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At least 199 records · Page 11Linked to original sources
PubMed1976

Regional changes in [3H]-noradrenaline uptake, catecholamines and catecholamine synthetic and catabolic enzymes in rat brain following neonatal 6-hydroxydopamine treatment.

6-Hydroxydopamine (6-OH-DA) treatment of rats at birth (with the analyses conducted in the adult stage) produced marked regional variations in changes in endogenous noradrenaline (NA) and [3H]NA uptake in the CNS. The most pronounced reductions were seen in the cerebral cortex, hippocampus and the spinal cord. Moderate changes or none at all were seen in the hypothalamus, septum and thalamus. Marked increases in endogenous NA and [3H]NA uptake were seen in the mesencephalon and the pons-medulla oblongata. There was in general a close correlation between the changes in endogenous NA and [3H]NA uptake. The results from the cerebellum varied, depending on the developmental stage at which the 6-OH-DA treatment was performed. 6-OH-DA treatment up to three days after birth generally led to a marked increase in both endogenous NA and [3H]NA uptake, while continuing the treatment caused a marked reduction of both parameters. The 6-OH-DA treatment caused no changes in endogenous dopamine (DA) in all regions analysed. Enzyme activity assays showed that DA-beta-hydroxylase (DBH) and tyrosine hydroxylase (TH) were greatly reduced in the cerebral cortex, while the activity of both enzymes was almost double in the pons-medulla. No changes in the activity of phenylethanol-amine N-methyltransferase (PNMT), DOPA decarboxylase, COMT and MAO were seen after 6-OH-DA at birth. Measurements of choline acetyltransferase activity displayed only minute changes. The present results strongly support the view that 6-OH-DA treatment in the neonate stage produces a very selective action on NA neurones belonging to the locus coeruleus system from a structural standpoint, leaving DA- and PNMT-containing neurones unaffected. [3H]NA uptake in whole CNS was almost unchanged, despite the marked regional variations. The results have been interpreted as being due to a 'pruning effect', where the permanent NA denervation in distant nerve terminal projections (e.g. cerebral cortex) leads to a compensatory sprouting and increased outgrowth of NA terminal projections in areas close to the perikarya (e.g. pons-medulla). Furthermore, the results support the view that the growing locus coeruleus neurones are strictly programmed to produce a certain quantity of nerve terminal volume and arborization during the postnatal development.

Age Factors↗
PubMed1997

Effects of N- and L-type calcium channel antagonists and (+/-)-Bay K8644 on nerve-induced catecholamine secretion from bovine perfused adrenal glands.

1. The effects of N- and L-type calcium channel antagonists and (+/-)-Bay K8644 on catecholamine release from chromaffin cells and acetylcholine release from splanchnic nerve terminals was investigated in bovine perfused adrenal glands. 2. Adrenal glands were perfused retrogradely and preloaded with [3H]-choline. Subsequent efflux of 3H-labelled compounds was taken as an index of acetylcholine release from the splanchnic nerve terminals. Noradrenaline and adrenaline release from the glands was measured by h.p.l.c. with electrochemical detection. 3. A maximally effective frequency of field stimulation of the adrenal nerves, 10 Hz, induced release of catecholamines and 3H-labelled compounds. Tetrodotoxin (1 microM) abolished release of both catecholamines and 3H-labelled compounds. A combination of mecamylamine (5 microM) and atropine (1 microM) inhibited nerve-induced catecholamine release by about 75% but did not inhibit release of 3H-labelled compounds. Reducing the concentration of extracellular calcium 5 fold to 0.5 mM inhibited nerve-induced catecholamine release by 80% and release of 3H-labelled compounds by 50%. 4. (+/-)-Bay K8644 (1 microM), nitrendipine (1 microM), omega-conotoxin-GVIA (10 nM) and the combination of nitrendipine and omega-conotoxin-GVIA each had no effect on nerve-induced release of 3H-labelled compounds. 5. (+/-)-Bay K8644 (1 microM) potentiated nerve-induced catecholamine release by 75%. Nitrendipine (1 microM) reduced release by 20% but this did not reach statistical significance, omega-Conotoxin-GVIA (10 nM) reduced nerve-induced catecholamine release by 75%, while the combination of omega-conotoxin-GVIA and nitrendipine reduced release to the same extent as omega-conotoxin-GVIA alone. 6. Exogenous acetylcholine perfusion through the glands produced a concentration-dependent increase in catecholamine release. The maximally effective concentration of acetylcholine for catecholamine release was > or = 300 microM, while 30 microM acetylcholine gave comparable catecholamine release to that obtained with 10 Hz field stimulation. 7. (+/-)-Bay K8644 (1 microM), nitrendipine (1 microM) and omega-conotoxin-GVIA (10 nM) each had no significant effect on catecholamine release evoked by perfusion of the gland with either a near maximally effective concentration of acetylcholine, 100 microM, or with the lower concentration of 30 microM. 8. The results show that the omega-conotoxin-GVIA-sensitive N-type voltage-sensitive calcium channels located on the chromaffin cells are largely responsible for catecholamine release induced by nerve stimulation in bovine adrenal glands. In contrast, N-type calcium channels are not involved in catecholamine release induced by exogenous acetylcholine. L-type voltage sensitive calcium channels do not play a major role in nerve-induced or exogenously applied acetylcholine-induced catecholamine release. However, the L-type calcium channels do have the potential to augment powerfully nerve-induced catecholamine release. N- and L-type calcium channels do not play a major role in the presynaptic release of acetylcholine.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1996

Human neuroblastoma cell lines regain catecholamine fluorescence when xenografted into athymic (nude) mice.

Detection of catecholamine production by neuroblastoma is a useful tumor marker. The majority of neuroblastoma patients have elevated levels of urinary catecholamines and/or their metabolites, and have tumors, which show histochemical evidence of catecholamines using glyoxylic acid-induced catecholamine fluorescence. By contrast, continuous cell lines derived from neuroblastomas lack catecholamine fluorescence in vitro. In this study, we report that 11 out of 12 human neuroblastoma cell lines established from catecholamine-positive tumors displayed histochemical evidence of catecholamines when grown as xenografts in athymic (nude) mice. Catecholamine fluorescence in these xenograft tumors decayed over a 5 day period when the cells were placed into tissue culture. Xenograft tumors of cell lines derived from four catecholamine-negative neuroblastomas or seven primitive neuroectodermal tumors (PNET) did not show catecholamine fluorescence. Ultrastructural comparisons of cell lines in vitro with their corresponding tumors in vivo showed that six of eight cell lines had fewer dense core (neurosecretory) granules in vitro compared to the more readily detectable dense core granules seen in nude mouse tumor tissue. These data indicate that catecholamine synthesis and/or storage in human neuroblastoma cells requires factor(s) not present in the in vivo environment. As neuroblastoma cell lines derived from catecholamine-positive tumors retain the ability to produce and store catecholamines in vivo, such cell lines can be used to identify factors critical to catecholamine production in human neurons.

Animals↗
PubMed1995

Differential regulation of sympathetic neuron neuropeptide Y and catecholamine content and secretion.

Cultured principal neurons of the superior cervical ganglion (SCG), which coexpress high levels of catecholamines and neuropeptide Y (NPY), were used as a model to simultaneously examine whether sympathetic neuronal peptide and transmitter content or secretion are differentially regulated. Accumulation of NPY immunoreactivity and the dopamine metabolites DOPAC and HVA in SCG neuronal conditioned culture medium was used as an index of NPY and catecholamine secretion, respectively. Release of NPY and catecholamines was linear with time; SCG neurons exhibited a basal NPY secretory rate of approximately 0.9-3 fmol NPY immunoreactivity/10(4) cells/hr, and basal DOPAC plus HVA accumulation was about 10-20 pmol total metabolites/10(4) cells/hr. While sympathetic neuronal NPY and total catecholamine cell content increased more than 6-10-fold by 14 d of culture, secretion remained constant. Depolarization stimulated the rate of NPY secretion 18-fold, whereas medium catecholamine metabolite levels increased 3-fold. Activation of intracellular signaling pathways was shown to be an important point of regulation of sympathetic neuron peptide and transmitter content and secretion. Differential regulation of SCG neuron NPY and catecholamine expression was second messenger system specific. Activation of the protein kinase A pathway with the cAMP analog dibutyryl cAMP, or the adenylyl cyclase activator forskolin, produced a concentration-dependent, sustained stimulation of NPY secretion; maximal stimulation resulted in decreased cellular NPY content. Parallel stimulated neuronal catecholamine release was observed, but in contrast to NPY, total cellular catecholamine content was also increased. Regulation of the protein kinase C pathway with phorbol myristate acetate (PMA) stimulated SCG neuronal NPY secretion to a lesser degree than activation of protein kinase A, but did not alter cellular NPY levels. PMA minimally stimulated catecholamine release and content. NPY secretion induced by the calcium ionophore A23187 was paralleled by a concomitant decrease in cellular NPY. A23187 decreased catecholamine release, but did not change cellular total catecholamine levels. The magnitude of the secretory responses of sympathetic neurons to these regulators was far greater than changes in NPY or catecholamine content, biosynthesis or mRNA levels, suggesting that release is a primary site of regulation. The independent regulation of sympathetic neuronal NPY and catecholamine content and release is consistent with the fundamental differences in the biosynthetic pathways, vesicular compartmentalization, uptake and metabolism of neuropeptides and neurotransmitters.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Time course of release of catecholamine and other granular contents from perifused adrenal chromaffin cells of guinea-pig.

Experiments were carried out to investigate the time course of the release of catecholamine, dopamine-beta-hydroxylase (DBH) and adenine nucleotides from isolated chromaffin cells of guinea-pig adrenal gland. When the isolated chromaffin cells were incubated with medium containing acetylcholine (ACh) (0.1 mM), veratridine (0.1 mM) or scorpion (Leiurus quinquestriatus) venom, (10 micrograms/ml.), catecholamine was released into the medium. Catecholamine secretion induced by veratridine or scorpion venom was inhibited by tetrodotoxin (1 microM) but not by atropine (0.1 mM) plus hexamethonium (0.1 mM). On the other hand, the secretory response to ACh was abolished by the cholinergic blocking drugs but not by tetrodotoxin. DBH was released together with catecholamine into the medium in which cells were suspended with these drugs. The ratio of catecholamine (n-mole) to DBH activity (n-mole/hr) appearing in the supernatant was 7.08 +/- 0.55, 6.60 +/- 0.27 and 8.91 +/- 0.47 for ACh, veratridine and scorpion venom, respectively. These values were close to that found in the lysate of chromaffin granules obtained from guinea-pig adrenal glands (7.37 +/- 0.39). The application of ACh or veratridine to perifused chromaffin cells was found to cause a parallel increase in catecholamine and DBH secretion in the perifusion medium without corresponding amounts of phenylethanolamine-N-methyltransferase leakage. However, DBH secretion tended to last for a longer period than catecholamine secretion. Adenine nucleotides were released from perifused chromaffin cells together with catecholamine, by ACh and veratridine. ATP added to the perifusion medium was metabolized to ADP and AMP, of which the ratio (ATP, 21.6%; ADP, 34%; AMP, 17.9%) was close to those of adenine nucleotides released from the cells. The secretion of adenine nucleotides induced by both secretagogues ceased much faster than the catecholamine secretion, so that molar ratio of catecholamine to adenine nucleotides was gradually increased during and after stimulation. The results indicate that catecholamine secretion is accompanied with a simultaneous release of DBH and ATP from adrenal chromaffin cells. Therefore, it is suggested that the delayed output of DBH, unlike catecholamine secretion, in perfused adrenal glands results from the presence of a diffusion barrier for this protein. The releasable secretory granules of isolated chromaffin cells are suggested to be heterogeneous with respect to the ratio of catecholamine to ATP.

Acetylcholine↗
PubMed1996

Consequences of catecholamine release on ventilation and blood oxygen transport during hypoxia and hypercapnia in an elasmobranch Squalus acanthias and a teleost Oncorhynchus mykiss

The marine dogfish (Squalus acanthias) and the seawater-adapted rainbow trout (Oncorhynchus mykiss) were exposed to acute environmental hypercapnia or hypoxia to evaluate (i) the dynamics of catecholamine release into the circulation and (ii) the impact of catecholamine release on gill ventilation and blood oxygen transport. This comparison was undertaken to test the hypothesis that the pattern and consequences of catecholamine release differ in the two species according to the presence or absence of a Root effect and a red blood cell (rbc) ss-adrenergic response. Hypercapnia and hypoxia elicited marked increases in plasma catecholamine levels in the trout but not in the dogfish. In the trout, catecholamine release occurred abruptly during hypoxia when arterial PO2 (PaO2) decreased below 2.7 kPa. In the dogfish, plasma catecholamine levels remained stable during hypoxia even when PaO2 fell below 2.0 kPa. Trout and dogfish displayed pronounced hyperventilatory responses during both hypercapnia and hypoxia. In trout, the hyperventilatory response consisted of an increase in ventilation amplitude (estimated by opercular cavity pressure changes) with no change in ventilation frequency (fv), whereas in the dogfish, both amplitude (estimated by spiracular cavity pressure changes) and fv increased significantly. The use of an extracorporeal circulation and frequent blood sampling demonstrated that plasma catecholamine levels and ventilation amplitude were not correlated during hypoxia in either species. During hypercapnia in trout, the bolus injection of a catecholamine cocktail (final nominal circulating levels 200 nmol l-1 adrenaline, 50 nmol l-1 noradrenaline) caused a rapid (within 2 min) 33 % reduction in ventilation amplitude that persisted for 3 min; fv was unaffected. This hypoventilatory response occurred concurrently with activation of rbc Na+/H+ exchange and an increase in arterial blood O2 content (CaO2) and O2 specifically bound to haemoglobin (O2/Hb). During hypoxia in trout, a similar injection of catecholamines activated rbc Na+/H+ exchange and increased O2/Hb yet was without effect on ventilation amplitude or fv. In dogfish during hypercapnia or hypoxia, injection of a catecholamine cocktail (final nominal circulating levels 125 nmol l-1 adrenaline, 125 nmol l-1 noradrenaline) caused slight but significant reductions in fv (3-4 min-1) without affecting ventilation amplitude. Catecholamine injections did not affect blood oxygen transport in dogfish. The results demonstrate significant differences in the nature of catecholamine release in dogfish and trout that may reflect, in part, the absence of a Root effect and rbc adrenergic Na+/H+ exchange in the elasmobranch. The present data do not support the hypothesis that circulating catecholamines play a major role in controlling breathing during hypoxia or hypercapnia.

Journal Article↗
PubMed1986

[Topography of the catecholamine neurons in the brain stem of the human fetus: an immunohistochemical study using antibodies to tyrosine hydroxylase].

Immunohistochemistry using antibodies to tyrosine hydroxylase (TH), a rate-limiting enzyme which catalyzes the initial step in the catecholamine synthesizing pathway, has been widely accepted as one of the methods for identification of catecholamine neurons in the nervous system. In the present study, we performed immunohistochemical examination to elucidate the distribution of catecholamine neurons in brain stem of human fetuses. The brain stems were obtained from 8 human fetuses (CRL: 120-275 mm, GA: 15-27 wks) 1-3 h after death following therapeutic or spontaneous abortion. They were immediately fixed with 4% paraformaldehyde in 0.1 M phosphate buffer, pH 7.4, dehydrated with graded ethanol, and embedded in paraffin. Serial 6 microns sections were cut from 7 different levels of the brain stem of each fetus. These sections were stained by peroxidase-antiperoxidase (PAP) technique using TH antisera. The TH antisera used were raised in rabbits by injecting purified TH from bovine adrenal medulla. The preparation and the specificity of TH antisera were described in detail elsewhere (Nakashima et al, 1983). Catecholamine neurons were clearly demonstrated in the brain stem of all fetuses. They could be recognized as catecholamine cell groups in the same manner as is done in experimental mammals. Among these cell groups, the catecholamine neurons showed distinct cytological features in shape and size. The distribution of catecholamine positive neurons in the brain stem was almost the same in the 8 human fetuses, and an atlas was given with anatomical explanation under the terminology of Olszewski and Baxter (1982) for the human brain stem. In the mesencephalon, a large number of catecholamine neurons lay in the nucleus substantiae nigrae, pars compacta, the nucleus paranigralis, the middle of the ventral tegmentum and the tractus tegmentalis centralis, and fewer catecholamine neurons were scattered in the other tegmental area. In addition, a group of small catecholamine neurons was located in the griseum centrale mesencephali near the aqueduct. In the pons, catecholamine neurons occurred mainly in the nucleus locus coeruleus and the nucleus subcoeruleus. A band of TH-positive neurons extended from the nucleus locus coeruleus to the dorsolateral tegmentum, and further to the roof of the fourth ventricle. Occasional catecholamine neurons were present in the area medial to the upper portion of the nucleus locus coeruleus. More caudally, a small number of catecholamine neurons were scattered in the area medial to the nervus facialis and adjacent to the nucleus facialis and the nucleus olivaris superior.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic Fibers↗
PubMed2001

The role of neuronal and extraneuronal plasma membrane transporters in the inactivation of peripheral catecholamines.

Catecholamines are translocated across plasma membranes by transporters that belong to two large families with mainly neuronal or extraneuronal locations. In mammals, neuronal uptake of catecholamines involves the dopamine transporter (DAT) at dopaminergic neurons and the norepinephrine transporter (NET) at noradrenergic neurons. Extraneuronal uptake of catecholamines is mediated by organic cation transporters (OCTs), including the classic corticosterone-sensitive extraneuronal monoamine transporter. Catecholamine transporters function as part of uptake and metabolizing systems primarily responsible for inactivation of transmitter released by neurons. Additionally, the neuronal catecholamine transporters, recycle catecholamines for rerelease, thereby reducing requirements for transmitter synthesis. In a broader sense, catecholamine transporters function as part of integrated systems where catecholamine synthesis, release, uptake, and metabolism are regulated in a coordinated fashion in response to the demands placed on the system. Location is also important to function. Neuronal transporters are essential for rapid termination of the signal in neuronal-effector organ transmission, whereas non-neuronal transporters are more important for limiting the spread of the signal and for clearance of catecholamines from the bloodstream. Besides their presynaptic locations, NET and DAT are also present at several extraneuronal locations, including syncytiotrophoblasts of the placenta and endothelial cells of the lung (NET), stomach and pancreas (DAT). The extraneuronal monoamine transporter shows a broad tissue distribution, whereas the other two non-neuronal catecholamine transporters (OCT1 and OCT2) are mainly localized to the liver, kidney, and intestine. Altered function of peripheral catecholamine transporters may be involved in disturbances of the autonomic nervous system, such as occurs in congestive heart failure and hypernoradrenergic hypertension. Peripheral catecholamine transporters provide important targets for clinical imaging of sympathetic nerves and diagnostic localization and treatment of neuroendocrine tumors, such as neuroblastomas and pheochromocytomas.

Carrier Proteins↗
PubMed1997

Congener specific effects by polychlorinated biphenyls on catecholamine content and release in chromaffin cells.

The effects of the non-planar polychlorinated biphenyl (PCB) congener 2,2',4,4'-tetrachlorobiphenyl (2,4-TCB) and of the coplanar PCB congener 3,3',4,4'-tetrachlorobiphenyl (3,4-TCB) were investigated on the catecholamine content and release from bovine adrenal chromaffin cells in culture. Each congener was tested at three concentrations (20, 50 and 100 microM) and two exposure periods (24 h and 5 days). Catecholamine release induced by K(+)-stimulation as well as catecholamine content of Triton X-100 treated cell cultures were examined using high-performance liquid chromatography (HPLC). 2,4-TCB showed dose- and time-dependent effects. 2,4-TCB at 100 microM reduced the K(+)-stimulated catecholamine release after 24 h of exposure. After 5 days of exposure, 2,4 TCB at 50 and 100 microM drastically reduced the K(+)-stimulated catecholamine release. 3,4-TCB even at a concentration of 100 microM over exposure of either 24 h or 5 days had no effects on the K(+)-stimulated secretion. When chromaffin cells, exposed to 2,4-TCB, were lysed with 0.5% Triton X-100, a dose- and time-dependent reduction of the catecholamine content appeared. The 3,4-TCB did not reduce the catecholamine content. Conversely there seemed to be a trend towards an increase in catecholamine content. Spontaneous release of catecholamines was strongly increased by the non-planar 2,4 TCB, while the coplanar 3,4 TCB showed no effects on this parameter. Furthermore, the effects of 2,4 TCB appeared to be reversible after replacing the highest concentration (100 microM) of the TCB-solution with culture-medium at the end of the 24-h exposure. Thus, K(+)-stimulated catecholamine release and the catecholamine content of bovine adrenal chromaffin cells was effectively reduced by the non-planar PCB congener whereas spontaneous catecholamine release was strongly increased. The coplanar PCB congener was ineffective at the same conditions.

Animals↗
PubMed1986

Simultaneous secretion of catecholamines from the adrenal medulla and of [3H]norepinephrine from sympathetic nerves from a single test preparation: different effects of agents on the secretion.

The uptake and release of catecholamines was investigated in the isolated perfused adrenal gland of the rat after preloading the preparation with [3H]norepinephrine, and the effects of various agents were examined on the stimulation-evoked secretion of catecholamines and total tritium. Large quantities of tritium were found in the adrenal medulla after either intravenous injection of [3H]norepinephrine to the rat, or perfusion of the isolated adrenal gland with Krebs-bicarbonate solution containing [3H]norepinephrine. The retention of the tritium was inhibited 90% by desipramine. Acute treatment with guanethidine and chronic treatment with 6-hydroxydopamine abolished the secretion of tritium without affecting the secretion of catecholamines evoked at 1 Hz. Nicotine, muscarine and acetylcholine enhanced the secretion of catecholamines but not tritium, whereas tyramine and ephedrine enhanced the secretion of tritium but not catecholamines. It is concluded that chromaffin cells do not possess the norepinephrine uptake mechanism and that the uptake of [3H]norepinephrine occurs mainly in sympathetic nerve terminals present in the adrenal gland and the surrounding blood vessels (adrenal and renal veins). The differential localization of [3H]norepinephrine and catecholamines allowed us to test the effects of a variety of pharmacological agents that alter neurotransmitter release by acting on receptors on the neuronal membrane, acting on sodium and potassium channels, or acting to alter the intracellular concentrations of adenosine 3',5'-cyclic monophosphate and protein kinase C. Transmural stimulation (1 Hz for a total of 300 pulses) markedly enhanced the release of catecholamines and tritium which was blocked by tetrodotoxin (sodium channel-blocker) and potentiated by tetraethylammonium and gallamine (potassium channel-blockers). Phentolamine, an alpha adrenergic blocking agent which acts on both alpha-1 and alpha-2 receptors, caused a 3- to 4-fold facilitation of the tritium secretion while inhibiting catecholamine secretion by 45%. [Met]enkephalin almost completely inhibited the evoked-secretion of tritium but had very little effect on the secretion of catecholamines. Forskolin inhibited the tritium secretion by 80% but produced more than a 2-fold facilitation of catecholamine secretion. Phorbol 12,13-dibutyrate caused facilitation of evoked secretion of both catecholamines and tritium. A combination of phorbol ester and forskolin had a synergistic effect on stimulation-evoked secretion of catecholamines, whereas phorbol ester partially reversed the inhibitory effects of forskolin on the tritium secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Medulla↗
PubMedDate not supplied

Relationship between catecholamine neurons and cerebral blood vessels studied by their simultaneous fluorescent revelation in the rat brainstem.

In order to study the relationship between catecholamine neurons and cerebral blood vessels, a technique was developed which permitted the simultaneous visualization of blue-green fluorescent catecholamine neurons and red fluorescent stained blood vessels in the brain of the normal rat. Sympathetic nerve fibers were found on the major arteries and in the pia-arachnoid at the base of the brainstem and also along paramedia and lateral perforating arteries as small as 10-12 microns within the brain. Running within the parenchyma, central catecholamine nerve fibers occasionally approached and intersected smaller blood vessels, either arterioles or venules of 8-12 microns, and infrequently climbed along or encircled these vessels for a limited distance, particularly within the lateral tegmentum. Across the nuclei of the brainstem, no overall contiguity of catecholamine terminals with capillaries was apparent, and no correlation between the density of catecholamine varicosities and that of capillaries existed. Only in regions with a high density of both catecholamine varicosities and capillaries, such as in the principal olivary nucleus, did a significant overlap of the two occur. But in most cases of moderately to densely innervated and vascularized regions, such as the solitary tract nuclei, the greatest concentration of terminals appeared over the parenchyma. Regarding the blood supply to the catecholamine neurons, their perikarya did not receive a particularly dense capillary supply relative to other nuclei. However, a special relationship of catecholamine cells to blood vessels was suggested, particularly in the case of dopamine neurons in the substantia nigra by the close apposition of cellular processes to adjacent small vessels. This morphological study was undertaken to determine whether central catecholamine neurons may significantly innervate cerebral blood vessels and accordingly, may function analogously to the peripheral sympathetic adrenergic neurons in the regulation of the vascular system. Although a limited number of associations between central catecholamine nerve terminals and small blood vessels suggested the possibility of an innervation in a few regions, the lack of an overall correspondence and correlation between the two across brainstem nuclei indicated that the analogy of central catecholamine neurons to the sympathetic nervous system was inappropriate. On the other hand, evidence of contact with vessels by presumed dendrites of the catecholamine neurons suggested a possible vascular sensory function.

Adrenergic Fibers↗
PubMed1979

Stimulation by catecholamine of purine catabolism in rats and chickens.

The effect of catecholamine in vivo was studied on purine catabolism in rats and chickens. Catecholamine, administered intraperitoneally in a high dose, markedly increased plasma uric acid and allantoin in rats, and an increase was also observed with intravenous infusion of a lower dose of catecholamine. The effects of catecholamine were characterized by inhibition with alpha and beta adrenoceptor antagonists. Regarding the mechanism of this catecholamine action on purine catabolism, it was shown that catecholamine stimulated degradation of tissue ATP into the end-product. Plasma allantoin, the final purine catabolite in rats, elicited by catecholamine could be maintained under conditions of renal failure, although the action of catecholamine in intact rat was short lasting. The effect of catecholamine was potentiated and/or prolonged by angiotensin-II and aminophylline, and a hyperuricemic state could be induced by catecholamine treatment in chickens. In addition, increase of plasma purine catabolite by immobilization stress in rats suggested the involvement of endogenous catecholamine. From these experimental results, it is considered that catecholamines probably play a important role in the pathogenesis of hyperuricemia.

Adrenergic alpha-Antagonists↗