Mammals that use the ventilatory system as the principal means of increasing heat loss, i.e. that pant, show two fundamental changes in the control of breathing at raised temperatures. First, alveolar ventilation increases by more than, rather than in proportion to, the increase in CO2 production. Second, hypocapnia no longer causes apnoea. Rats do not use the ventilatory system as the principal means of increasing heat loss, so we have investigated whether rats also show these two changes at raised temperatures. Breathing was detected from diaphragmatic electromyogram (EMG) activity. Anaesthesia and hyperoxia were used to minimise behavioural and hypoxic drives to ventilation and arterial PCO2 (Pa,CO2) was controlled using mechanical ventilation. At 36.6 ± 0.1 °C, breathing was absent as long as Pa,CO2 was held below a threshold level of 32.9 ± 0.7 mm Hg (n = 14) under steady-state conditions. When body temperature in rats was raised above 37 °C, both fundamental changes in the control of breathing became apparent. First, at 39 °C the mean Pa,CO2 level during spontaneous breathing (39.6 ± 5.4 mm Hg, n = 4) fell by 3.9 ± 1.4 mm Hg (P < 0.05, Student's paired t test). Second, at 39.9 ± 0.1 °C breathing was present when mean Pa,CO2 levels were only 18.2 ± 1.5 mm Hg (n = 14), the lowest mean Pa,CO2 level we could achieve with mechanical ventilation. We calculate, however, that at 39.9 °C, the drive to breathe from the increased CO2 production alone would not sustain breathing below a Pa,CO2 level of 27.8 ± 1.4 mm Hg (n = 13). In rats at raised body temperatures therefore a respiratory drive exists that is in addition to that related to the increase in CO2 production. Experimental Physiology (2000) 85.3, 309-319.