The vagal branches, the recurrent and superior laryngeal nerves (RLN and SLN), which innervate the intrinsic muscles and the mucosa of the larynx, contain paraganglia in both humans and rat (1–3). These paraganglia resemble morphologically the carotid body and are composed of clusters of dense-cored vesicle cells, sustentacular cells, and thin-walled blood vessels. Unmyelinated nerve fibers occur in the connective tissue of the paraganglia, and nerve endings are in contact with the vesicle-containing cells (3). Histofluorescence studies have revealed the storage of catecholamines in the paraganglia of the rat, and biochemical analysis have shown that dopamine and noradrenaline are present in the laryngeal nerves, the amines probably being stored in the paraganglia (4). Another possible storage site of catecholamines in the laryngeal nerves is sympathetic nerve fibers located within the nerve trunks.

The catecholamines in the recurrent and superior laryngeal nerves of the rat were assayed by high performance liquid chromatography. The nerves were shown to contain high levels of dopamine (1.9 +/- 0.6 and 2.3 +/- 0.4 pmol, respectively) and noradrenaline (1.3 +/- 0.3 and 0.9 +/- 0.2 pmol, respectively). No adrenaline could be detected in any of the nerves. Reserpine markedly depleted the stores of these amines in both nerves. A significant increase in dopamine level was seen in the superior laryngeal nerve after treatment with a monoaminoxidase inhibitor, but not in the recurrent laryngeal nerve. The high levels of dopamine detected are presumably derived from endoneurial paraganglia which were demonstrated by glyoxylic acid-induced fluorescence. The source of noradrenaline is less evident, but noradrenaline is probably stored in both endoneurial paraganglia and in sympathetic nerve endings.

A micro-organ composed of islands resembling carotid body cells located in the endoneural space of the rat recurrent laryngeal nerve is described. The microglomus is located 5 to 6 mm from the nerve entrance into the laryngeal wall. The characteristic cells, containing numerous membrane-bound granules, or dense-cored vesicles, are surrounded by bundles of myelinated as well as unmyelinated nerve fibres. Ultrastructurally the cells are very similar to the chemoreceptor cells of the carotid body. Unlike the carotid body, however, the morphometric measurements showed the recurrent laryngeal nerve microglomus to consist of a homogeneous cell type with respect to their content and size of dense-cored vesicles (profile diameter range 20–160 nm, median value 110 nm). Only occasionally was a granulated type of cell with smaller and fewer dense-cored vesicles found.

Long-term exposure to hypoxia (10%O2 + 90%N2) elicits an increase in the dopamine content of the carotid body after 2 days and in the noradrenaline content after one week. When hypoxia is extended to 4 weeks the dopamine and noradrenaline content increase 15- and 12-fold, respectively. These changes are associated with an increase in size and protein content of the carotid body. Removal of the superior cervical ganglion, which causes a 50% reduction of the noradrenaline content, fails to prevent the increase in amine content elicited by hypoxia. Exposure to hypoxia for 4 weeks slightly increases the dopamine and 3,4-dihydroxyphenylacetic acid content in superior cervical ganglia and that of dopamine in adrenal glands, but fails to alter the levels of noradrenaline, adrenaline and 3-methoxy-4-hydroxyphenylglycol in heart and adrenal glands, that of noradrenaline in superior cervical ganglia and that of dopamine and 3,4-dihydroxyphenylacetic acid in the caudate nucleus.

Short-term or long-term administration of dexamethasone (1 mg/kg, i.p.) increases the concentrations of both dopamine and noradrenaline in rat carotid body. This increase in catecholamine content elicited by dexamethasone also occurs after transection of th. carotid sinus nerve or removal of the superior cervical ganglion. Injections of cycloheximide curtail the dexamethasoneinduced increase in noradrenaline content but the increase in dopamine content remains unchanged. The rate of elimination of dihydroxyphenylacetic acid is decreased by more than 50% 12 h following the injection of dexamethasone, while the steady-state content of dopamine is increased.

1. The mechanism whereby hypoxia lasting 20 min elicits a decrease in the dopamine content of rat carotid bodies was studied. 2. The concentrations of dopamine, noradrenaline, dihydroxyphenylacetic acid and homovanillic acid in carotid body were measured by a mass‐fragmentographic procedure. The turnover rate of dopamine was determined by measuring the elimination rate of dihydroxyphenylacetic acid immediately after inhibition of monoamine oxidase by injection of pargyline. The turnover rate of noradrenaline was derived from measurements of the rate of decline of noradrenaline content after injection of L‐methyl‐p‐tyrosine. 3. The results indicate that hypoxia increases the rate of dopamine release without changing its turnover rate thereby accounting for the decrease in dopamine content. The content and turnover rate of noradrenaline remained unchanged during exposure to hypoxia. 4. Neither the carotid sinus nerve nor the sympathetic innervation appeared to participate in the regulation of dopamine content or turnover rate in carotid bodies of rats either before or during hypoxia. 5. Since transection of the carotid sinus nerve or/and ganglionectomy failed to prevent the decrease of dopamine content caused by hypoxia, it is inferred that low arterial PO2 depletes dopamine stores independently of the above mentioned innervation.