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PubMed1985

[Free and conjugated plasma catecholamines, lactate behavior and oxygen uptake at rest and in staged physical exertion as well as alpha receptor density in intact thrombocytes in trained athletes].

The influence of chronic static training on free and conjugated plasma catecholamines was investigated in 8 statically trained athletes (21 +/- 2 years of age) at rest and during incremental ergometric cycling. Plasma catecholamines are seen as biochemical indicators of the over-all sympathetic activity. Alpha-2-adrenoreceptors were additionally determined as one parameter of the organism's sensitivity to catecholamines. During modest and heavy exercise, free plasma noradrenaline and adrenaline are comparably low in statically and endurance trained athletes. They are lower than in untrained subjects. During exhaustion, however, free adrenaline responses of the statically trained athletes only amount to 30-50% of the concentrations observed in endurance trained athletes and untrained subjects. Free plasma dopamine and conjugated plasma catecholamines do not show any significant changes during ergometric exercise. Free and conjugated catecholamines correlate positively. Positive correlations are also observed between blood pressure and plasma catecholamines. These correlations however are clearer between conjugated catecholamines and blood pressure. This is also recognizable for the negative correlation between alpha-2-receptor density on intact platelets (1078 +/- 323 binding sites per cell) and conjugated catecholamines. In conclusion, statically trained athletes also show an alteration of sympathetic tone (catecholamines) comparable to that observed in endurance trained athletes. Maximal adrenaline responses however are lower in statically trained athletes than in endurance trained or untrained subjects. The alpha-adrenoreceptor density on intact thrombocytes seems to be increased in statically trained athletes.

Adult↗

PubMed1986

Catecholamine secretion from the adrenal medulla of the fetus, regulation by hormones.

In the ovine fetus, the adrenal medulla activity secretes catecholamines into the circulation under normal and stress conditions. Little is known regarding the endocrine regulation of adrenal medullary catecholamine secretion in the fetus. The present study was undertaken to investigate the direct effects of the hormones prolactin, angiotensin II and cortisol on catecholamine release from fetal adrenal medulla, and to determine whether the effect of the hormones change during development into adulthood. Adrenal medulla from fetal, newborn and adult pregnant sheep was collected, dispersed into single cells and plated. Following preincubation, the cells were treated with ovine prolactin or angiotensin II at 8, 40 and 200 micrograms/ml; or cortisol at 10(-8), 10(-7) and 10(-6)M for 24 h. Catecholamine release into the medium were measured at 3, 6, 12 and 24 h. Ovine prolactin at 8 to 200 micrograms/ml significantly stimulated the release of total catecholamines after 12 h of incubation. The effect of prolactin was dose-dependent such that the magnitude of the response increased and the response time shortened with increasing concentrations of prolactin. In addition, the release of all three catecholamines--dopamine, norepinephrine and epinephrine--was significantly elevated. In newborn cells, only the highest concentration of 200 micrograms/ml ovine prolactin stimulated total catecholamine release at 6 h and 12 h, with significant increases of the three catecholamines at 12 h. In maternal cells, stimulation of catecholamine release was observed also with the highest concentration of prolactin tested (200 micrograms/ml) and after 12 h of incubation, when only the release of epinephrine was significantly enhanced by 324%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗

PubMed1980

Poststimulation catecholamine synthesis and tyrosine hydroxylase activation in central noradrenergic neurons. II. Depolarized hippocampal slices.

The ability of neuronal depolarization to increase catecholamine biosynthesis in the poststimulation period was investigated in a preparation of central noradrenergic tissue, maintained in vitro. Rat hippocampal slices were superfused with oxygenated Krebs-Ringer phosphate saline (KRP) or depolarized with KRP containing 55 mM KCl. Slices were then transferred to fresh, nondepolarizing KRP containing [3H]tyrosine for further incubation. Ten minutes of K+ depolarization resulted in a 78% increase in [3H]catecholamine synthesis, measured in the poststimulation period, relative to nondepolarized, control slices. This activation of catecholamine synthesis was maintained for up to 10 min following termination of K+ depolarization. Depolarization in the presence of tetrodotoxin did not block the poststimulation increase in catecholamine synthesis. The increased catecholamine synthesis in the poststimulation period can be accounted for by increased tyrosine hydroxylation since: 1) the synthesis of [14C]catecholamines from [14C]dopa was not increased by K+ depolarization and 2) K+ depolarization led to a 71% increase in the accumulation of [3H]dopa newly synthesized from [3H]tyrosine in the presence of the decarboxylase inhibitor, brocresine. Under these conditions, no significant depletion of tissue norepinephrine could be detected. The depolarization-induced increase in catecholamine synthesis was independent of the presence of Ca++ in the superfusion and/or incubation media, suggesting its dissociation from Ca++-dependent transmitter release. The absence of enhanced [3H]catecholamine synthesis following depolarization of slices in a Ca++-free K+-KRP containing 1.0 mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) suggested that there is an absolute requirement for tissue Ca++ during the stimulation-induced synthesis activation process. There appears to be a depolarization-related phenomenon whose triggering is Ca++-independent, but which, in the presence of Ca++, is manifested as an increase in catecholamine biosynthesis (tyrosine hydroxylase activity).

Animals↗

PubMed1995

[The catecholamine concentrations of collected autologous blood during adrenalectomy for pheochromocytoma].

We studied the catecholamine concentrations in collected autologous blood of a patient undergoing adrenalectomy for pheochromocytoma. In the preoperative laboratory data, plasma concentrations (normal ranges) of epinephrine, norepinephrine and dopamine were 60180 pg.ml-1 (< 100), 11090 pg.ml-1 (100-450) and 104 pg.ml-1 (< 20), respectively. The catecholamine levels of collected blood were epinephrine 2490000 pg.ml-1, norepinephrine 352300 pg.ml-1 and dopamine 6100 pg.ml-1 before wash. Wash of collected blood with 1000 ml saline diluted the catecholamines to epinephrine 212000 pg.ml-1, norepinephrine 18700 pg.ml-1 and dopamine 4900 pg.ml-1. Platelet activation by contact with tissue collagen or thrombin results in the release of catecholamine concentrated in the dense body. The mechanical stimulation by suction, roller pump and centrifugation during blood collection may accelerate the catecholamine release from platelets. Thus, saline wash hardly reduces catecholamine concentrations of collected blood from a patient with pheochromocytoma. In this particular case, plasma catecholamines seem to exceed the potential capacity of platelets in amount. The dilution effect for epinephrine and norepinephrine probably reflects the washout of greater amount of plasma catecholamines. However, saline wash was unable to reduce catecholamines contained in the collected blood to a safe level, and hypertension following autotransfusion was predictable. We conclude that hemodynamic change should be monitored carefully during intraoperative autotransfusion in a case of pheochromocytoma.

Adrenal Gland Neoplasms↗

PubMed1994

Clinical implications of genetic and acquired defects in catecholamine synthesis and metabolism.

All major enzymes involved in catecholamine synthesis and metabolism have been cloned. In addition to some genetic defects of these enzymes responsible for well-defined clinical syndromes, several enzymatic abnormalities may be due to environmental (e.g. pharmacological and nutritional) or biological (e.g. aging) factors, which may modify genome expression. The enzymes involved in catecholamine metabolism either lead to metabolites which cannot be reconverted to the parent catecholamine (such as products of monoamine oxidation and catechol-O-methylation), or metabolites, which can be reconverted to the free catecholamine from which they are generated (such as products of sulfoconjugation). Reversible sulfoconjugation is partly regulated by the recently cloned enzyme, sulfatase. The importance of this reversible step is that it reconverts inactive into biologically active catecholamines. The balance of the sulfoconjugation-deconjugation interplay may have physiological implications; in addition to catecholamine release, it may determine the availability of free catecholamines during diurnal rhythms and stress or modify their renal excretion. Circumstantial evidence, including a close homology within the aryl sulfatases and steroid sulfatase gene, the first implicated in catecholamine metabolism, the second in steroid metabolism, suggests a genetic defect of sulfatases in essential hypertension. A similar, but secondary, sulfatase defect may affect catecholamine metabolism and action in chronic renal failure.

Animals↗

PubMed1990

Substance P has biphasic effects on catecholamine secretion evoked by electrical stimulation of perfused rat adrenal glands in vitro.

The adrenal medulla is innervated by the splanchnic nerve which contains substance P-immunoreactive fibres originating in the dorsal root ganglia but whose function in the adrenal medulla is not known. In the present study, we have examined the effect of exogenous substance P on catecholamine secretion and [3H]-choline overflow evoked by field stimulation of the perfused rat adrenal gland. Substance P had biphasic effects on catecholamine secretion evoked by field stimulation: at the lower concentrations (10(-7)-3 x 10(-6) M), substance P facilitated catecholamine secretion whereas at higher concentrations (3 x 10(-5) M), substance P inhibited catecholamine secretion. The effects of substance P were long-lasting: substance P at all concentrations present during the second of three 6-min stimulations increased catecholamine secretion during the third stimulation. The enhancement of catecholamine secretion by substance P during field stimulation was not blocked by atropine but was substantially blocked by hexamethonium plus atropine. Substance P at all concentrations inhibited the evoked [3H]-choline overflow with a maximal inhibition of 60% (at 10(-6) M). In the absence of stimulation, substance P (10(-7)-3 x 10(-5) M) had no effect on the basal catecholamine secretion or basal [3H]-choline overflow. These results indicate that substance P has modulatory effects on adrenal catecholamine secretion and [3H]-choline overflow evoked by electrical stimulation. Presynaptically, substance P inhibits transmitter overflow from cholinergic nerve terminals and post-synaptically substance P has biphasic effects on catecholamine secretion dependent on the substance P concentration. These results suggest a functional role for substance P-containing fibres innervating the adrenal medulla.

Adrenal Glands↗

PubMed2001

Correlation of increased grooming behavior and motor activity with alterations in nigrostriatal and mesolimbic catecholamines after alpha-melanotropin and neuropeptide glutamine-isoleucine injection in the rat ventral tegmental area.

1. We wished to further study the behavioral effects of alpha-melanotropin (alpha-MSH), melanin-concentrating hormone (MCH), and neuropeptide glutamine-isoleucine (NEI). 2. To this effect we administered alpha-MSH, MCH, and NEI in the ventral tegmental area of the rat, a structure where these neuropeptides are highly concentrated. To further elucidate the biochemical mechanisms of the behavioral effect of these neuropeptides, we determined the degree of grooming behavior and the levels of catecholamines. after neuropeptide administration. 3. We preselected those animals responding to the central injection of alpha-MSH with excessive grooming behavior. We administered the neuropeptides at the dose of 1 microg/0.5 microL, in each side of the ventral tegmental area, bilaterally. We studied grooming behavior, locomotor activity, and total behavior scores, 30 and 65 min after administration of the peptides. 4. Three groups of animals were decapitated immediately after the injection of the neuropeptides, and 30 or 65 min after injection. We measured dopamine (DA), noradrenaline (NA), and the dopac/dopamine ratio (DOPAC/DA) to determine steady state levels of catecholamines and an indirect measure of DA release and metabolism, respectively. 5. Injections of alpha-MSH produced significant elevations in grooming behavior, locomotor activity, and total behavior scores, both 30 and 65 min after peptide administration. This was correlated with significant decreases in DA content, increases in DOPAC content, and increases in the DOPAC/DA ratio. In the caudate putamen, changes in catecholamines occurred both at 30 and 65 min after injection. In the nucleus accumbens, changes were present at 65 min after injection. Conversely, there were no alterations in NA content, either in the caudate putamen or in the nucleus accumbens, at any time after the injection. 6. Injections of NEI resulted in significant elevations in grooming behavior, locomotor activity, and total behavior scores, both 30 and 65 min after peptide administration. This was correlated with increased DOPAC/DA ratio in the nucleus caudatus but not in the nucleus accumbens. Conversely, NEI produced increased NA concentrations in the nucleus accumbens, but not in the nucleus caudatus. 7. Injections of MCH did not produce significant changes in behavior or significant changes in nucleus caudatus or nucleus accumbens catecholamines. 8. Our results indicate (a) There is a correlation with alterations in behavior as induced for the neuropeptides injected here, and changes in extrapyramidal catecholamines. (b) There is a correlation between alterations in behavior and increases in DOPAC/DA ratio in the nucleus caudatus. (c) There is a correlation between alterations in behavior and alterations in catecholamines in the nucleus accumbens. In the nucleus accumbens, DOPAC/DA ratio is changed after alpha-MSH, and NA ratio is changed after NEI injection. (d) Absence of alterations in extrapyramidal catecholamines, and in particular in catecholamines in the nucleus accumbens, correlates with absence of behavioral alterations after neuropeptide administration to the ventral tegmental area. 9. In conclusion, the behavioral effect of exogenous administration of neuropeptides in the ventral tegmental area is peptide-specific, and is probably associated with alterations in catecholamine metabolism and release in the nucleus caudatus and the nucleus accumbens. Both alpha-MSH and NEI seem to stimulate the nigrostriatal DA system. While alpha-MSH appears to stimulate the mesolimbic DA system as well, NEI may exert its actions not through the DA, but through the NA mesolimbic system. The precise contribution of DA and NA, and the relative role of the nucleus caudatus and nucleus accumbens in these behaviors remain to be elucidated.

Animals↗

PubMed1999

Unexpected changes in the catecholamine content of platelets and plasma during exercise.

Catecholamines are retained within platelets for several hours after plasma catecholamine concentrations have returned to baseline. To determine whether platelet catecholamine concentrations may provide an index of short-term elevations in plasma adrenaline (A) and noradrenaline (NA), the response of plasma and platelet catecholamines to an interval supramaximal, Max (107% VO(2) Max), and submaximal, Submax (37% VO(2) Max), cycling protocol was examined in seven healthy male volunteers, 22-34 years. Despite large rises in plasma NA and A in the Max study (12- and 8-fold increases above baseline, respectively) and smaller rises in the Submax study, the baseline platelet concentrations of A and NA fell significantly in the first 15 min of exercise in both groups. This fall was greater in the SubMax protocol. Catecholamine concentrations then increased slowly in the second half of exercise, but never returned to baseline. The circulating platelet count almost doubled during the exercise period, increasing from 308 to 569 X 10(3) platelets/ml plasma in both studies, returning close to baseline in recovery. These results indicate that at the beginning of exercise there is large rise in plasma catecholamines and the circulating platelet count, with a fall in the platelet catecholamine concentrations. This suggests that a sequestered platelet population, free of catecholamines, is released at the beginning of exercise. This release most probably occurs from the spleen. If this is the case, the reason for a propagation of platelets in the spleen, free of catecholamines, requires further investigation.

Journal Article↗

PubMed1983

Influence of vagotomy on changes in feline plasma catecholamine levels induced by occlusion of either the left or right coronary vessel.

The purpose of this study was two-fold: (1) to determine the effect of occlusion of the left anterior descending branch (LAD) of the left coronary artery or the right coronary (RC) artery on plasma catecholamine levels, and (2) to determine whether bilateral vagotomy has an effect on changes in plasma catecholamine levels evoked by coronary occlusion. Chloralose anaesthetised cats subjected to LAD occlusion exhibited increases in plasma noradrenaline and adrenaline at 3 min post-occlusion. The increases in noradrenaline and adrenaline were unrelated to the hypotension that occurred at this time. Bilateral vagotomy did not appear to alter the effect of LAD occlusion on catecholamine release into the circulation but did unmask a significant correlation between the degree of hypotension and the magnitude of increase in plasma catecholamines. Right coronary occlusion in animals with intact and sectioned vagus nerves evoked noradrenaline and adrenaline release that was significantly correlated with a fall in arterial pressure. Bilateral vagotomy per se caused an increase in baseline plasma catecholamine levels. Pretreatment with atropine mimicked the increase in baseline catecholamine levels seen with vagotomy. These results indicate that occlusion of the LAD and RC arteries increase the release of catecholamines into the circulation. The role of the vagus nerves in this response was observed only with LAD occlusion and consisted of altering the relationship between the degree of hypotension and the magnitude of increase in plasma catecholamines. That is, after vagotomy, the decrease in blood pressure following LAD occlusion was effective in causing release of catecholamines, presumably because of the hypotension causing a decrease in baroreceptor stimulation. Finally, it appeared that vagotomy increases the release of noradrenaline into the circulation by removing efferent vagal tone that inhibits noradrenaline release. This inhibitory action is mediated by activation of muscarinic receptors.

Animals↗

PubMed1998

Usefulness of plasma catecholamines during head-up tilt as a measure of sympathetic activation in vasovagal patients.

Vasovagal syncope is a common clinical disorder which has been traditionally related to a vasovagal reflex precipitated by an initial excess sympathetic stimulation. We hypothesized that the increase in plasma catecholamines during head-up tilt is more accentuated in patients with tilt induced vasovagal syncope. To test this hypothesis, plasma catecholamines were measured in supine posture and during head-up tilt in patients with a history suggestive of vasovagal syncope. Of these, 13 had a normal response to tilt (nonvasovagal group; age 41 +/- 19 [SD]years) and 11 had a vasovagal response to tilt (vasovagal group; 39 +/- 20 years). In the supine posture at rest, plasma epinephrine and norepinephrine were not significantly different between the nonvasovagal and the vasovagal groups (39 +/- 28 ng/L vs 46 +/- 38 ng/L, P = 0.5792, 335 +/- 158 ng/L vs 304 +/- 124 ng/L, P = 0.6007, respectively). Furthermore, the tilt induced changes in plasma epinephrine and norepinephrine were not different between the two groups (20 +/- 20 ng/L vs 35 +/- 55 ng/L, P = 0.3562, 264 +/- 158 ng/L vs 242 +/- 205 ng/L, P = 0.7724, respectively) suggesting that differences in the hemodynamic response to tilt are not predictable by the supine levels of circulating plasma catecholamines, and that the extent of plasma catecholamines increase during tilt does not determine the hemodynamic outcome of the tilt test. Since orthostatic changes of plasma catecholamines could be influenced by volume factors, we assessed plasma renin activity and aldosterone as surrogates of blood volume. Baseline plasma renin activity and aldosterone were not significantly different between the two groups. We conclude that inasmuch as plasma catecholamines reflect the status of sympathetic activity, our data do not support the hypothesis that accentuation of sympathetic activity precedes necessarily the tilt induced vasovagal syncope. However, one should take in consideration that multiple factors may influence catecholamine levels and catecholamines kinetics. A hyperresponsiveness of beta-receptors to catecholamines in patients with vasovagal syncope may be suggested but needs to be tested.

Adolescent↗

PubMed1995

Effect of corticosteroids on free and sulfoconjugated catecholamines at birth in premature newborn sheep.

We previously demonstrated that prenatal corticosteroids attenuated the expected exponential increase in circulating catecholamines at birth. The present studies were undertaken to determine if alteration in sulfoconjugation could account for this attenuation. Catheterized fetal lambs received saline (n = 6) or corticosteroids (n = 8) intravenously for 60 h. The lambs were delivered by cesarean section at 130 +/- 1 days gestation. Ventilatory and cardiovascular responses and plasma catecholamine concentrations were measured for 2 h after birth. Although plasma free catecholamines levels were higher in controls than in corticosteroid-treated fetuses, the sulfoconjugated levels were similar in the two groups. Thus the corticosteroid-treated fetuses had a higher proportion of plasma sulfoconjugated catecholamines consistent with the possibility that sulfoconjugation was augmented during intrauterine life. After birth, the corticosteroid-treated animals showed an attenuated increase in plasma free catecholamine levels compared with controls but a similar increase in sulfoconjugated catecholamine levels to the control animals. The proportion of plasma sulfoconjugated catecholamines was higher in the corticosteroid-treated animals; however, the increase in sulfoconjugated catecholamines was insufficient to account for the attenuated overall increase in total catecholamines in the corticosteroid-treated animals.

Adrenal Cortex Hormones↗

PubMed2001

Opioids suppress basal and nicotine-induced catecholamine secretion via a stabilizing effect on actin filaments.

Catecholamine secretion and actin filament disassembly are closely coupled in chromaffin cells. Opioid suppression of catecholamine secretion is fast and transient, both characteristics of actin filament involvement. The aim of the present work was to test the hypothesis that opioids suppress catecholamine secretion via an inhibitory effect on actin filament disassembly. For this purpose we used the PC12 rat pheochromocytoma cell line. Norepinephrine and dopamine were measured by enzyme-linked immunosorbent assay or RIA. Polymerized actin was measured by rhodamine-phalloidin and visualized by confocal laser scanning microscopy. Opioids suppressed basal catecholamine secretion. The onset of this effect was fast and transient, peaking at 2 min, and was reversible by opioid antagonists. Synchronously, opioids suppressed actin filament disassembly; this was also reversible by opioid antagonists. Cytochalasin B prevented the inhibitory effect of opioids on catecholamine secretion. In addition, opioids suppressed the stimulatory effect of nicotine on catecholamine secretion and actin depolymerization. Changes in actin cytoskeleton in neuron-like PC12 cells make them resistant to both effects of opioids, i.e. on catecholamine secretion and actin disassembly. In conclusion, our data suggest that the suppressive effect of opioids on basal and nicotine-induced catecholamine secretion may result from an opioid-provoked stabilization of cortical actin. It also appears that basal catecholamine secretion is associated with opioid-sensitive machinery regulating the continuous formation of short-lived areas of cortical actin filament disassembly.

Actins↗

PubMed1994

THE EFFECTS OF ACCLIMATION TEMPERATURE ON THE DYNAMICS OF CATECHOLAMINE RELEASE DURING ACUTE HYPOXIA IN THE RAINBOW TROUT ONCORHYNCHUS MYKISS

The response of cannulated rainbow trout (Oncorhynchus mykiss) to acute hypoxia was studied in fish acclimated to two temperatures (5 and 15 °C). Blood/water respiratory variables and plasma catecholamine levels were measured before and 15 min after exposure to hypoxic water varying between 4.0 and 10.7 kPa (3080 mmHg) oxygen partial pressure (PwO2). Arterial blood PO2 (PaO2) and oxygen content (CaO2) fell during hypoxia in a similar manner at both temperatures, although the changes in CaO2 were often more pronounced in the fish acclimated to 15 °C. Regardless of acclimation temperature, plasma catecholamine levels were consistently elevated at PwO2 values below 8.0 kPa (60 mmHg); the largest increases in plasma catecholamine levels occurred below PwO2=5.3 kPa (40 mmHg). Adrenaline was the predominant catecholamine released into the circulation. Adrenaline was released at PwO2 values of 8.0 kPa or below, whereas noradrenaline was released at PwO2 values of 6.7 kPa or below. The construction of in vivo oxygen dissociation curves demonstrated an obvious effect of acclimation temperature on haemoglobin (Hb) oxygen-affinity; the P50 values at 15 °C and 5 °C were 3.6 kPa (26.7 mmHg) and 1.9 kPa (14.0 mmHg), respectively. At 15 °C, catecholamines were released into the circulation abruptly at a PaO2 threshold of 4.6 kPa (34.5 mmHg) while at 5 °C the catecholamine release threshold was lowered to 3.3 kPa (24.5 mmHg). The difference in the PaO2 catecholamine release thresholds was roughly equivalent to the difference in the P50 values at the two distinct temperatures. Catecholamine release thresholds, calculated on the basis of arterial blood oxygen-saturation (expressed as CaO2/[Hb]), were similar at both temperatures and were approximately equal to 5355 % Hb O2-saturation. The results support the contention that the lowering of blood oxygen content/saturation rather than PO2 per se is the proximate stimulus/signal causing catecholamine release in rainbow trout during acute hypoxia.

Journal Article↗

PubMed1996

Control of catecholamine and serotonin release from the chromaffin tissue of the Atlantic hagfish

An in situ saline-perfused systemic heart/posterior cardinal vein preparation of the Atlantic hagfish (Myxine glutinosa) was used to assess (1) the ability of the chromaffin tissue to release catecholamines in response to adrenocorticotropic hormone (ACTH; 7.5 i.u. kg-1), serotonin (250 nmol kg-1), carbachol (100 µmol kg-1), [Asn1-Val5]angiotensin II (Ang II; 100 nmol kg-1), histamine (0.3300 µmol l-1) and a high-[K+] saline (60 mmol l-1), (2) whether serotonin is co-released with the catecholamines of the chromaffin tissues, and (3) the potential modulatory effects of NECA, an adenosine receptor agonist, and DPSPX, an adenosine receptor antagonist, on catecholamine release. Bolus injections of ACTH, serotonin or carbachol, or perfusion with high-[K+] saline, all elicited the release of both adrenaline and noradrenaline. Pre-treatment with the serotonergic receptor antagonist methysergide or the cholinergic receptor antagonist hexamethonium abolished the serotonin- and carbachol-mediated catecholamine releases, respectively. Neither receptor antagonist affected the ACTH-mediated catecholamine release. Bolus injections of Ang II or perfusion with a range of histamine concentrations, two potent secretagogues in other vertebrates, did not elicit catecholamine secretion in hagfish. While injections of Ang II or perfusion with the high-[K+] saline both elicited the release of serotonin, treatments with ACTH, carbachol or histamine did not. Hence, co-release of catecholamines and serotonin was elicited by non-specific cell membrane depolarization using K+, but not by the specific secretagogues assessed in this study. The adenosine receptor agonist NECA and antagonist DPSPX significantly modified the secretory responses elicited by ACTH, serotonin and carbachol. The results suggest that adenosine may inhibit catecholamine release induced by serotonin or carbachol, while stimulating ACTH-induced release. Although the contribution of the different secretagogues identified in this study has yet to be explored in vivo, our results suggest that the control of catecholamine and serotonin release from the aneural chromaffin tissue of the Atlantic hagfish can be achieved through hormonal and/or paracrine means.

Journal Article↗

PubMed1989

Catecholamines: study of interspecies variation.

In the last three decades, numerous articles on plasma catecholamine concentrations in various settings have been published in the medical literature. Despite this abundance of information, no summary article has analyzed the species variations in circulating catecholamine concentrations. In this paper, the plasma catecholamine responses to various stresses in 31 animal groups have been compiled from greater than 200 publications (with greater than 5000 animal subjects). Primitive cartilaginous fish such as the shark and the lamprey have the highest reported basal plasma catecholamine concentrations. Birds, mammals, and teleost fish have the lowest concentrations. The lower circulating catecholamine concentrations parallel anatomical changes in the development of the adrenal medulla and the development of the nervous system. Decapitation, hypoxia, hemorrhage, and hypothermia are the experimental conditions associated with the greatest stress-induced changes in plasma catecholamine concentrations. The differences in experimental design are tabulated to afford the reader an opportunity to compare catecholamine levels among species. The table provides a detailed guide to normal concentrations and normal responses in 31 species. This report gives a dynamic overview of catecholamine concentrations in human and animal physiology and may be particularly helpful to investigators involved in catecholamine research.

Animals↗

PubMed1981

(3-H)-dihydrotestosterone in catecholamine neurons of rat brain stem: combined localization by autoradiography and formaldehyde-induced fluorescence.

A combined formaldehyde-induced fluorescence (FIF)-autoradiography procedure was used to determine how and where the androgen, dihydrotestosterone (DHT), is associated with catecholamine systems in the rat brain. With this dual localization method, (3H)-DHT target sites can be visualized in relation to catecholamine perikarya and terminals. In the hindbrain, catecholamine neurons adjacent to the fourth ventricle (group A4), the nucleus (n.) olivaris superior (group A5), the n. parabranchialis medialis (group A7), and in the locus coeruleus (group A6) and subcoeruleal regions, as well as in the substantia grisea centralis, concentrate (3H)-DHT in their nuclei. (3H)-DHT target neurons appear to be innervated by numerous catecholamine terminals in the following hindbrain regions: n. motorius dorsalis nervi vagi, n. tractus solitarii, n. commissuralis, n. raphe pallidus, n. olivaris inferior, the ventrolateral portion of the substantia grisea centralis, n. cuneiformis, and the ventrolateral reticular formation in the caudal mesencephalon. In the forebrain, (3H)-DHT concentrates in nuclei of catecholamine neurons located in the n. arcuatus and n. periventricularis (group A12). In addition, (3H)-DHT target neurons appear to be innervated by numerous catecholamine terminals in the following forebrain regions: n. periventricularis rotundocellularis, n. paraventricularis, n. dorsomedialis, n. periventricularis, area retrochiasmatica, n. interstititalis striae terminalis (ventral portion), and n. amygdaloideus centralis. The disclosure of a morphologic association between (3H)-DHT target sites and certain brain catecholamine systems suggests a close functional interdependence between androgens and catecholamines.

Animals↗

PubMed1985

Catecholamine innervation of the caudal spinal cord in the rat.

By means of the aluminum-formaldehyde (ALFA) fluorescence technique for monoamine visualization the distribution of catecholamines was studied in the caudal spinal cord, particularly in relation to motoneurons innervating pelvic structures. In the lumbosacral cord all parts of the spinal gray matter were found to contain catecholamines. In the dorsal horn the most intense fluorescence was seen in the superficial layers. The motoneuron neuropil exhibited the most prominent catecholamine-fluorescence of the ventral horn layers. In the sixth lumbar segment, which contains the motor nuclei that innervate the pelvic striated muscles as well as one innervating muscles in the lower limb, a differential distribution of the density of catecholamine fluorescence was presented by the individual nuclei. The catecholamine fibers in the motoneuron neuropil were seen closely surrounding the motoneuron somata, suggesting the existence of axosomatic contacts, and by utilizing the fluorescent retrograde tracer True Blue in combination with the ALFA method tentative axosomatic noradrenergic synapses on identified neurons innervating small striated pelvic muscles could be visualized in the light microscope. In the intermediate gray the intermediolateral nucleus in thoracic and upper lumbar segments was the most heavily innervated area, followed by the medial lumbar sympathetic group, which contains the majority of the sympathetic preganglionic neurons innervating the pelvic organs. The parasympathetic intermediolateral nucleus in the upper sacral segments received a catecholamine innervation of moderate density. The catecholamine innervation pattern is discussed in relation to the patterns of other putative transmitters. The distribution of catecholamine fluorescence in relation to nuclei that control the pelvic organs differs from the arrangement of other transmitters in this region. The complexity of the innervation of the pelvic organs and their related striated muscles is thus further stressed.

Animals↗

PubMed1994

The pattern of catecholamine response to burst activity in leopard frogs, Rana pipiens.

It is well known that burst activity causes a rapid breakdown of muscle glycogen and extensive accumulation of lactate in frogs. During recovery, it has been shown that lactate is nearly totally recycled into muscle glycogen. Since catecholamines are likely to play some role in the regulation of postexercise repletion of muscle glycogen, the pattern of catecholamine response was assessed in frogs during intense physical activity and the ensuing recovery period. Chronically cannulated frogs were forced to swim until exhaustion, and serial blood samples were taken at regular time intervals for the measurements of catecholamines. The pattern of changes in plasma and muscle lactate and glucose and muscle glycogen during and after burst activity is similar to that reported in previous studies using noncannulated frogs, a result which indicates that the animals recover well from the surgical trauma associated with cannulation. The concentrations of plasma catecholamines in frogs at rest are comparable to those measured in other amphibians, and the levels of plasma epinephrine in resting frogs are much higher than those of norepinephrine. Burst activity causes a marked increase in plasma catecholamines, with higher levels reached by epinephrine. During recovery, the concentration of plasma catecholamines returns to normal within 30 min. Although this pattern of catecholamine response to intense physical activity may be favorable to the repletion of muscle glycogen postexercise, it remains to be clarified how critical the low levels and fast reduction in plasma catecholamines are for optimum glycogen resynthesis.

Animals↗