The present study was undertaken to evaluate the effects of hypercapnia on the cardiorespiratory control in normovolemic and hypovolemic rabbits during exogenous hyperthermia. Hypovolemia was induced by administration of furosemide, the body temperature (Tb) was gradually elevated to 42 degrees C by body surface heating. Subsequently, Tb was lowered back to the initial values by gradual cooling. Recordings were done at normothermia (TN=38 degrees C), during heating at 40 degrees C (TH1) and 42 degrees C (TH2), and in the course of Tb reverting toward the baseline values back at 40 degrees C (TC1), and finally after full return to the initial temperature value (TC2). The hypercapnic ventilatory response (HCVR) was estimated as the slope of minute volume (VE) on end-tidal CO2 (ETCO2) curves. We found that heating caused an increase in the VE slope in the normovolemic (NV), but not in hypovolemic (HV), rabbits. Between-group comparison revealed a significant increase in HCVR at TH2 and TC1 in NV vs. HV rabbits. Hypercapnia in hyperthermia (at TC2) was accompanied by a significant decrease in heart rate only in the hypovolemic group. Recovery of Tb was unaccompanied by appreciable changes in HCVR in either NV or HV groups. In the course of cooling, a decrease in heart rate during hypercapnic challenge was present in both group, in HV the drop was less prominent. We conclude that hypercapnia during heat stress in both normovolemic and hypovolemic rabbits is associated with altered cardiorespiratory responses. HCVR during exogenous hyperthermia is augmented in normovolemic, but not in hypovolemic, rabbits.