Reflex apnea, bradycardia, and hypotension produced by serotonin and phenyldiguanide acting on the nodose ganglia of the cat.

Five to 20 jug of phenyldiguanide or serotonin (5-HT) injected into the common carotid arteries of cats (anesthetized with chloralose and urethan) elicited an immediate apnea, usually accompanied by bradycardia and hypotension. The response persisted after ligation of the external carotid and lingual arteries. Since the internal carotid is occluded in the cat, the receptors must be in the distribution of the occipital or ascending pharyngeal arteries. Denervation of the carotid sinus and carotid body, removal of the superior cervical ganglion, section of the vagosympathetic trunk below the nodose ganglion, and extracranial section of cranial nerves IX, XI, and XII did not diminish the response. Section or procaine block of die extracranial supranodose vagus or removal of the nodose ganglion usually abolished the apnea and bradycardia; hypotension still occurred in many cats. Examination of the nodose ganglion by fluorescence microscopy revealed nests of intensely fluorescent cells similar to type 1 carotid body cells. Although previous investigators have reported that veratrum alkaloids or acetylstrophanthidin causes vomiting or bradycardia by an action on the nodose ganglion, this is the first demonstration that a naturally occurring substance (5-HT) stimulates receptors in the nodose ganglion, causing reflex apnea and hypotension in addition to bradycardia.