suppression of baroreflex control of RSNA could contribute to hypothermic hypotension and may primarily reflect an effect of Tb on central drive. The marked attenuation of the baroreflex control of HR during hypothermia was likely due to an impairment of both the central and peripheral components of the reflex arc. Baroreflex control of RSNA and HR was similar between both groups of rats, which implied that the control was non-adaptive on chronic cold exposure.