Plasma catecholamines and pituitary adrenal hormones related to mental task demand under quiet and noise conditions

Plasma levels of catecholamines and pituitary adrenal hormones were measured in 20 min samples from eight subjects, in one control session and two experimental sessions, while they performed a short-term memory task under quiet or noise conditions.

Performing the task led to significant increase in the plasma levels of cortisol, adrenaline and noradrenaline, whereas no variations in growth hormone and dopamine were observed. Similarly, significant changes occurred in urinary catecholamine excretion. A significant correlation was found between individual plasma cortisol increments and error-rates assessed from an accuracy of recall variable. For adrenaline and noradrenaline, an early response apparently linked with an anticipatory process preceded the task. Exposure to noise did slightly amplify cortisol response to the task, but during the first experimental session, with or without noise, the task elicited greater cortisol increases in all subjects than during the second session.

These results provide evidence for a relationship between sympathoadrenocortical activity and attentional demand, whereas cortisol increments seem to be more specifically related to better coping with the task. Frequent hormone level measurements during a prolonged mental task might clarify the complex relationship between time-related bodily hormonal changes, performance and subjective feelings.     

A quantitative analysis of rat adrenal chromaffin tissue: Morphometric analysis at tissue and cellular level correlated with catecholamine content

A morphometric analysis of normal Wistar rat adrenal medulla following perfusion fixation and Araldite embedding, was correlated with catecholamine levels on fresh tissue, measured by high-performance liquid chromatography. The mean volume of whole adrenal is 13.2 mm³ and the mean medullary volume 1.3mm³. Volume density estimates showed that the medulla is composed of 63% chromaffin tissue with an adrenaline to noradrenaline storing cell ratio of 4.4:1. The vasculature occupies 20%, neuronal tissue 5% and interstitial tissues 12% of the medulla. A comparison was made of cell volumes, cell numbers and volume and surface density estimates of cytoplasmic organdies in adrenaline and noradrenaline storing cells. The mean cell volume of adrenaline storing cells at 1300 μm³ is larger than that of noradrenaline storing cells at 980 μm³. A single adrenal medulla contains4.4−5.7 × 10⁵ adrenaline cells and1.5−1.9 × 10⁵ noradrenaline cells. Chromaffin granules account for approximately 30% of the volume of the cytoplasm; the numerical density of granules at different sites in the cell was calculated for adrenaline cells. The volume density of mitochondria (4%) and the surface density of mitochondrial membranes (the ratio of outer to inner membrane being approximately 1:2.3) were similar in both cell types. Rough endoplasmic reticulum was the only organelle to show a significant difference in volume and surface density between the two cell types. Adrenaline storing cells have stacks of rough endoplasmic reticulum which have two to three times the surface and volume densities of that found diffusely scattered throughout noradrenaline cells. The adrenaline content of an adrenaline storing cell is0.14 × 10⁻⁶ μM and that of a granule 3.0 × 10⁻¹² or3.8 × 10⁻¹² μ moles depending on the method of calculation. The noradrenaline content of noradrenaline storing cells can only be calculated on the assumption that all noradrenaline is stored in this cell type though it is likely that some is contained within adrenaline cells. Based on this assumption the noradrenaline content is0.17 × 10⁻⁶μ moles per cell and5 × 10⁻¹² μ moles per granule. The present study provides baseline morphometric data on the rat adrenal medulla at tissue and cellular level correlated with amine levels in adrenaline and noradrenaline storing cells and granules.     

Conditioned reflex responses of the sympathetico-adrenal system to an aversive taste stimulus

Studies were carried out on male and female rats in which the effects of isolated presentation of a conditioned stimulus (a saccharine solution) to which the animals had previously developed conditioned reflex taste aversion (RTA) on the level of urinary catecholamine secretion were determined. The studies showed that presentation of an aversive taste stimulus without reinforcement by a negative stimulus increased the levels of urinary adrenaline, noradrenaline, and dopamine secretion; this repeated, albeit more weakly, the effects of the negative reinforcement (angular acceleration) used for development of RTA. After presentation of the isolated aversive taste stimulus, the greatest increase in catecholamine excretion affected adrenaline, which indicates an anxiety state (fear). There was also a significant increase in noradrenaline excretion in these conditions. The accompanying increase in dopamine excretion in experimental and control animals showed this change to be largely nonspecific in nature, and to result from the experimental procedures. Isolated presentation of the conditioned taste stimulus elicited significantly greater increases in urinary catecholamine excretion in males than in females. It is suggested that the time for which the RTA is retained could be increased by activation of the sympathetico-adrenal system resulting from presentation of the nonreinforced taste stimulus which had acquired aversive properties. Laboratory for the Ontogenesis of Higher Nervous Activity, I. P. Pavlov Institute of Physiology, Russian Academy of Sciences, 199034 St. Petersburg. Translated from Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 82, No. 3, pp. 57–65, March, 1996.     

Hypoxia and hypercapnia increase the sympathoadrenal medullary functions in anesthetized, artificially ventilated rats

Graded hypoxia (FETO2 14-6%) and hypercapnia (FETCO2 6-10%), which were applied for 45s and 2 min, respectively, to urethane anesthetized and artificially ventilated rats produced an increase in adrenal sympathetic efferent nerve activity in parallel with increases in adrenaline and noradrenaline secretion measured in the adrenal venous effluent. Percentage increases in adrenaline and noradrenaline were almost equal. In rats whose carotid sinus nerves (CSN) were bilaterally cut, hypoxia did not produce any effect on adrenal sympathetic nerve activity or catecholamine secretion. In contrast, excitatory adrenal nerve and catecholamine secretory responses to hypercapnia remained unchanged in CSN denervated rats. After severing a splanchnic nerve whose branches innervated the adrenal gland, while maintaining the resting level of catecholamine secretion by low-frequency stimulation of the peripheral end of the splanchnic nerve, hypoxia did not produce any increase in catecholamine secretion. Hypercapnia (FETCO2 8 and 10%), however, induced catecholamine secretion from denervated adrenal medulla, although the magnitude of the response was significantly lower than that in animals with adrenal nerve intact. It is concluded that hypoxia stimulates the adrenal medulla via the carotid chemoreceptor reflex whereas hypercapnia acts mainly via mechanisms besides carotid chemoreceptors such as central chemoreceptors with some direct stimulatory effect on the adrenal medulla. The functional significance of these dual mechanisms of sympathoadrenal excitation during hypoxia and hypercapnia is discussed.     

Acute administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine affects the adrenal glands as well as the brain in the marmoset

A parkinsonian syndrome was induced in marmosets by administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for 4 days. Ten days following the onset of drug administration, brainstem and adrenal tissues were assayed for levels of monoamines and their metabolites. In the brainstem tegmentum, dopamine, its metabolites homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC), and noradrenaline were reduced, whereas 5-hydroxytryptamine (5-HT) levels were elevated, in comparison with untreated controls. In the adrenal gland, 5-HT and adrenaline levels were unchanged, but dopamine and noradrenaline were substantially elevated.     

Chromaffin granules in the rat adrenal medulla release their secretory content in a particulate fashion

Exocytosis is considered the main route of granule discharge in chromaffin cells. We recently provided ultrastructural evidence suggesting that piecemeal degranulation (PMD) occurs in mouse adrenal chromaffin cells. In the present study, we processed rat adrenal glands for transmission electron microscopy (TEM), and examined chromaffin cells for changes characteristic of PMD. Both adrenaline (A)- and noradrenaline (NA)-storing cells express ultrastructural features suggestive of a slow and particulate mode of granule discharge. In adrenaline-containing cells, some granules present enlarged dimensions accompanied by eroded or dissolved matrices. Likewise, a number of granules in NA-releasing cells show content reduction with variably expanded granule chambers. Dilated, empty granule containers are recognizable in the cytoplasm of both cell types. Characteristically, altered granules and empty containers are seen intermingled with normal, resting granules. In addition, chromaffin granules often show irregular profiles, with budding or tail-like projections of their limiting membranes. Thirty 150-nm-diameter membrane-bound vesicles with a moderately electron-dense or -lucent internal structure are observable in the cytoplasm of both cell types. These vesicles are seen among the granules and some of them are fused with the perigranule membranes in the process of attachment to or budding from the granules. These data add further support to the concept that PMD may be an alternative secretory pathway in adrenal chromaffin cells.     

Catecholamine synthesis inhibitors increase pineal adrenaline content by stimulating adrenal medullary activity

Estimation of noradrenaline and adrenaline utilization in the pineal gland of female rats was attempted using inhibitors of the enzymes that catalyse the catecholamine biosynthetic pathway. Treatment with FLA63, an inhibitor of dopamine beta-hydroxylase (10 mg/kg, 2 h before killing), induced depletion of noradrenaline and adrenaline in the preoptic area and median eminence (sites, respectively, inside and outside the blood-brain barrier) but, paradoxically, resulted in a significant increase (+77%) in the pineal content of adrenaline without affecting that of noradrenaline. Treatment with LY134046, an inhibitor of phenylethanolamine N-methyltransferase (40 mg/kg, 5 and 2 h before killing), induced depletion of adrenaline in the preoptic area and median eminence but, again, resulted in a paradoxical and large increase in pineal adrenaline (+224%); this increase was prevented by prior adrenalectomy. Blood samples taken from free-moving rats fitted with intravenous and intraperitoneal cannulae revealed a marked increase in plasma levels of adrenaline after each injection of LY134046. These results suggest that the adrenal medulla is the primary source for the increase in pineal adrenaline seen after administration of the enzyme inhibitors. The precise site of uptake and the biological implications of this phenomenon remain to be elucidated. Nevertheless, interpretation of in vivo experiments involving these catecholamine synthesis inhibitors should take this adrenal response into account.     

Long-term exposure to noise modifies rat adrenal cortex ultrastructure and corticosterone plasma levels

Female rats were exposed to noise 6 h daily for 7 or 21 days running. The effects of stress were evaluated both on adrenal cortex ultrastructure and on plasma corticosterone levels. Subcellular examination showed a marked involvement of each zona of the adrenal cortex. In particular, we observed various alterations, the most frequent consisting of diluted matrix and cristolysis of mitochondria and swelling of smooth endoplasmic reticulum membranes. These morphological changes were most prominent after longer exposure to noise. Similarly, corticosterone plasma levels significantly increased over the time of application of noise stimulus. The present findings indicate that prolonged exposure to loud noise induced structural and functional modifications in the adrenal gland. These data might be potentially relevant in contributing to explain the effects induced in humans exposed to loud noise in a variety of environmental conditions.     

Diseases of the adrenal medulla

The adrenal glands are vital in the organism's response to environmental stress. The outer cortex releases steroid hormones: glucocorticoids, mineralocorticoids and sex hormones, which are crucial to metabolism, inflammatory reactions and fluid homeostasis. The medulla is different developmentally, functionally and structurally. It co-releases catecholamines (primarily adrenaline and to some extent noradrenaline) as well as peptides by the all-or-none process of exocytosis from chromaffin granules, to aid in blood pressure and blood flow regulation, with regulated increments during the activation of the sympathetic nervous system. The co-released peptides function to regulate catecholamine release, blood vessel contraction and innate immune responses. Pathology within the adrenal medulla and the autonomic nervous system is primarily because of neoplasms. The most common tumour, called phaeochromocytoma when located in the adrenal medulla, originates from chromaffin cells and excretes catecholamines, but may be referred to as secreting paragangliomas when found in extra-adrenal chromaffin cells. Neoplasms, such as neuroblastomas and ganglioneuromas, may also be of neuronal lineage. We will also briefly discuss the catecholamine deficiency state.     

Phaeochromocytoma, Electron microscopic study on catecholamine storage.

The biochemical and electron-microscopical findings of eight cases of phaeochromocytoma and the ultrastructure of two cases of human adrenal medulla are presented here as regards catecholamine storage. Due to the rarity of phaeochromocytoma, other ultrastructural features are also described. The morphological characteristics of catecholamine-containing granules are considered on the basis of our investigations and results of other authors. These characteristics are discussed from the point of view of their value in the morphological differentiating of granules storing norepinephrine and those storing epinephrine.     

The Secretion of Adrenaline and Noradrenaline in 20° C and 3° C Acclimated Rats Injured by Limb Ischemia

The effects of hind-limb ischemia on the concentrations of adrenaline and noradrenaline in the adrenals, heart and spleen, on the excretion of these compounds and their 3-0-methylated metabolites in the urine and on the uptake of (°)-noradrenaline-7-³H by the adrenals, kidneys. spleen and heart have been studied in 20° C and 3° C acclimated rats at an environmental temperature of 20° C. The adrenals of uninjured 3° C acclimated rats contained more adrenaline and noradrenaline than those from 20° C acclimated rats. In a 20° C environment both types of rat excreted the same amounts of these compounds. Hind-limb ischemia increased the rate of secretion of adrenaline and noradrenaline since the adrenal contents of these compounds were reduced, their excretion and that of two of their metabolites was increased and tissue uptake was not reduced. The response was the same in 20° C and 3° C acclimated rats after a 4 hr period of bilateral hind-limb ischemia. According to the assay methods used adrenaline secretion preceded that of noradrenaline and the secretion of both continued for up to 26 hrs after the injury. The possible factors in the injury leading to the increase in catecholamine secretion are discussed and also the relation between these changes and some of the biochemical sequelae of limb ischemia.     

Renal extraction of endogenous and radiolabelled catecholamines in the dog

Efferent renal nerve activity can be studied by measurements of the renal venous outflow of noradrenaline and dopamine. Accurate estimates of the intrarenal release to plasma of these catecholamines, however, require determinations of the net contribution of the catecholamines in arterial plasma to their renal venous outflow. We therefore studied the extractions of endogenous noradrenaline, dopamine and adrenaline, as well as 3H-labelled tracer amounts of noradrenaline, and dopamine in innervated and denervated canine kidneys. Approximately two-thirds of noradrenaline and dopamine in arterial plasma were extracted in the kidney, while 80-90% of adrenaline in arterial plasma was extracted. The fractional extractions of the three catecholamines were not substantially altered when the sympathetic nervous system was moderately activated by bilateral carotid occlusion or when the renal nerve activity was abolished by acute denervation. It is concluded that biochemical assessment of renal sympathetic nerve activity by studies of the renal venous noradrenaline and dopamine outflow requires some estimate of the net arterial contribution to the renal venous outflow. Ideally, catecholamine extraction by the kidney should be evaluated by studies of the renal extraction of 3H-labelled noradrenaline and dopamine, but the extraction of endogenous adrenaline may also be useful for this purpose.     

Fine ultrastructure of chromaffin granules in rat adrenal medulla indicative of a vesicle-mediated secretory process

Observation by transmission electron microscopy, coupled with morphometric analysis and estimation procedure, revealed unique ultrastructural features in 25.94% of noradrenaline (NA)-containing granules and 16.85% of adrenaline (A)-containing granules in the rat adrenal medulla. These consisted of evaginations of the granule limiting membrane to form budding structures having different morphology and extension. In 14.8% of NA granules and 12.0% of A granules, outpouches were relatively short, looked like small blebs emerging from the granule surface and generally contained electron-dense material. A proportion of 11.2% of NA granules and 4.9% of A granules revealed the most striking ultrastructural features. These secretory organelles presented thin, elongated, tail-like or stem-like appendages, which were variably filled by chromaffin substance and terminated with spherical expansions of different electron density. A cohort of vesicles of variable size (30–150 nm in diameter) and content was found either close to them or in the intergranular cytosol. Examination of adrenal medullary cells fixed by zinc iodide–osmium tetroxide (ZIO) revealed fine electron dense precipitates in chromaffin granules, budding structures as well as cytoplasmic vesicles. These data indicate that a common constituent is revealed by the ZIO histochemical reaction in chromaffin cells. As catecholic compounds are the main tissue targets of ZIO complexes, catecholamines are good candidates to be responsible for the observed ZIO reactivity. This study adds further to the hypothesis that release of secretory material from chromaffin granules may be accomplished by a vesiclular transport mechanism typical of piecemeal degranulation.     

Centrally evoked increase in adrenal sympathetic outflow elicits immediate secretion of adrenaline in anaesthetized rats

To examine whether feedforward control by central command activates preganglionic adrenal sympathetic nerve activity (AdSNA) and releases catecholamines from the adrenal medulla, we investigated the effects of electrical stimulation of the hypothalamic locomotor region on preganglionic AdSNA and secretion rate of adrenal catecholamines in anaesthetized rats. Pre- or postganglionic AdSNA was verified by temporary sympathetic ganglionic blockade with trimethaphan. Adrenal venous blood was collected every 30 s to determine adrenal catecholamine output and blood flow. Hypothalamic stimulation for 30 s (50 Hz, 100–200 μA) induced rapid activation of preganglionic AdSNA by 83–181% depending on current intensity, which was followed by an immediate increase of 123–233% in adrenal adrenaline output. Hypothalamic stimulation also increased postganglionic AdSNA by 42–113% and renal sympathetic nerve activity by 94–171%. Hypothalamic stimulation induced preferential secretion of adrenal adrenaline compared with noradrenaline, because the ratio of adrenaline to noradrenaline increased greatly during hypothalamic stimulation. As soon as the hypothalamic stimulation was terminated, preganglionic AdSNA returned to the prestimulation level in a few seconds, and the elevated catecholamine output decayed within 30–60 s. Adrenal blood flow and vascular resistance were not affected or slightly decreased by hypothalamic stimulation. Thus, it is likely that feedforward control of catecholamine secretion from the adrenal medulla plays a role in conducting rapid hormonal control of the cardiovascular system at the beginning of exercise.     

Localization of angiotensin II binding sites in the bovine adrenal medulla using a labelled specific antagonist

Angiotensin II binding sites have been localized in sections of bovine adrenal glands and on living cultured bovine adrenal medullary cells using [125I]-[Sar1,Ile8]-angiotensin II and autoradiographic techniques. Binding sites were observed over both adrenaline and noradrenaline chromaffin cells. However, they were present in higher density over adrenaline cells, as determined by the distribution of phenylethanolamine N-methyltransferase mRNA by in situ hybridization histochemistry and of glyoxylic acid-induced fluorescence of noradrenaline. Binding sites were also observed in low density over nerve tracts within the bovine adrenal gland. Living cultured bovine adrenal medullary cells possessed angiotensin II binding sites. Not all cells were labelled. At least 73% of identified dispersed chromaffin cells in these cultures were labelled. Some chromaffin cells were not labelled with the ligand, and at least some non-chromaffin cells in the cultures did possess angiotensin II binding sites. The results provide direct anatomical support for the known ability of angiotensin II to elicit catecholamine secretion from perfused adrenal glands and from cultured adrenal chromaffin cells. They also suggest that some of the effects of angiotensin II on calcium fluxes and second messenger levels measured in cultured adrenal medullary cell preparations may be due to angiotensin II acting on non-chromaffin cells present in these cultures.     

The metabolic requirements from catecholamine release from the adrenal medulla

1. The metabolic requirements for catecholamine secretion elicited by acetylcholine or by calcium plus high K(+) were studied on acutely denervated perfused cat adrenal glands.2. Glucose-deprivation plus anoxia caused an increase in the spontaneous catecholamine output from adrenal glands perfused with normal Locke solution, which was abolished by the removal of calcium from the perfusion medium.3. Anoxia plus glucose-deprivation did not depress the secretory response to repeated exposures of a low concentration of acetylcholine, but did depress the response to a higher concentration of acetylcholine. Glucose-deprivation and nitrogen, when imposed either separately or together, did not inhibit total catecholamine output in response to calcium. Differential analysis of the calcium-evoked secretion showed that during anoxia, catecholamine output was maintained primarily by adrenaline secretion.4. Cyanide (0.2 mM) potentiated the secretory response to calcium in the presence of glucose, but when glucose was omitted from the perfusion medium, cyanide caused a gradual decline in calcium-evoked secretion. Iodoacetic acid (IAA) (0.2 mM) depressed the response to calcium by about 50% under aerobic conditions and by 90% under anaerobic conditions.5. The glycogen content of medullae was profoundly depleted under anoxic conditions.6. It is concluded that energy is required for the secretory action of calcium on medullary chromaffin cells. The energy may be derived from glycolysis or oxidative metabolism. A possible interaction between calcium and adenosine triphosphate acid (ATP) in eliciting catecholamine secretion is discussed.7. The alteration in the percent adrenaline and noradrenaline secreted during anoxia indicates that anoxia may regulate medullary catecholamine secretion through a peripheral, as well as a central mechanism.     

Influence of food restriction on dopamine receptor densities, catecholamine concentrations and dopamine turnover in chicken brain

To investigate further a putative role of dopamine in control of food restriction-induced behavioural stereotypies, chickens were fed during rearing on either a daily restricted ration recommended by a breeding company, twice the recommended restricted ration, or ad libitum food. They were killed at 60 days of age and their excised brains were dissected into six regions and homogenized. Densities of dopamine D1 and D2 receptors were assessed, after first estimating binding parameters for [3H]SCH 23390 (D1) and [3H]spiperone (D2) in chicken brain homogenates. Specific binding of both ligands was highest in basal telencephalon. Concentrations of dopamine and its metabolites 3,4-dihydroxyphenylacetic acid and homovanillic acid were also highest in basal telencephalon, whereas noradrenaline and adrenaline levels were highest in diencephalon. Dopamine concentration in basal telencephalon and noradrenaline concentration in diencephalon were increased significantly in response to food restriction, but no effect of feeding treatment was found in dopamine turnover, adrenaline levels, or D1 and D2 receptor densities in any brain region studied. The observed changes in brain catecholamine levels are consistent with roles for dopaminergic and adrenergic mechanisms in the control of food restriction-induced behavioural stereotypies in chickens.     

Catecholamine secretion by the adrenal medulla of the foetal and new-born foal

1. The content and output of adrenaline and noradrenaline from the equine adrenal medulla has been investigated under different conditions in foetuses, foals and adult mares.2. In the foetus only small amounts of both amines were secreted in response to stimulation of the peripheral ends of the splanchnic nerves to the gland; during anoxia the adrenal discharge was far greater and was independent of any nervous mechanism.3. Whereas in the ruminant a direct adrenal response to low P(O2) is confined to the noradrenaline cells during foetal life only, the adrenal medulla of the foetal foal secreted both adrenaline and noradrenaline during asphyxia, and the direct response persisted for some days after birth. Noradrenaline was the amine predominantly released during asphyxia in the foetus.4. Catecholamine output from the equine adrenal medulla changed with age, in that there was a gradual increase in both the absolute and relative amount of adrenaline released, irrespective of the stimulus applied, although at any given stage of development a higher proportion of adrenaline was secreted in response to stimulation of the splanchnic nerves than during anoxia.5. The relative proportions of the two amines in the effluent blood bore little resemblance to those found in the glands, removed after prolonged asphyxia, in either foetuses or foals. Preliminary observations have indicated that more noradrenaline is present in the glands when the foetus remains relatively undisturbed within the uterus.6. The possible significance of the larger adrenal response to asphyxia in the foetal foal in comparison with other species is discussed in relation to the development of the innervation and the growth of the adrenal cortex.     

Effects of hypoxia lasting up to one month on the catecholamine content in rat carotid body

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.From these data it can be inferred that the increase in dopamine and noradrenaline content occurs as a specific response to long-term hypoxia and may involve both induction of tyrosine hydroxylase and hyperplasia of glomus cells of carotid bodies.     

The content and localization of catecholamines in the carotid labyrinths and aortic arches of Rana temporaria

1. The catecholamine content of the carotid labyrinth of Rana temporaria was estimated by two different methods, and compared with that of the aortic arch. In both tissues adrenaline was found as the dominant amine, with traces of dopamine and noradrenaline detectable in the labyrinth only.2. Per gram of fresh tissue, the labyrinth usually contained more adrenaline than the aortic arch.3. On microscopic examination, the aortic arch was found to contain nerve fibres which fluoresced after treatment with formaldehyde, whereas within the carotid labyrinth the formaldehyde-induced fluorescence was localized in the cytoplasm of clusters of small cells. This fluorescence resembled that exhibited by glomus cells in the mammalian carotid body.