Incomplete understanding of heat stroke pathophysiology makes an efficient treatment of this deadly condition difficult. There is a general agreement that heat stress leads to a hyperadrenergic state, however information about the parasympathetic activity is virtually absent. To further clarify the role of the autonomic nervous system in heatstroke development, 4-month old Wistar-Kyoto male rats (n=8) were implanted with telemetric transmitters (anesthetized with ketamine 120 mg/kg, xylazine 6mg/kg, atropine 0.12mg/kg, i.p.). After the recovery period of 1 month, rats were placed into the climatic chamber (air temperature 44°C, relative humidity 20%). During exposure to the heat stressor, aortic pressure, ECG, core body temperature, and animal activity were continuously monitored. Recorded waveforms were used to derive information about the sympathetic (low-frequency power of systolic pressure variability, LF SPV) and parasympathetic activity (high-frequency power of heart rate variability, HF HRV) as well as spontaneous baroreflex sensitivity (sBRS). Time-frequency analysis based on the Wigner-Ville transform was applied to assess cardiovascular variability in 1 second-long intervals and sBRS was estimated with the cross-spectral method. Values are means (SD), compared with the repeated measures ANOVA. Body temperatures of animals placed into the preheated climatic chamber steadily rose with the speed of 0.09 (0.001) 0C/min. Arterial pressure elevation followed approximately hyperbolic kinetics, reaching the maximum of 200 (14) mmHg within 43 (9) min. In contrast, heart rate increase resembled exponential kinetics. Tachycardia initially progressed slowly at 2.8 (1.2) bpm/min, however speed of heart rate rise accelerated later to 10.2 (3.4) bpm/min, P<0.05. Cardiac parasympathetic drive based on HF HRV was 2.1 (0.5) ms2 outside the climatic chamber and augmented to 15.2 (4.8) ms2 (P<0.05) during the period of slow heart rate increase. The break point in the speed of heart rate rise appeared 41 (9) min after placing animals into the climatic chamber and coincided with the rapid decline of HF HRV to 1.2 (0.1) ms2. A similar pattern was seen in changes of the sBRS: an increase from preheating values of 1.3 (0.3) ms/mmHg, to 1.9 (0.4) ms/mmHg, followed by rapid decline to very low values of 0.25 (0.09) ms/mmHg, P<0.05. Vascular sympathetic activity based on LF SPV increased evenly during warm air exposure from 3.8 mmHg2 to a maximum of 13.8 mmHg2 (P<0.05) attained during the heatstroke when parasympathetic activity was barely measurable. Thus, exposure to the hot environment activated both branches of the autonomic nervous system. However, parasympathetic activation was only temporary and its decline could be related to the uncontrolled tachycardia and transition to heatstroke.