Searching for an arterial chemosensory drive exerted upon the cardiovascular system under eucapnic normoxia, we performed experiments on spontaneously ventilated, pentobarbitone-anesthetized cats, in which ventilatory flow through a pneumo-tachograph, instantaneous respiratory frequency, end-tidal pressure of CO(2), arterial pressure, and instantaneous heart frequency were simultaneously recorded. Repeated exposures to 100% O(2) breathing for 5 to 60 s caused the well-known transient decreases in tidal ventilatory volume and instantaneous respiratory frequency, after which minor decreases in systolic, diastolic and mean arterial pressures, as well as in instantaneous heart frequency were observed. After selective bilateral denervation of carotid sinuses (barodenervation), hyperoxia-induced falls in arterial pressure and heart rate became more evident. Subsequent bilateral section of the carotid nerves (with or without section of the aortic nerves) suppressed these effects. Present results indicate the presence of a chemosensory drive of the cardiovascular system under eucapnic normoxia, although considerably smaller than that exerted upon ventilation. The small magnitude of the decreases in arterial pressure and heart rate observed under control conditions suggests that cardiovascular effects elicited by hyperoxic challenges are normally buffered by carotid baroreflexes.