The effects evoked by 1 min occlusions of the common carotids were studied in 16 spontaneously breathing pentobarbitone anesthetized cats. Unilateral occlusions induced increases in systemic arterial pressure (to 111.5% of basal), but no changes in ventilation. Bilateral occlusions provoked larger increases in systemic arterial pressure (to 137.5% of basal) and mild tachycardia, associated with pulmonary and alveolar hyperventilation. Breath-by-breath minute volume augmented (to an averaged maximum of 144.7% of basal), the increase in tidal volume being more important than that of respiratory frequency. The maximal changes occurred shortly after occlusion and they were inversely but not linearly related to the minimal levels of intrasinusal pressure attained. Changes were subsequently attenuated during each occlusion, depending on the partial restoration of intrasinusal pressure. After barosensory denervation of the carotid sinuses, the cardiovascular responses to bilateral occlusions were reduced, but the respiratory ones were not affected. During 100% O2 breathing in cats with intact innervation or carotid barodenervation, the respiratory responses to bilateral occlusions were much reduced and delayed, or even absent. That the above circulatory and respiratory effects of carotid occlusions were of reflex nature was demonstrated by their elimination after bilateral section of the carotid (sinus) nerves. Results indicate that while barosensory withdrawal during carotid occlusion is mostly responsible for reflex hypertension and bradycardia, chemosensory excitation induced by this maneuver is the major cause of reflex hyperventilation.