Ventilatory responses to CO 2 were studied m awake Peking ducks before (intact) and after chronic bilateral carotid body denervation ( cbd) or after sham operation (s.o.), in nonnoxic (Pao;, = 100 torr) and hypoxic conditions (Pa O 2 =60 torr). During breathing of CO 2-free gas mixtures, normoxic cbd ducks were chronically hypercapnic; hypoxic intact and s.o. ducks hyperventilated, while cbd animals did not. Steady-state ventilation (V), arterial P CO 2 relationships were determined. For intact and s.o. ducks, the slopes of the V, Pacoi curves were steeper in hypoxia than in normoxia, and shifted toward lower Pa CO 2 values. For cbd ducks, the curves were shifted to the right with lower slopes and became virtually independent of the level of oxygénation. Transient changes in P CO 2 were induced in both intrapulmonary gas and arterial blood by abruptly modifying the CO 2 concentration in the inspired gas or in an abdominal air sac. cbd ducks exhibited depressed ventilatory responses, and the maximal ventilatory change came later than in intact ducks. In both cbd and intact ducks, the early ventilatory increase was significant at the second respiratory cycle following the CO 2 change. An early ventilatory change was also observed when CO 2 concentra- tion was abruptly raised in the interclavicular air sac, a procedure which did not modify Paco, but transiently increased P CO 2 in the bronchial gas. It is concluded that in awake Peking ducks (1) the normal arterial chemoreflex drive of ventilation, dependent on the integrity of afferent fibers from the carotid body, is essential in determining the, eupneic level of ventilation in normoxia as well as during acute hypoxia, and is also essential for normal ventilatory responses to CO 2 either in transient or in steady-state conditions; (2) possibly, other receptors, presumably located in the pulmonary tract, play a role in the fast component of ventilatory responses to CO 2 in physiological conditions.