Recent neuroanatomical investigations revealed the intrapulmonary neuroepithelial bodies (NEB) to be innervated to a large extent by sensory nerve fibers, displaying peripheral nerve endings of afferent as well as efferent morphology and having their cell bodies in the nodose ganglion of the vagus nerve. Earlier studies also revealed that upon exposure to acute hypoxia NEB exhibit a distinct secretory response, including as well a decrease in the cytoplasmic fluorescence as an increased basal exocytosis and indicating the secretion of serotonin. In the present study, we have tried to establish whether or not this secretory behavior is neurally controlled by combining an exposure to hypoxia with various vagotomy procedures. After long-term (3 days) infranodose vagotomy, the ipsilateral NEB nerve endings have degenerated. The secretory response to hypoxia is modified: the cytoplasmic fluorescence intensifies, while the basal exocytosis remains unchanged. After short-term (1 hour) infranodose as well as long-term (3 days) supranodose vagotomy, the NEB nerve endings are still intact, though no longer connected to the central nervous system. In these circumstances, the hypoxic NEB secretory behavior is indistinguishable from that of intact NEB. From these experimental findings we conclude that the hypoxic NEB secretory response is neurally controlled, since it no longer occurs when the normal innervation has degenerated. This modulation is however not by CNS motor nerve impulses, but probably by intrapulmonary axon reflexes in sensory nerve fibers.