Central vascular blood flows and ventilation were measured in conscious toads (Bufo marinus) at 15 and 25 degrees C. The animals were exposed to hypoxia (Fi(O)(sum)=0.10 and 0.05, where Fi(O)(sum) is the fractional oxygen concentration of inspired air) at both temperatures. In addition, the cardiorespiratory responses to hypercapnia (Fi(CO)(sum)=0.05) and atropine injection (5 mg kg(−)(1); 7.4 μmol kg(−)(1)) were studied at 25 degrees C. At 25 degrees C, systemic blood flow (q_dot (sys)) exceeded pulmocutaneous blood flow (q_dot (pc)), indicating a large net right-to-left shunt (q_dot (pc)/ q_dot (sys) was 0.39). q_dot (pc)/ q_dot (sys) was reduced significantly to 0.22 at 15 degrees C. At both temperatures, q_dot (pc) increased significantly during hypoxia (from 26.2 to 50.8 ml min(−)(1)kg(−)(1) at 25 degrees C and from 11. 2 to 18.9 ml min(−)(1)kg(−)(1) at 15 degrees C), whereas q_dot (sys) changed little (from 77.2 to 66.2 ml min(−)(1)kg(−)(1) at 25 degrees C and from 54.3 to 50.1 ml min(−)(1)kg(−)(1) at 15 degrees C). As a result, the net right-to-left shunt was greatly reduced, while total cardiac output remained almost unaffected. The ventilatory response was more pronounced during hypercapnia but, since q_dot (pc) and q_dot (sys) were affected similarly, there was no change in the shunt pattern. In undisturbed toads at 25 degrees C, atropine injection increased q_dot (pc) and eliminated the net right-to-left shunt. This is consistent with the known vagal innervation of the pulmonary artery.The present study shows that the cardiac right-to-left shunt that prevails in undisturbed and resting toads is reduced with increased temperature and during hypoxia. These findings are consistent with the general view that the cardiac right-to-left shunt is regulated and reduced whenever oxygen delivery is compromised or metabolic rate is increased.