Baroreflex was repeatedly postulated as an essential mechanism of hemodynamic adaptation to elevated ambient temperature. However, the exact role of the baroreflex in this adaptation is less clear. Because tachycardia leads to increased myocardial oxygen demand, reduced myocardial perfusion, and ventricular filling, we have hypothesized that baroreflex restraining effect on heart rate elevation is an important component of the adaptation to the hot environment. To confirm the role of unharnessed tachycardia in heatstroke development, we used a muscarinic blocker to remove vagal restraint on the heart rate by desensitizing the baroreflex. If baroreflex heart rate control is an important adaptive mechanism during passive heating, a sudden increase in the heart rate should induce heatstroke. Wistar-Kyoto male rats 13-week old were implanted with telemetric transmitters to monitor ECG, aortic pressure and body temperature. During the surgery, general anesthesia with ketamine 120 mg/kg and xylazine 6mg/kg was used. The rats were randomly divided into 2 groups (n = 10) and examined in a climatic chamber with an air temperature of 44.4 °C. Time-frequency analysis (Wigner-Ville) was applied to estimate the high-frequency power of RR-interval variability (HFRRI), a measure of cardiac parasympathetic activity. The spontaneous baroreflex sensitivity (sBRS) was estimated with the cross-spectral method. Values represent the mean (standard deviation) compared with the t-test. During the passive heating, RR-interval (RRI) became progressively shorter with an average speed of 1.4 (0.2) ms/min. The permanent decline in the arterial pressure that began at the core body temperature (Tc) of 43 (0.4)°C heralded the beginning of the heatstroke; the RRI reached 110 (14) ms and systolic pressure 218 (5) mmHg at this moment. Oxyphenonium (10 µmol/kg) i.p. injection at Tc of 40°C abruptly reduced RRI from 183 (12) to 120 (7) ms (p < 0.001), sBRS from1.5 (0.05) to 0.1 (0.03) ms/mmHg (p < 0.001) and HFRRI from 13.8 (0.7) to 0.6 (0.06) ms2(p < 0.001). Heart rate-pressure double product rose from 5.6×104 (0.4×104) to 8.4×104 (0.7×104) bpm.mmHg (p < 0.001), suggesting a strongly elevated myocardial oxygen demand. Although hemodynamic remained stable and the arterial pressure and RRI rose steadily further, the time needed to develop the heatstroke was significantly (p < 0.002) shorter by 4.2 (0.3) min. This was associated with the increased speed of Tc elevation from 0.093 (0.008) to 0.112 (0.009)°C/min (p < 0.001), probably a consequence of reduced salivation after oxyphenonium parasympatholysis, which is documented by strongly diminished HFRRI. Conclusion: Muscarinic blockade mildly accelerated heatstroke development, however probably not as a consequence of tachycardia, but because of the interference with evaporation cooling.