Even in virtually identical conditions, tolerance of hot environment is greatly variable in mammals, including humans. Understanding the mechanisms of this variability may help prevent negative consequences of prolonged hyperthermia. We tested the hypothesis that changes in spontaneous cardiovagal baroreflex sensitivity (cBRS) could be related to hypotension development during passive hyperthermia. Anesthetized (120 mg.kg-1 ketamine & 6 mg.kg-1 xylazine i.p.) male Wistar-Kyoto rats (12-week old, n = 10) were implanted with telemetric transmitters (HD-S11, Data Sciences, USA) to monitor aortic pressure, ECG, core body temperature (Tc) and locomotor activity. Animals were exposed to hot air (44°C, humidity 13%) in a climatic chamber 1 month after implantation surgery (1). Rats in this hot environment feel discomfort but not pain (2). The transfer function between systolic pressure and R-R interval changes in the low-frequency band (0.2-0.7 Hz) was used to estimate cBRS in the 10-s windows, moved by 1-s steps. Exposure to hot air immediately, before any change in Tc, doubled cBRS from 1.3 (0.3) ms.mmHg-1 to 3.0 (1.4) ms.mmHg-1, p<0.001 (pairwise comparison with Bonferroni test after repeated measure ANOVA with Greenhouse-Geisser correction; numbers in brackets are standard deviations). High frequency power of heart rate variability, a surrogate measure of vagal drive to the heart, increased simultaneously from 3.9 (1.7) ms2 to 47.3 (17.9) ms2, p<0.001. The period of high cBRS values ended at a Tc of 38.8 (0.6) °C. During further elevation of Tc, cBRS receded from its maximal values but remained above the reference baseline cBRS. Tc of 40.9 (0.4) °C marked the beginning of the phase with below-baseline cBRS. Cardiovagal baroreflex desensitization was accelerated with increasing Tc, and above a Tc of 42.1 (0.4) °C, the baroreflex was essentially non-operative in heart rate control. Despite progressive desensitization of cardiovagal baroreflex, arterial pressure continuously increased and started to decline only when Tc reached 42.5 (0.3) °C. Thus, it is not likely that hypotension of heatstroke is caused by cardiovagal baroreflex failure. However, we found a positive correlation between the maximal cBRS reached during the initial period of exposure to hot air and the time to onset of arterial pressure decline, r2 = 0.5713, p = 0.01144, i.e. the degree of initial baroreflex sensitization explains 57% of the variance in the onset of circulatory failure. In conclusion, exposure of rats to hot air transiently sensitizes cardiovagal baroreflex, probably by increased vagal activity. The strong initial increase in cBRS was associated with delayed appearance of arterial pressure decline suggesting that parasympathomimetic intervention may improve thermotolerance.