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PubMed1989

Catecholamine activity in paraventricular hypothalamus after hemorrhage in cats.

Temporal changes in catecholamine activity within the paraventricular nucleus (PVN) of the hypothalamus were assessed using in vivo voltammetry after moderate hemorrhage in chloralose-anesthetized cats. Oxidation current was measured with carbon microelectrodes, and the change at +250 mV was used as an estimate of catecholamine activity. The magnitude and directional change in catecholamine activity was assessed for each site during the initial 3 min of blood loss. Of 62 recording sites, 45 sites were located along the rostrocaudal extent of the medial PVN. Fifteen of these 45 sites exhibited an increase, 15 others exhibited a decrease, and the remaining 15 sites exhibited no change in catecholamine activity. The magnitude of change in oxidation current was independent of the magnitude of the decrease in arterial pressure after hemorrhage. Twelve of the 15 sites that exhibited increases in catecholamine activity were located in the caudal PVN along its dorsomedial aspect, whereas the location of sites that exhibited decreases in catecholamine activity were more widely distributed throughout the nucleus. These data are consistent with the hypothesis that an increase in the release of catecholamines within the caudal PVN in response to hemorrhage is facilitatory for the release of adrenocorticotropin and/or vasopressin.

Adrenocorticotropic Hormone↗
PubMed1992

Evidence against a humoral control mechanism in adrenal catecholamine secretion during insulin-induced hypoglycemia.

The present study tested the hypothesis that a humoral control mechanism is involved in the enhanced adrenal catecholamine secretion during insulin-induced hypoglycemia. The experiments were carried out in anesthetized dogs in which neuronal and humoral components were simultaneously determined by measuring catecholamine output from the right innervated and the left acutely denervated adrenal gland, respectively. Different levels of hypoglycemia were induced by intravenous injection of insulin with doses of 0.075 (n = 6), 0.150 (n = 6), and 0.300 IU/kg (n = 6) in three separate groups of dogs. Catecholamine output in the right innervated gland increased dose dependently (P less than 0.05), reaching a maximum level 45 min after insulin administration. By contrast, catecholamine output from the left denervated adrenal gland remained unchanged at all doses tested. In sham-denervated animals (n = 7), catecholamine output from the left adrenal gland increased to a magnitude similar to that observed in the right innervated gland after insulin administration. Plasma glucose concentration significantly decreased in a dose-dependent manner, reaching a nadir 30 min after insulin administration. Maximum decreases in plasma glucose concentration could be strongly correlated with maximum increases in catecholamine output from the right innervated adrenal gland (r = -0.66, n = 18, P = 0.011), but not with those from the left denervated gland (r = -0.32, n = 18, P = 0.455). The present results do not support the functional existence of a humoral mechanism permitting the release of adrenal catecholamines during insulin-induced hypoglycemia.

Adrenal Glands↗
PubMed2004

Expression of tyrosine hydroxylase in lymphocytes and effect of endogenous catecholamines on lymphocyte function.

OBJECTIVES: To comprehend the changes and significance of the endogenous catecholamines in the immune system, we explored the synthesis of catecholamines by lymphocytes in various lymphoid organs and in different activated states, and the effect of the endogenous catecholamines synthesized by lymphocytes on the function of the lymphocytes themselves. METHODS: Immunohistochemistry for lymphoid organs (mesenteric lymph nodes, spleen and thymus) and lymphocytes was used to observe their expression of tyrosine hydroxylase (TH), an initial rate-limiting enzyme of the catecholamine synthesis. The contents of catecholamines, including norepinephrine (NE), dopamine (DA) and epinephrine (E), in lymphocytes were tested by means of high-performance liquid chromatography with electrochemical detection. Western blot was used to examine the character and relative quantity of TH-stained protein in lymphocytes, lymph nodes and adrenal medullary tissue. The effect of alpha-methyl-P-tyrosine (alpha-MT), an inhibitor of TH activity, on concanavalin A (Con A)-induced interleukin-2 (IL-2) production was determined by MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay. RESULTS: TH-positive cells were found in the three examined lymphoid organs, but the lymph nodes had the highest and the thymus had the lowest density. Both TH expression and the contents of NE, DA and E in the Con A-activated lymphocytes were markedly increased in comparison with those in the nonactivated lymphocytes. A band with TH immunoreactivity was seen in the extracts from either Con A-activated lymphocytes or nonactivated cells and the molecular weight of the protein was 59.4 +/- 0.3 kD. However, the relative quantity of the protein was notably higher in the activated lymphocytes than in the nonactivated cells. As a positive control, a similar band of TH immunoreactivity in the adrenal medullary tissue was also obtained. Alpha-MT at the doses of 10(-11), 10(-10) and 10(-9) M was found to significantly facilitate the Con A-induced IL-2 production. CONCLUSIONS: These results suggest that lymphocytes can synthesize catecholamines and their synthesis levels may increase in the activated state, and that endogenous catecholamines synthesized by the lymphocytes can regulate the function of the lymphocytes themselves.

Animals↗
PubMed1984

Modulation of luteinizing hormone release and catecholamine activity by opiates in the female rat.

Previous studies have shown that the stimulation of LH release by the opiate receptor blocker, naloxone, can be prevented by catecholamine synthesis inhibitors, suggesting opiate regulation of catecholamine release. The present study tested whether an opiate agonist and antagonist would affect the depletion of hypothalamic catecholamines observed after synthesis inhibition, as a measure of catecholamine activity, concomitant with changes in LH secretion. Administration of naloxone to estradiol-primed rats increased LH release and potentiated the depletion of norepinephrine in the preoptic-anterior hypothalamus and medial basal hypothalamus, and enhanced the decline of epinephrine and of dopamine in the medial basal hypothalamus, suggesting increased catecholamine activity in these regions. Administration of the opiate agonist, morphine, to estrogen/progesterone pretreated females decreased LH and decreased the depletion of the catecholamines in the above mentioned areas, suggesting reduced activity. In most cases, naloxone antagonized the inhibitory effect of morphine. These findings indicate that naloxone may stimulate LH release by enhancing hypothalamic catecholamine turnover, possibly by removing the inhibitory influence of an endogenous opioid neuropeptide.

Animals↗
PubMedDate not supplied

Catecholamines in discrete kidney regions. Changes in salt-sensitive Dahl hypertensive rats.

Steady state levels of catecholamines (dopamine, norepinephrine, and epinephrine) were measured by the use of radioenzymatic techniques in discrete areas of the kidney (outer and inner cortex, outer and inner medulla) dissected by a "punch" technique from frozen kidney sections of salt-sensitive (DS) and salt-resistant (DR) Dahl rats fed a low or high salt diet. All three catecholamines were present in all areas of the kidney examined. There were gradients of concentrations of each catecholamine in different kidney areas. Renal medullary areas contained proportionally more dopamine than cortical areas. The proportion of epinephrine with respect to the total catecholamine content was relatively high in the inner medulla. Genetic factors and the amount of dietary salt influenced the catecholamine content in specific kidney areas, and these changes were different according to the area considered. DS rats when fed a high salt diet presented increased systolic blood pressure but no increased levels of dopamine in the inner medulla nor of norepinephrine in the outer medulla and outer cortex. Results suggest that either the uptake, release, storage, synthesis, or catabolism of kidney catecholamines is altered in Dahl salt-sensitive (DS) hypertensive rats and suggest specific roles for each catecholamine in discrete areas of the kidney.

Animals↗
PubMed2002

Phaeochromocytoma with normal urinary catecholamines: the potential value of urinary free metadrenalines.

BACKGROUND: Normal urine catecholamine values in patients with phaeochromocytoma is an occasional finding and may lead to a missed diagnosis. Additional urinary free metadrenaline analysis may be of value in this situation. METHODS: In addition to vanillylmandelic acid, homovanillic acid and the catecholamines, urinary free normetadrenaline (fNMA) and free metadrenaline (fMA) were measured. This report describes six confirmed cases of phaeochromocytoma showing normal urinary catecholamine output and compares fMA results and tumour size with other confirmed cases where the urine catecholamines were increased. RESULTS: Urine catecholamines in these patients with, on average, smaller tumours, were all normal. Urinary fNMA and fMA were available on five patients, and were increased in three. The data suggest that, unlike the catecholamines, urinary fNMA and fMA could be a useful predictor of tumour size. CONCLUSION: The inclusion of fNMA and fMA in the test profile is likely to be of additional benefit in tumour detection, particularly when catecholamines or other metabolites are normal.

Adult↗
PubMed1993

Ca(2+)-dependent stimulatory effect of pituitary adenylate cyclase-activating polypeptide on catecholamine secretion from cultured porcine adrenal medullary chromaffin cells.

Pituitary adenylate cyclase-activating polypeptide (PACAP) stimulates catecholamine secretion from cultured porcine adrenal medullary chromaffin cells in a dose-dependent manner with the half-maximal and maximal doses of 30 nM and 1 microM, respectively. Either removal of extracellular Ca2+ or addition of Gd3+, an inorganic Ca2+ channel blocker, very potently inhibits PACAP-induced catecholamine secretion. Both nicardipine (1 microM) and methoxyverapamil (1 microM), blockers of voltage-dependent Ca2+ channels, are also effective in inhibiting PACAP-induced catecholamine secretion. When the intracellular free Ca2+ concentration ([Ca2+]i) is measured in a fura 2-loaded single chromaffin cell, PACAP is found to cause a sustained increase in [Ca2+]i by mobilizing Ca2+ from both extra- and intracellular pools. It is also found that PACAP stimulates the production of inositol phosphates in a dose-dependent manner, which is not abolished by removal of extracellular Ca2+ unlike the case of nicotine. PACAP increases cAMP content in chromaffin cells in a dose-dependent manner. Removal of extracellular Ca2+ enhances PACAP-induced cAMP production but strongly inhibits PACAP-induced catecholamine secretion. Pretreatment of cells with adenosine-3':5'-monophosphothioate, cyclic, Rp-isomer, a cAMP antagonist, does not block PACAP-induced catecholamine secretion. The addition of forskolin or 3-isobutyl-1-methylxanthine does not enhance the PACAP-induced catecholamine secretion. These results indicate that PACAP activates voltage-dependent Ca2+ channels and phospholipase C as well as adenylate cyclase in cultured porcine adrenal medullary cells and strongly suggest that PACAP-induced catecholamine secretion is mainly mediated by activation of voltage-dependent Ca2+ channels.

Adrenal Medulla↗
PubMed1978

Suppression of plasma catecholamines and flushing by clonidine in man.

Administration of the anti-hypertensive agent clonidine as a single (0.5 mg) oral dose or as multiple doses (0.2-0.4 mg/day for 4 days) markedly reduced plasma catecholamines (decrement = 81 +/- 3% and 68 +/- 5%, respectively; X +/- SE, % of basal; both P less than 0.001) in normal male volunteers. Five patients with various metabolic disorders showed similar responses. The absolute decrements in plasma catecholamines correlated significantly with basal catecholamine levels (P less than 0.001). Clonidine-induced decrements in mean arterial blood pressure correlated significantly with decrements in plasma catecholamines (P less than 0.001). The clonidine effect upon catecholamine levels was reversed by phentolamine (clonidine = -68 +/- 5%; clonidine with phentolamine = -1 +/- 16%). The decrements in catecholamines induced by clonidine in normal subjects were associated with increased sensitivity to the pressor effect of infusion of exogenous norepinephrine. In an analogous fashion flushing associated with endogenous adrenergic discharge was blocked by clonidine, whereas that due to exogenous catecholamines was intensified. These data are compatible with data in experimental animals suggesting that clonidine acts at least in part by interaction with a central alpha adrenergic receptor.

Adenoma, Islet Cell↗
PubMed2001

NPY regulates catecholamine secretion from human adrenal chromaffin cells.

The aim of the present work was to find out whether NPY synthesized in human adrenal chromaffin cells controls in an autocrine/paracrine fashion the release of catecholamines by these cells. Accordingly, the constitutive and regulated release of both NPY and catecholamines was measured simultaneously in cultured human chromaffin cells. In addition, by using both RT-PCR and a combination of specific agonists and antagonists, we characterized the expression of NPY receptors on these cells as well as their pharmacology. Our results were as follows. 1) Human chromaffin cells constitutively secrete NPY. 2) Nicotine elicits a rapid increase in the release of both catecholamines and NPY; this release of NPY is more sustained than that of catecholamines. 3) RT-PCR shows expression of Y1, Y2, Y4, and Y5 receptor mRNA by chromaffin cells; these receptors are functional, as various receptor specific agonists elicit an increase in intracellular calcium. 4) Peptide YY, in contrast to NPY, is not able to stimulate the release of catecholamines. This finding was corroborated by the observation that no receptor-specific antagonists were able to reduce constitutive catecholamine release, whereas an NPY-immunoneutralizing antibody markedly attenuated the secretion. Taken together, these data suggest that NPY originating from the adrenal medulla locally enhances the secretion of catecholamines, presumably by acting via the putative y3 receptor.

Adolescent↗
PubMed2001

Catecholamines in patients with 22q11.2 deletion syndrome and the low-activity COMT polymorphism.

OBJECTIVE: To investigate catecholamine phenotypes and the effects of a tyrosine hydroxylase inhibitor in individuals with the 22q11.2 deletion syndrome and low-activity catechol-O-methyltransferase (COMT). BACKGROUND: Many persons with the 22q11.2 deletion syndrome suffer severe disability from a characteristic ultrarapid-cycling bipolar disorder and associated "affective storms." One etiologic hypothesis for this condition is that deletion of the COMT gene from one chromosome 22 results in increased catecholamine neurotransmission, particularly if the undeleted chromosome 22 encodes a variant of COMT with low activity. METHODS: In a preliminary study, plasma, urine, and CSF catecholamines and catecholamine metabolites were measured in four teenage patients with a neuropsychiatric condition associated with 22q11.2 deletion and the low-activity COMT polymorphism on the nondeleted chromosome. In these four patients, and an additional institutionalized adult with the condition, an uncontrolled, open-label trial of metyrosine was administered in an attempt to lower catecholamine production and to alleviate symptoms. RESULTS: Mild elevations of baseline CSF homovanillic acid (HVA) were found in three of four patients and a moderate reduction in CSF HVA after metyrosine treatment in the patient with the highest pretreatment concentration. The course of the five patients during the clinical trial is described. CONCLUSIONS: In patients with the 22q11.2 deletion syndrome and low-activity COMT, controlled studies of pharmacologic agents that decrease catecholamine production, block presynaptic catecholamine storage, or enhance S-adenosylmethionine, the cosubstrate of COMT, are warranted.

Abnormalities, Multiple↗
PubMed1988

Morphological, cytochemical and neuropharmacological evidence for the presence of catecholamines in hydrozoan planulae.

Planula larvae of Halocordyle disticha were examined for the presence of catecholamines using a multipronged approach. Transmission electron micrographs of planular sensory cells and ganglionic cells demonstrated dense-cored vesicles and electron-dense droplets in both cell types. These vesicles and droplets were similar in morphology to catecholamine-containing granules of vertebrates. Planulae processed with the SPG histofluorescence technique, specific only for catecholamines, exhibited blue-green fluorophores which were most prominent in the anterior ectoderm. Such fluorescence was associated with sensory cells, ganglionic cells and the neural plexus. Pretreatment of planulae with neuropharmacological agents which prevent reuptake (reserpine) or cause release (nicotine, ephedrine) of catecholamines caused a diminution of the fluorophores. Pretreatment of animals with 6-hydroxydopamine, which causes destruction of catecholamine-containing cells, prevented any fluorescent response. Ultrastructural examination of reserpine-treated planulae revealed a dramatic reduction in the populations of dense-cored vesicles and electron-dense droplets. Furthermore, many of the vesicles and droplets remaining in reserpinized animals appeared washed out, i.e. stained faintly. Exposure of planulae to exogenous norepinephrine caused premature, rapid metamorphosis and produced polyps with slightly stunted tentacles and pitted, irregular hypostomes. Exposure of planulae to nicotine caused similar effects. Rearing planulae in sea water containing alpha blockers, phentolamine and tolazoline, had no discernible effect on behaviour (motility, phototactic response) or gross morphology. However, planulae raised in sea water containing propranolol, a beta blocker, ceased all movement, became tack-shaped and died within 72 h. These results meet multiple criteria for the identification of catecholamines in hydrozoan planulae and suggest that such catecholamines may function as neurotransmitters, neurohormones or neuromodulators during larval development.

Animals↗
PubMed2002

[Possible role of a neuropeptide PACAP (pituitary adenylate cyclase-activating polypeptide) on stimulus-secretion coupling in catecholamine neuron].

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide first isolated from ovine hypothalamic tissue. This peptide stimulates adenylate cyclase activation. However, few details were known of the function of this peptide on stimulus-secretion coupling in neuronal cells. The authors have investigated the role of PACAP on catecholamine biosynthesis and secretion using cultured bovine adrenal chromaffin cells as a model for catecholamine-containing neurons. PACAP38, the 38-amino acid form of PACAP, increased cAMP formation in bovine adrenal chromaffin cells. In addition, PACAP38 increased [Ca2+]i associated with PI turnover and Ca2+ influx into the cells. The synthesis of catecholamine and the phosphorylation of tyrosine hydroxylase, a rate-limiting enzyme of catecholamine biosynthesis, stimulated by the maximal effective concentration of dibutyryl cAMP or a high concentration (56 mM) of K+ were further enhanced by PACAP38. Thus PACAP38 stimulated the pathway of catecholamine biosynthesis mainly by both activation of cAMP- and Ca2(+)-dependent protein kinases. On catecholamine secretion from the cells, the effect of PACAP38 was markedly potentiated by addition of ouabain, an inhibitor of Na+/K+ ATPase. This markedly potentiated secretion was greatly reduced with Na+ omitted-sucrose medium. PACAP38 increased 22Na+ influx into the cells treated with ouabain. Thus PACAP38 with ouabain stimulated catecholamine secretion by accumulation of intracellular Na+, resulting in an increase in Ca2+ influx. These results indicate that the neuropeptide PACAP has an important role in stimulus-secretion coupling in adrenal chromaffin cells.

Animals↗
PubMed1990

Stimulatory action of Ba2+ on catecholamine biosynthesis in cultured bovine adrenal chromaffin cells: possible relation to protein kinase C.

The effect of Ba2+ on the catecholamine biosynthetic activity was studied by measuring the formation of [14C]catecholamines from L-[14C]tyrosine in cultured adrenal chromaffin cells. In the absence of Ca2+, [14C]catecholamine formation was markedly stimulated by Ba2+, and this stimulation was observed in a manner dependent on its concentration. The stimulation of [14C]catecholamine formation by relatively low concentrations of Ba2+ was suppressed by polymyxin B, a typical inhibitor of Ca2+/phospholipid-dependent protein kinase (protein kinase C); and this inhibitory action of polymyxin B was attenuated by increasing the Ba2+ concentration. On the other hand, a tendency toward the enhancement of Ba2+-stimulated [14C]catecholamine formation was observed by a protein kinase C activator, 12-O-tetradecanoylphorbol 13-acetate (TPA). In contrast to the acute effect of TPA, [14C]catecholamine formation stimulated by Ba2+ was reduced by long-term exposure of chromaffin cells to a high concentration of TPA, which has already been reported to cause the reduction of protein kinase C activity as a result of the down-regulation of this enzyme. These findings suggest that Ba2+ stimulates catecholamine biosynthesis, probably through its direct action on protein kinase C in adrenal chromaffin cells.

Adrenal Glands↗
PubMed1977

[Effect of phentolamine on the catecholamine output from the perifused pig adrenal medulla in response to infusions of acetylcholine (author's transl)].

The effect of phentolamine (regitine) on the in vitro release of catecholamines from adrenal medulla has been studied. Firstly, a continuous flow incubation (perifusion) system was developed in which secretory responses of adrenal medulla to acetylcholine were characterized by serial fluorimetric assay of catecholamine in the effluent medium. There was an initial massive release of catecholamine, which in the absence of acetylcholine, declined to a low basal level. The basal level was stable. Following 2.5 h preincubation, catecholamine release rose abruptly after addition of 10(-2) M acetylcholine to the medium and returned promptly to baseline after withdrawal. Pretreatment of pig adrenal medulla with 10(-2) M phentalamine blocked the increase of catecholamine overflow by 10(-2) M acetylcholine. It was also found that phentolamine, itself, caused no effect on catecholamine release from adrenal medulla. These results show that phentolamine blocked the catecholamine release from perifused pig adrenal medulla in response to acetylcholine infusion.

Acetylcholine↗
PubMed1999

Catecholamine production in patients with gastroenteropancreatic neuroendocrine tumors.

OBJECTIVE: Amine precursor uptake and decarboxylation is a classical feature of gastroenteropancreatic (GEP) neuroendocrine tumors (NET). Production of catecholamines was studied in GEP NET and non-NET patients. DESIGN: A cross-sectional study was undertaken. METHODS: We studied catecholamine and metabolite secretion in 115 consecutive GEP NET patients and in 20 patients with non-NET. After specific extraction, vanilmandelic acid, homovanilic acid, catecholamines (norepinephrine, epinephrine, dopamine) and methoxylated derivates (metanephrine, normetanephrine, methoxytyramine) in urinary extracts were analyzed by high performance liquid chromatography. Results were indexed to the 24-h urinary creatinine levels. RESULTS: Among the 115 patients with NET, 9 (8%) had an increase of at least one urinary catecholamine or metabolite; in 7 out of the 9 the increase was slight being less than twice the upper value of the normal range. Elevated urinary dopamine (3 patients), methoxytyramine (6 patients), norepinephrine (2 patients) and normetanephrine (2 patients) were found. No increased urinary excretion of epinephrine nor metanephrine was observed. An adrenal mass existed in one of these nine patients but metaiodobenzylguanidine scintigraphy was negative as was immunohistochemistry for epithelial markers. None of the 20 patients with non-NET demonstrated an increased excretion of catecholamine or metabolites. No relationships were found between catecholamine and metabolite excretions and patients' tumor and treatment characteristics. CONCLUSION: Production of catecholamines and metabolites is a rare event in GEP NET patients. Histological results, including positive immunohistochemistry for epithelial markers may help to diagnose GEP NET.

Adult↗
PubMed2003

Adhesion molecules, catecholamines and leucocyte redistribution during and following exercise.

The circulating blood normally contains no more than 1-2% of the body's population of leucocytes. The numbers and phenotypes of circulating leucocyte subsets can change dramatically during and immediately following exercise. The surface expression of adhesion molecules makes an important contribution to such responses by changing patterns of cell trafficking. Alterations in the surface expression of adhesion molecules could reflect a shedding of molecules, selective apoptosis or differential trafficking of cells with a particular phenotype, effects from mechanical deformation of the cytoplasm, active biochemical processes involving cytokines, catecholamines, glucocorticoids or other hormones, or changes in the induction of adhesion molecules. The expression of adhesion molecules changes with maturation and activation of leucocytes. Typically, mature cells express lower densities of L-selectin (CD62L), the homing receptor for secondary lymphoid organs, and higher densities of LFA-1 (CD11a), the molecule associated with trafficking to non-lymphoid reservoir sites. The neutrophils and natural killer cells that are mobilised during exercise also express high levels of Mac-1 (CD11b), a marker associated with cellular activation. Possibly, exercise demarginates older cells that are awaiting destruction in the spleen. Plasma concentrations of catecholamines rise dramatically with exercise, and there is growing evidence that catecholamines, acting through a cyclic adenosine monophosphate second messenger system, play an important role in modifying the surface expression of adhesion molecules. Analogous changes can be induced by other forms of stress that release catecholamines or by catecholamine infusion, and responses are blocked by beta(2)-blocking agents. Catecholamines also modify adherence and expression of adhesion molecules in vitro. Cell trafficking is modified by genetic deficiencies in the expression of adhesion molecules, but leucocyte responses to exercise and catecholamines are generally unaffected by splenectomy. A number of clinical conditions including atherogenesis and metaplasia are marked by an altered expression of adhesion molecules. The effects of exercise on these molecules could thus have important health implications.

Apoptosis↗
PubMed1994

Changes in plasma catecholamines during fever induced by bacterial endotoxin and interleukin-1 beta.

We have examined whether or not the release of catecholamines into the blood circulation of rabbits during fever is mediated by prostaglandins. The plasma levels of catecholamines (epinephrine and norepinephrine) were measured in 2 ml of blood withdrawn from the marginal ear vein. At an ambient temperature of 21 +/- 1 degree C, intravenous injection of either lipopolysaccharide (LPS, 4 micrograms/kg) or human recombinant interleukin-1 beta (rIL-1 beta, 1 microgram/kg) produced a biphasic fever accompanied by an increase in the plasma level of catecholamines. Pretreatment with intravenous indomethacin (1 mg/kg) markedly suppressed the increase in catecholamines induced by LPS and rIL-1 beta. In contrast, although intracerebroventricular injection of rIL-1 beta (20 ng) produced fever, it did not produce a significant change in plasma catecholamine levels. Similarly, intrahypothalamic injection of prostaglandin E2 (200, 800 ng) induced fever, but did not cause a significant change in catecholamine concentrations. These results suggest that IL-1 acts via prostaglandins on the peripheral tissues to release catecholamines into the circulation.

Animals↗
PubMed1985

Circadian variations of free and sulfoconjugated catecholamines in normal subjects.

Normotensive recumbent subjects exhibit an early (11 p.m.) nocturnal increase in plasma dopamine, norepinephrine and epinephrine sulfates. In individual patients, this peak value is followed by a smaller nocturnal peak of catecholamine sulfates, while free catecholamine levels change in a direction opposite to catecholamine sulfates. This reciprocity of changes cannot however be demonstrated in the whole group. The origin of the nocturnal peaks of catecholamine sulfates is unknown. It may be due to a nocturnal decrease of the renal clearance of catecholamine sulfates, an increased generation of sulfates for reasons other than an increase in the free catecholamine substrate, or possibly a release of catecholamine sulfates from the brain.

Adult↗