Activation of carotid sinus (CS) baroreceptors has been shown to increase inspiratory time (TI) and expiratory time (TE) and to have a varied effect on tidal volume. The contribution of two functionally different types of baroreceptors to changes in respiratory function were examined in the current study. The techniques of DC anodal block and bupivacaine anesthetic block were used to selectively block fibers, from largest (type I) to smallest (type II) and smallest to largest, respectively, in the CS nerve (CSN) from an isolated CS in an anesthetized, paralyzed, vagotomized, artificially ventilated dog. Anodal blocking currents from 25 to 60 µA, which blocked primarily large A fibers, produced significant decreases in TI and TE and increased the slope of the average phrenic neurogram [PNG(t)], with no change in peak PNG(t). Further increases in blocking current to levels that also blocked small C fibers did not result in additional changes. Bupivacaine blockade using concentrations that blocked primarily C fibers did not block changes in TI and TE to step CS pressure changes. Increasing bupivacaine concentration to 20 mg/100 ml blocked all CSN conduction, and respiratory responses were eliminated. Therefore respiratory responses arising from CS baroreceptors appear to originate from the larger type I baroreceptors.