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At least 19 recordsLinked to original sources
PubMed1985

The effects of acute and chronic treatment with triiodothyronine and thyroxine on the hypothalamic and telencephalic catecholamine nerve terminal systems of the hypophysectomized male rat. Chronic treatment modulates catecholamine utilization in discrete catecholamine nerve terminal systems.

Using catecholamine (CA) fluorescence histochemistry in combination with quantitative microfluorimetry, it has been shown that chronic treatment with triiodothyronine (T3) and thyroxine (T4; 2 X 10 and 2 X 36 micrograms/kg i.p., respectively, twice daily for 10 days), but not acute treatment (1 and 3.6 mg/kg i.p., respectively, 2 h before killing), increases CA utilization in the medial and lateral palisade zones of the median eminence and reduces noradrenaline (NA) utilization in the parvocellular part and magnocellular part of the paraventricular hypothalamic nucleus of the hypophysectomized male rat. Following chronic T4 treatment it could also be shown that the CA levels in the medial and lateral palisade zones of the median eminence were increased, while the NA levels were reduced in the parvocellular part of the paraventricular hypothalamic nucleus. Chronic T3 treatment induced similar changes - increased CA levels in the medial palisade zone and reduced NA levels in the magnocellular part of the paraventricular hypothalamic nucleus. Within the telencephalon, chronic but not acute treatment with T3 or T4 selectively increased dopamine (DA) utilization within the diffuse type of DA nerve terminal systems of the nucleus accumbens. This action of chronic treatment of T3 or T4 was highly selective and no changes in DA levels could be demonstrated in any DA nerve terminals analyzed in the nucleus caudatus putamen; nucleus accumbens and tuberculum olfactorium. In all the experiments the TSH levels remained undetectable and the low basal serum prolactin levels were not modulated in any experimental group in spite of the treatment with a tyrosine hydroxylase inhibitor in the CA utilization experiments. Following 2-3 weeks after hypophysectomy, serum T3 and T4 were decreased by 30-50%. In the acute experiments with T3 or T4, serum T3 levels and T3 as well as T4 levels were markedly elevated after the respective treatments. In the chronic experiments, the T4 treatment resulted in significant increases in the serum levels of both T3 and T4. The present results indicate that discrete DA and NA nerve terminal systems within the median eminence (DA), nucleus accumbens (DA) and paraventricular hypothalamic nucleus (NA) can slowly respond to chronic treatment with T3 or T4. This effect is the result of a direct action of the thyroid hormones on the brain since TSH is absent in the hypophysectomized rat.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Restoration of catecholamine content of previously depleted adrenal medulla in vitro: importance of synthesis in maintaining the catecholamine stores.

The functional integrity of adrenal chromaffin storage vesicles was studied in the perfused rat adrenal gland subjected to intense exocytosis. Continuous perfusion with 55 mM K+-Krebs solution produced a large and uninterrupted secretion of catecholamines. Total amounts secreted within 45 min were 4.66 micrograms and represented almost 30% of the total tissue catecholamine content. If perfusion with excess K+ was extended to 90 min, the secretion increased further to 5.76 micrograms. Despite such a large secretory response, the catecholamine content of the K+-stimulated adrenal medulla was comparable to that of unstimulated control, suggesting an enhanced resynthesis to maintain the normal levels. Pretreatment of rats with alpha-methyl-p-tyrosine, and including this agent in the perfusion medium during stimulation with K+, caused a marked reduction in catecholamine content. The degree of depletion depended on the extent of stimulation with K+ (45% in 45 min and 60% in 90 min). Although depleted catecholamine stores did not show spontaneous recovery in 2 h, inclusion of tyrosine, L-3,4-dihydroxyphenylalanine or dopamine (but not epinephrine or norepinephrine) completely restored the catecholamine content of previously depleted adrenal medulla. Repletion achieved by tyrosine was time dependent (evident in 30 min and maximum in 2 h) and blocked by alpha-methyl-p-tyrosine but not by calcium deprivation. The ratio of epinephrine to norepinephrine remained constant during various stages of the experiment, suggesting both types of vesicles were equally affected by different treatments. The secretory response (10 Hz for 30 s) was unaffected even though tissue catecholamine stores were significantly depleted (50%). In summary, we have demonstrated that catecholamine content of the isolated perfused adrenal gland can be reduced by stimulation of exocytotic secretion in the presence of tyrosine hydroxylase inhibitor. Since the depleted stores can be fully refilled by synthesis of catecholamines from its precursors, it is suggested that chromaffin vesicles may be reutilized for the purpose of synthesis, storage, and secretion of adrenal medullary hormones.

Adrenal Medulla↗
PubMed1990

Catecholamines and catecholamine-synthesizing enzymes in guinea-pig sensory ganglia.

Cranial and spinal sensory ganglia of the guinea-pig were investigated by means of histochemistry and biochemistry for the presence of catecholamines and catecholamine-synthesizing enzymes. Sensory neurons exhibiting immunoreactivity to the rate-limiting enzyme of catecholamine synthesis, tyrosine hydroxylase (TH), were detected by immunohistochemistry in lumbo-sacral dorsal root ganglia, the nodose ganglion and the petrosal/jugular ganglion complex. The carotid body was identified as a target of TH-like-immunoreactive (TH-LI) neurons by the use of combined retrograde tracing and immunohistochemistry. Double-labelling immunofluorescence revealed that most TH-LI neurons also contained somatostatin-LI, but TH-LI did not coexist with either calcitonin gene-related peptide- or substance P-LI. TH-LI neurons did not react with antibodies to other enzymes involved in catecholamine synthesis, i.e., aromatic amino acid decarboxylase (AADC), dopamine-beta-hydroxylase (D beta H), and phenylethanolamine-N-methyl-transferase (PNMT). Petrosal neurons as well as their endings in the carotid body lacked dopamine- and L-DOPA-LI. Sensory neurons did not display glyoxylic acid-induced catecholamine fluorescence. Ganglia containing TH-LI neurons were kept in short-term organ culture after crushing their roots and the exiting nerve in order to enrich intra-axonal transmitter content at the ganglionic side of the crush. However, even under these conditions, catecholamine fluorescence was not detected in axons projecting peripherally or centrally from the ganglia. Sympathetic noradrenergic nerves entered the ganglia and terminated within them. Accordingly, biochemical analyses of guinea-pig sensory ganglia revealed noradrenaline but no dopamine. In conclusion, catecholamines within guinea-pig sensory ganglia are confined to sympathetic nerves, which fulfill presently unknown functions. The TH-LI neurons themselves, however, lack any additional sign of catecholamine synthesis, and the presence of enzymatically active TH within these neurons is questionable.

Animals↗
PubMed1991

Catecholamine metabolic pathways and exercise training. Plasma and urine catecholamines, metabolic enzymes, and chromogranin-A.

BACKGROUND: Because acute exercise increases systemic catecholamines, we sought to determine whether exercise training would alter daily or exercise-related catecholamine release and inactivation. METHODS AND RESULTS: In 24-hour urine collections, catecholamines and metabolites provided indexes of overall oxidative deamination, sulfation, and O-methylation. Plasma catecholamines, the sulfoconjugates of each, and chromogranin-A were determined at rest and during exercise in 10 well-trained male subjects and nine minimally trained male subjects (maximal oxygen uptake 55.2 and 42.5 ml/kg/min, respectively), and levels of activities of catechol-O-methyltransferase (COMT), monoamine oxidase B (MAO-B), and thermolabile phenolsulfotransferase (TL-PST) were also determined. Plasma-free catecholamines showed minimal differences between the two groups at submaximal exercise (4 minutes) but large differences at maximal exercise, reflecting the different exercise levels attained. Inactivation of plasma catecholamines by sulfation across rest and exercise tended to be greater in the well-trained group, with small increases in both plasma sulfoconjugated dopamine and sulfoconjugated norepinephrine. In the well-trained group, urinary metabolites demonstrated trends toward increased dopamine release (p less than 0.07) and small increases in the daily release of epinephrine and its sulfoconjugated metabolites. Indexes of deamination, sulfoconjugation, and O-methylation, with the exception of a reduced deamination of dopamine and the activities of COMT, MAO-B, and TL-PST were not different in the two groups. CONCLUSIONS: Despite considerable differences in the exercise activities per week between well-trained and minimally trained individuals, there were minimal differences in the release and metabolism of catecholamines at rest or during exercise.

Adult↗
PubMed1986

An in-situ isolated rat adrenal perfusion system for study of neurally mediated catecholamine secretion: effects of morphine, a Met-enkephalin analogue, and naloxone on catecholamine secretion.

An in-situ isolated rat adrenal perfusion technique has been devised to study the opioid control of neurally mediated adrenomedullary catecholamine release. Adrenomedullary catecholamine secretion was induced by electrical stimulation of the cut end of the left descending thoracic sympathetic chain on platinum electrodes. The half-maximal stimulatory potential (ED50) of the system was 8 V, 20 Hz, with 300 microseconds pulse width. Basal release of catecholamine from the adrenal was constant using a perfusion flow rate of 100-300 microliter/min, but increased significantly with increasing perfusion temperature over the range 36-38 degrees C. Following repetitive 30-s stimulation of the left thoracic sympathetic chain, and 3-min fraction collections, the total amount of catecholamine released per fraction remained within 80-100% of the maximum release for up to eight consecutive stimuli. The release of catecholamines was completely blocked by hexamethonium (0.1 mmol/l), but recovered to pre-blockade values within two further stimuli. Using the ED50 and the first three stimuli as control, the effects of morphine (10 nmol/l-l mmol/l), D-Ala2-MePhe4-Met-enkephalin-(O5)-ol (DAMME; 10 nmol/l-0.1 mmol/l) and naloxone (10 nmol/l-10 mumol/l) on the response to the next three stimuli were compared. Morphine, DAMME or naloxone did not significantly alter the amount of catecholamine released by this form of stimulation. Therefore in the rat, under the conditions used, there is no evidence for mu (mu) or delta (delta) opiate modulation of neurally mediated catecholamine release from the rat adrenal medulla.

Adrenal Glands↗
PubMed1975

Effects of catecholamines on rat myocardial metabolism. II. Influence of catecholamines on 32p-incorporation into rat myocardial adenylic nucleotides and their turn-over.

1. The influence of catecholamines (adrenaline and noradrenaline) on 32Pi incorporation into intracellular phosphate and adenylic nucleotides has been studied on rat myocardium slices; consequently, the turn-over of nucleotides could be determined and compared under the influence of these two hormones. 2. In order to specify the site of action of these catecholamines, several inhibitors and activators of energetic metabolism were included in the incubation medium: 3'5'-AMP, caffein, ouabain, oligomycin, rotenone + antimycin. 3. Both catecholamines favour Pi exchanges between intra and extracellular spaces; ATP turn-over is greatly increased, while ADP turn-over is slightly decreased, and 32P-incorporation into ADP is increased. 4. 3'5'-AMP and caffein are without effect on Pi penetration; however, caffein increases catecholamine effects on this penetration. ATP turn-over is slightly increased by 3'5'-AMP or caffein. 5. Ouabain decreases ATP turn-over but does not prevent the adrenaline induced acceleration. Inhibitors of oxidative phosphorylation and electron transport decrease ATP-turn-over severely; this inhibition is not released by catecholamines. 6. It is concluded that the catecholamine effects observed are dependent on the oxidative phosphorylations process. The increase of Pi exchange by catecholamines may be related to the increase of extracellular space and cation translocations we observed with the hormones.

Adenine Nucleotides↗
PubMed1985

Catecholamine-induced myocardial cell damage: catecholamines or adrenochrome.

Recent evidence suggests that catecholamine-induced myocardial damage may be due to the cardiotoxic property of its non-physiological metabolite, adrenochrome. We investigated whether catecholamine-mediated myocardial damage is the result of catecholamine stimulation per se or the consequence of physiological or non-physiological metabolites. In the Langendorff perfused rat heart, fresh epinephrine (10(-6) M) solution increased cumulative lactate dehydrogenase (LDH) release when the perfusion pressure was 100 cm but not 65 cm, 3640 +/- 665 v. control 545 +/- 45 mIU/g/35 min respectively (P less than 0.01). In the left atrial perfused rat heart working against a hydrostatic pressure of 100 cm, fresh epinephrine (10(-6) M) solution produced the greatest increase in cumulative LDH release, 9346 +/- 1806 v. control 472 +/- 47 mIU/g/45 min respectively (P less than 0.01). Beta 1 but not alpha 1 adrenergic stimulation provoked enzyme leakage. Beta-adrenoceptor antagonism with atenolol 10(-5) M prevented catecholamine-induced leakage. Physiological metabolites of epinephrine viz metanephrine 10(-6) M, dihydroxymandelic acid 10(-6) M, vanillylmandelic acid 10(-6) M, and the non-physiological metabolite adrenochrome 10(-6) M to 10(-4) M did not increase the cumulative LDH release over 45 min. When adrenochrome 10(-4) M was perfused for 120 min enzyme release occurred, albeit only a third of that induced by epinephrine 10(-6) M over 45 min. We demonstrate that epinephrine-induced myocardial cellular damage is due to the direct effect of catecholamine stimulation acting on the beta-adrenergic receptor. The amount of left ventricular work appears to determine the extent of cellular damage. Physiological metabolites and the non-physiological metabolite, adrenochrome are not responsible for catecholamine-induced myocardial cellular damage. Epinephrine 10(-6) M caused a positive inotropic effect, whereas adrenochrome 10(-4) M induced contractile failure. Contractile failure was due to a negative inotropic effect and coronary artery vasoconstriction. Adrenochrome induces myocardial cellular damage and contractile failure but only in a concentration of 10(-4) M, this concentration does not appear to have pathophysiological relevance.

Action Potentials↗
PubMed1991

Catecholamine determination in sequential urine voiding: a method for detecting pheochromocytoma in patients without elevated urinary catecholamines.

The biochemical diagnosis of pheochromocytoma is based on the demonstration of increased amounts of catecholamines, or catecholamine metabolites, in 24-h urine samples. In patients whose 24-h urine catecholamines are within normal limits, and in whom short duration catecholamine elevations are suspected, timed urine collections have been used to detect these elevations. In this study, determination of catecholamines in sequential urine voidings and consideration of their relative values are suggested as a further method to detect pheochromocytomas, especially in cases without extended elevation of urinary catecholamine levels. The use of this method is demonstrated in three cases in which pheochromocytoma would not otherwise have been proven by laboratory determination.

Adrenal Gland Neoplasms↗
PubMed1987

Neuronal colocalization of peptides, catecholamines, and catecholamine-synthesizing enzymes in guinea pig paracervical ganglia.

The patterns of colocalization of neuropeptides, catecholamines, and catecholamine-synthesizing enzymes were examined in principal neurons and nerve terminals in guinea pig paracervical ganglia using a double-labeling immunohistochemical procedure. A small proportion of nerve cell bodies (less than 10%) had the characteristics of catecholamine-synthesizing neurons and presumably were noradrenergic. Another 50% of the nerve cell bodies contained immunoreactivity (IR) to dopamine-beta-hydroxylase (DBH), but did not have any other characteristics of noradrenergic neurons; they did not contain detectable catecholamines, or IR to dopa decarboxylase (DDC) or tyrosine (TH) hydroxylase, nor did they take up exogenous catecholamines. Half of the catecholamine neurons had neuropeptide Y (NPY)-IR, and a small number (0.5% total neurons) had somatostatin (Som)-IR. Most of the non-noradrenergic neurons with DBH-IR (40-50% total neurons) contained IR for dynorphin (Dyn), NPY, and vasoactive intestinal peptide (VIP), and about half of them (20-25% total) also contained Som-IR. Ten to twenty percent of neurons contained IR to Som, but not to any other antigen examined here. Nerve terminals with substance P (SP)-IR or enkephalin (Enk)-IR were prominent in all ganglia. SP-IR fibers formed dense baskets only around those neurons with DBH/Dyn/NPY/VIP (+/- Som)-IR, while fibers with very bright Enk-IR were associated selectively with those neurons with Som-IR alone. In addition, most TH-IR nerve cell bodies were surrounded by NPY-IR varicose nerve fibers. In conclusion, this analysis of combinations of peptides and enzymes contained in principal neurons of the paracervical ganglia allows us to identify as many as 11 different neuron populations. The functional significance of the presence of the same neuropeptide (e.g., NPY) in different neuron populations is as yet unknown. Some of these classes of neurons are associated specifically with immunohistochemically distinct types of presynaptic nerve fibers, which suggests that different immunohistochemically defined classes of neurons represent different functional pathways.

Animals↗
PubMed1985

Plasma catecholamines and modes of delivery: the relation between catecholamine levels and in-vitro platelet aggregation and adrenoreceptor radioligand binding characteristics.

Catecholamines were measured in maternal venous, and mixed umbilical cord blood. Maternal catecholamines were significantly (P less than 0.01) reduced by epidural analgesia with a 36% reduction in noradrenaline and a 33% reduction in adrenaline. Fetal catecholamines were elevated at birth with a 3-8 fold increase in noradrenaline but not adrenaline during spontaneous vaginal delivery. The lowest fetal catecholamines were obtained in the group delivered under epidural analgesia; lower plasma catecholamines were not associated with adverse respiratory effects. Fetal platelets showed impaired alpha 2-adrenoceptor function with absent aggregatory responses to adrenaline in vitro. The defect in platelet function was unlikely to be related to changes in the number of fetal platelet alpha-receptors or to changes in receptor affinity for adrenaline, as fetal platelets failed to aggregate to adrenaline from deliveries with high and low cord blood catecholamines.

Adult↗
PubMed1991

Catecholamine sulfates as internal standards in HPLC determinations of sulfoconjugated catecholamines in plasma and urine.

A method is described to measure catecholamine sulfates from human plasma and urine by isocratic reversed-phase high-performance liquid chromatography with electrochemical detection. For this measurement we use catecholamine 3-sulfate isomers as internal standards and determine the sulfoconjugates only after eliminating the catecholamines. Catecholamines that have previously been used as internal standards are shown to cause a significant overestimation (P less than 0.05) of the catecholamine sulfates--by 10% to 25% and 20% to 42% in human plasma and urine, respectively. The detection limits (signal-to-noise ratio greater than 3) in plasma and urine samples were about 80 pmol/L for each analyte. The intra-assay and interassay CVs were less than 4.0% and 10.6% in human plasma and less than 6.6% and 12.8% in human urine, respectively. The calibration curves for all catecholamine sulfates in human plasma and urine were linear (r greater than 0.96; P less than 0.001) over the respective concentration ranges of 0.1-100 nmol/L and 5-1000 nmol/L.

Adrenal Gland Neoplasms↗
PubMed1990

Dietary calcium deprivation increased the levels of plasma catecholamines and catecholamine-synthesizing enzymes of adrenal glands in rats.

Rats on calcium-deficient diets developed hypocalcemia, hyperparathyroidism and hypertension and showed an increase in plasma catecholamines. Adrenal gland catecholamines were decreased while tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) were found to be increased, as compared to controls. In contrast, no significant differences were found between controls and parathyroidectomized rats in plasma catecholamines, and catecholamines, TH and DBH of the adrenal gland. These findings seem to indicate that the genesis of hypertension in rats on a low calcium diet is secondary to hyperparathyroidism caused by a low calcium diet. Furthermore, some relation between catecholamines and parathyroid hormone seems to exist in the regulation of blood pressure in rats.

Adrenal Glands↗
PubMed1977

Relaxation of heart muscle by catecholamines and by dibutyryl cyclic adenosine 3',5'-monophosphate. Similarity of beta-adrenoceptors mediating contractile and relaxant effects of catecholamines in kitten pipillary muscle.

1. In isometrically contracting kitten papillary muscles, dibutyryl cyclic AMP (DBcAMP) enhanced peak tension, increased rates of contraction and relaxation, decreased tension of a phasic but not of a small tonic component of KCl-contractures, and caused aftercontractions. These effects resemble closely those of catecholamines. 2. The effects of DBcAMP on kitten papillary muscle were not influenced by (-)-bupranolol, a beta-adrenoceptor antagonist. 3. DBcAMP decreased KCl-contractures in strips of frog ventricle. 4. Phasic KCl-contractures in kitten papillary muscles were decreased by (-)- and (+)-isoprenaline. For similar effects, 100-fold higher concentrations of (+)-isoprenaline than of (-)-isoprenaline were required. 5. Increases in maximum rates of contraction and relaxation, increases in peak tension of isometric contractions and reduction of phasic KCl-contractures by catecholamines were antagonized competitively to a similar extent by (-)-bupranolol. Mean apparent equilibrium constants for the beta-adrenoceptor-(-)-bupranolol complex of 0.46-0.70 nM were estimated. These constants were quite similar irrespective of whether (-)-isoprenaline, (+)-isoprenaline or (-)-noradrenaline were used as agonists. 6. Increases in contractile strength, maximum rates of contraction and of relaxation of isometric contractions and decreases in KCl-contractures by (-)-isoprenaline were surmountably blocked by (+)-bupranolol. Mean apparent equilibrium constants for the receptor-(+)-bupranolol complex were 40-50 nM. 7. The equilibrium constants of (-)- and (+)-bupranolol for the receptors mediating positive inotropic and relaxant effects of catecholamines were not significantly different from constants for bupranolol-receptor complexes in cell-free membrane particles of kitten heart ventricle. It is suggested that the same beta-adrenoceptor triggers positive inotropic, relaxant and adenylyl cyclase-activating effects of catecholamines in kitten papillary muscle. 8. The partial agonist (-)-dichloroisoprenaline (DCI) (1 muM) reduced by 79% the phasic KCl-contractures of the kitten papillary muscles. DCI stimulates adenylyl cyclase activity of ventricle membranes to less than 1/4 of maximum stimulation by (-)-isoprenaline. If cyclic AMP produced by DCI is involved in the decrease of phasic KCl-contracture, small increase in cyclic AMP should be sufficient to induce this effect.

Adrenergic beta-Antagonists↗
PubMed1992

Effects of clentiazem (TA-3090) and nifedipine on basal circulating catecholamine levels and on stimulation-evoked adrenal catecholamine secretion in anesthetized dogs.

The effects of TA-3090 (clentiazem) and nifedipine on basal sympathoadrenal activity and on the adrenal medullary response during splanchnic nerve stimulation were studied in dogs anesthetized with sodium pentobarbital. Plasma concentrations of epinephrine and norepinephrine were measured in aortic and adrenal venous blood before and after acute administration of the drugs, as well as during left splanchnic nerve stimulation before and after administration of drugs. Following intravenous injections, TA-3090 (30, 100, and 300 micrograms/kg) did not affect basal circulating catecholamine levels, whereas nifedipine (10, 30, and 100 micrograms/kg) markedly increased aortic epinephrine and norepinephrine concentrations in a dose-dependent manner in correlation with progressive decreases in mean arterial pressure. The changes in aortic epinephrine and norepinephrine concentrations were inversely related to those in mean arterial pressure (r = 0.603, p < 0.01; r = 0.536, p < 0.01; respectively). In response to direct splanchnic nerve stimulation (2 Hz, 2 ms, 1 min, 12 V), adrenal venous epinephrine and norepinephrine concentrations significantly increased, with a high degree of reproducibility. The catecholamine responses to splanchnic nerve stimulation were not affected by either TA-3090 or nifedipine at any dose tested. The present results suggest that the increases in circulating catecholamine levels following nifedipine administration are due to baroreflex activation secondary to the drug-induced hypotension. The study indicates that both TA-3090 and nifedipine did not significantly affect L-type Ca2+ channels related to catecholamine release in the adrenal medulla under the present experimental conditions.

Adrenal Glands↗
PubMed1992

Urinary excretion of catecholamines and their metabolites in relation to circulating catecholamines. Six-hour infusion of epinephrine and norepinephrine in healthy volunteers.

Some depressed patients have been shown to excrete abnormal amounts of catecholamines and their metabolites in urine. Some studies suggest that hypersecretion of epinephrine by the adrenals and of norepinephrine by the peripheral sympathetic system cause increased excretion of urinary catecholamines and their metabolites in a subgroup of patients. To evaluate the effect of increased catecholamine levels in the peripheral circulation on urinary catecholamine and metabolite levels, we infused healthy volunteers during 6 hours with epinephrine, norepinephrine, or placebo, respectively, in a three-period, double-blind, crossover design. The results indicate that (1) urinary epinephrine and norepinephrine levels were the most sensitive indicators of increased circulating epinephrine and norepinephrine levels, respectively; (2) changes in circulating epinephrine or norepinephrine levels were not readily reflected in changes in urinary vanillylmandelic acid or 3-methoxy-4-hydroxyphenylglycol levels; and (3) increased normetanephrine excretion was not only induced by infusion of norepinephrine but also by epinephrine. This last finding may be due to activation of the sympathetic nervous system by circulating epinephrine. These results may help to explain the mechanism of adrenal epinephrine and sympathetic nervous system norepinephrine hypersecretion observed in subgroups of depressed patients.

Adult↗
PubMed1989

Catecholamine release by catecholamines in the eel does not require the presence of brain or anterior spinal cord.

The catecholamine-producing chromaffin cells of the American eel are strongly innervated by fibers, which, by ultrastructural criteria, seem to be cholinergic. However, neither removal of the brain nor removal of the brain combined with extirpation of the anterior spinal cord prevents the release of catecholamines into the circulation by catecholamines. It appears that the chromaffin cells are controlled by both nervous and humoral stimuli, and that at least some of the latter do not require the presence of "preganglionic" innervation.

Anguilla↗
PubMed1992

Catecholamine metabolism in the vas deferens and the adrenal gland with special reference to the central catecholamine-depleted state.

Experiments were carried out to elucidate the role of central catecholamines in regulating catecholamine metabolism in the vas deferens and adrenal gland of the rat. Rats were injected intracerebroventricularly (i.c.v.) with either vehicle or 6-hydroxydopamine (6-OHDA). Groups of animals pretreated with vehicle or 6-OHDA (i.c.v.) were injected intraperitoneally (i.p.) with alpha-methyl-para-tyrosine (AMT), a tyrosine hydroxylase inhibitor. Catecholamine turnover rates were estimated by determining norepinephrine or epinephrine content after administering AMT. Central norepinephrine and dopamine contents decreased significantly (p less than 0.05) after treatment with 6-OHDA and AMT. The norepinephrine content of the vas deferens of rats pretreated with 6-OHDA was markedly reduced (p less than 0.001) after administration of AMT, whereas that of the vehicle-treated rats remained unchanged. Administration of 6-OHDA had no effect on the norepinephrine or epinephrine content of the adrenal gland. The present results indicate that central monoaminergic neurons have an inhibitory effect on the adrenergic neurons of the vas deferens. In contrast, this inhibitory regulation does not appear to be exerted on the adrenal glands.

Adrenal Glands↗
PubMed1985

Conjugates of catecholamines. 6. Synthesis and beta-adrenergic activity of N-(hydroxyalkyl)catecholamine derivatives.

A new series of catecholamines has been prepared in which the N-alkyl substituent of dl-epinephrine or dl-isoproterenol has been extended by a methylene chain terminated by a hydroxyl group or derived functionality (e.g., carbamate or ester). These functionalized catecholamines (congeners) and model compounds were prepared with the goal of eventual attachment to polymeric carrier molecules. The beta-adrenergic agonist activity of the derivatives was evaluated in vitro by measuring the intracellular accumulation of cyclic AMP in S49 mouse lymphoma cells and by the displacement of iodocyanopindolol (ICYP). A n-butylcarbamate derivative (compound 15) was the most active compound in this series with a potency 190 times greater than dl-isoproterenol in the S49 assay. The biological results indicate that minor modifications in structure in the N-alkyl substituent of the catecholamine can influence the pharmacologic activity.

Adrenergic beta-Agonists↗