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PubMed1987

Effects of 2-hydroxyoestradiol, oestradiol and testosterone on FSH-induction of catecholamine- and gonadotrophin-responsive progesterone biosynthesis in rat granulosa cell cultures.

Catecholamine- and gonadotrophin-responsive progesterone biosynthesis increases during FSH-induced granulosa cell maturation. In this study, we compared in vitro effects of interrelated classes of follicular steroid on both endpoints: an androgen (testosterone), an oestrogen (oestradiol) and an oestradiol metabolite (2-hydroxyoestradiol). Granulosa cells from diethylstilboestrol-pretreated, immature rat ovaries were cultured for 48 h (pretreatment) in serum-free medium containing human FSH with or without steroid. The cell monolayers were then washed and reincubated for a further 24 h (test-treatment) in fresh medium with and without a catecholamine (isoproterenol or norepinephrine) or a gonadotrophin (FSH or hCG); test-treatment culture medium was collected and assayed for progesterone content. At concentrations up to 10(-6) M, each steroid enhanced dose-dependently basal and catecholamine-responsive progesterone production with a ranked potency-order of testosterone greater than 2-hydroxyoestradiol much greater than oestradiol. All three compounds also enhanced FSH and hCG responsiveness but this endpoint was affected most markedly by oestradiol. Pretreatment in the presence of specific antiandrogen (hydroxyflutamide; SCH16423) blocked the stimulatory effects of testosterone and 2-hydroxyoestradiol but did not inhibit stimulation by oestradiol, highlighting similarities between the actions of testosterone and the catechol oestrogen distinct from that of oestradiol. Test-treatment in the presence of beta-adrenergic antagonist (propranolol) blocked the stimulatory action of isoproterenol and reduced the response to FSH, suggesting the involvement of beta-adrenergic receptors in FSH as well as catecholamine action on steroidogenesis. We conclude that testosterone and catechol oestradiol have major effects on FSH-induced development of catecholamine responsive steroidogenesis whereas oestradiol mainly affects gonadotrophin responsiveness in this granulosa cell culture system. All three steroid types could interact with gonadotrophins and locally produced catecholamines to influence granulosa cell function in vivo.

Animals↗
PubMed1995

Age-related changes in plasma catecholamine responses to chronic intermittent stress.

We examined habituation and sensitization of plasma catecholamine responses to stressful stimulation in young adult (3 months) and aged (22 months) Fischer 344 (F-344) male rats. Aged rats had greater elevations in plasma levels of norepinephrine (NE) and epinephrine (EPI) following exposure to restraint stress compared to young adult controls. Within ages, plasma catecholamine responses were similar in rats stressed for the first time compared to those stressed for the 27th time. When chronically stressed young adult and aged F-344 rats were exposed to a novel stressor, swim stress at 25 degrees C, plasma catecholamine responses were significantly greater than for age-matched handled controls. The magnitude of sensitization of plasma catecholamine responses to the novel stressor was similar for young adult and aged F-344 rats. These results indicate that aged rats have enhanced plasma catecholamine responses to acute restraint stress compared to young adults. In addition, rats of both ages displayed comparable levels of sensitization of plasma catecholamine responses to a novel stressor. These findings emphasize that aged rats differ from young adult rats in some but not all aspects of sympathetic-adrenal medullary regulation. Further, these age-related differences in sympathetic-adrenal medullary responses are unmasked when animals are exposed to stressful stimulation.

Adrenal Medulla↗
PubMed1989

Evidence that hypoxemia promotes catecholamine release during hypercapnic acidosis in rainbow trout (Salmo gairdneri).

The concentrations of plasma catecholamines, epinephrine and norepinephrine, were monitored in rainbow trout (Salmo gairdneri) after acute (30 min) exposure to various levels of external hypercapnia (water PCO2 (PwCO2) = 0-11.3 Torr) under normoxic (water PO2 (PwO2) = 153 +/- 1.1 Torr) or hyperoxic (PwO2 = 653 +/- 27.0 Torr) conditions. Whole blood pH decreased to a similar extent as a function of external carbon dioxide tensions in both the normoxic and hyperoxic hypercapnic groups. Arterial oxygen content, however, declined only during normoxic hypercapnia. Similarly, plasma catecholamines (primarily epinephrine) increased only during normoxic hypercapnia in proportion to the severity of the whole blood acidosis. Epinephrine levels were elevated 10-fold from 0.70 +/- 0.06 nM to 7.06 +/- 3.7 nM at the highest concentration of external CO2 (11.3 Torr) whereas norepinephrine increased 3-fold from 0.56 +/- 0.07 nM to 1.62 +/- 0.40 nM. The absence of catecholamine release into the circulation during hyperoxic hypercapnia was not due to inhibition of the 'catecholamine-releasing process' by abnormally elevated arterial oxygen tensions (PaO2 = approximately 400 Torr) because acutely anaemic and thus hypoxemic fish (haematocrit = 4.9 +/- 0.7%) displayed identical elevations of plasma catecholamines under both normoxic and hyperoxic conditions. The results of these experiments demonstrate that arterial hypoxemia, rather than blood acidosis per se, is the proximate stimulus causing catecholamine mobilization in rainbow trout during short-term environmental hypercapnia.

Acidosis↗
PubMed1990

Catecholamine release controlled by blood oxygen tension during deep hypoxia in trout: effect on red blood cell Na/H exchanger activity.

Changes in plasma catecholamine levels were measured in trout exposed to acute hypoxia, in order to correlate with acid-base disturbances due to activation of the cAMP-dependent Na+/H+ antiporters of red blood cells, as previously described (Fiévet B., Respir. Physiol. 74, 99-114, 1988). The extracellular acidosis corresponding with the stimulation of the exchangers, occurred when arterial oxygen partial pressure (PaO2) reached around 15 Torr (Thomas S., Respir. Physiol. 74, 77-90, 1988). This blood pH drop coincided with a marked increase in plasma catecholamine levels. The catecholamine secretion was transient and the hormones were cleared provided PaO2 remained above 10 Torr. On the other hand, when PaO2 remained below 10 Torr, there was a persistent secretion of catecholamines. This is in agreement with the fact that the exchangers are 'turned off' or sustained when PaO2 remains above or below 10 Torr respectively, as previously described. Following the transient hormone peak when PaO2 stabilized above 10 Torr, it was possible to trigger the second pattern of continuous catecholamine secretion by controlling water PO2 so that PaO2 declined below 10 Torr. We conclude that the blood oxygen level controls catecholamine secretion during deep hypoxia.

Acid-Base Imbalance↗
PubMedDate not supplied

Neuropeptide tyrosine (NPY)-induced potentiation of the pressor activity of catecholamines in conscious rats.

IV bolus administration of 2.5-50 micrograms NPY (0.6-12.5 nmol) to conscious rats produced a dose- and time-dependent increase in systolic and diastolic blood pressure. Following priming with 2.5 micrograms NPY, or larger doses, the subsequent administrations of noradrenaline produced pressor responses that were potentiated both in magnitude and duration. The NPY-induced potentiation of the pressor response to noradrenaline was dose-dependent and extended to the pressor action of adrenaline and angiotensin II but not to the hypotensions produced by bradykinin or isoproterenol. The potentiation was not related to the fact that multiple doses of catecholamines were repeated. Reserpine did not substantially modify the NPY-induced potentiation of the pressor activity of the catecholamines. Chemical sympathectomy following 6-hydroxydopamine caused a marked supersensitivity to the catecholamines and NPY but obliterated the NPY-induced potentiation of the pressor effect of adrenaline. Nifedipine reduced the pressor action of the catecholamines and NPY but did not attenuate the NPY-induced potentiation of the pressor action of catecholamines. It is concluded that the acute pressor effect of NPY and of the potentiation of the catecholamine pressor effects involve different mechanisms.

Animals↗
PubMed1979

L-Dopa repairs deficits in locomotor and investigatory exploration produced by denervation of catecholamine terminal fields in the forebrain of rats.

In a previous study rats were shown to have decreased locomotor and investigatory exploration after bilateral microinjections of 6-hydroxydopamine into the anterolateral hypothalamus. These deficits correlate with the loss of catecholamine terminals in neocortical, limbic, and anteromedioventral striatal brain sites. To test whether this correlation was causal, central catecholamines were increased by the intraperitoneal administration of L-3,4-dihydroxyphenylalanine (L-dopa), 10--40 mg/kg) after inhibition of extracerebral L-amino acid decarboxylase. Such treatment repaired the deficits in locomotor exploration and investigation in 6-hydroxydopamine rats. Pretreatment with the catecholamine antagonist chlorpromazine (1--2 mg/kg) blocked the increase in locomotor exploration and investigation produced by L-dopa in 6-hydroxydopamine rats. The results suggest, but do not prove, that L-dopa produced these behavioral effects by increasing central catecholamines at the denervated catecholamine receptor sites in the forebrain. These data and the data from the previous study are complementary evidence for the hypothesis that forebrain catecholamine synaptic action is necessary for normal exploratory behavior.

Animals↗
PubMed1984

Glucocorticoids and catecholamines as mediators of acute-phase proteins, especially rat alpha-macrofoetoprotein.

Adrenal hormones were studied as possible triggering substances of the synthesis of acute-phase reactants in rats. alpha-Macrofoetoprotein, which rises sharply in concentration during inflammation, was used to monitor the acute-phase reaction. In normal rats glucocorticoids and catecholamines induce alpha-macrofoetoprotein synthesis; glucocorticoids only increase alpha-macrofoetoprotein to moderate levels in plasma, but catecholamines enhance alpha-macrofoetoprotein synthesis to very high levels, comparable with those observed in the post-injury phase. However, catecholamines in vivo also activate the adrenal cortex, suggesting a synergistic effect of both kinds of adrenal hormones. Our study showed that in adrenalectomized rats, the effect of catecholamines on alpha-macrofoetoprotein synthesis is greatly diminished, whereas the moderate effect of glucocorticoids remains. Combination of glucocorticoids and catecholamines induces extremely high alpha-macrofoetoprotein levels in both adrenalectomized and normal rats. With crossed immunoelectrophoresis it was shown that other acute-phase reactants, such as haptoglobin and alpha 1-major acute-phase protein, are affected differently by the hormones. Contrary to glucocorticoids, catecholamines give a pattern comparable with that found after surgical injury.

Acute-Phase Proteins↗
PubMed1998

Catecholamines, hypoxia and high altitude.

Hypoxia is a potent activator of the sympathetic nervous system by stimulating arterial chemoreceptors. However, out of 15 laboratory studies on the effects of acute and prolonged hypoxia on catecholamines, 14 failed to show any changes in plasma or urinary noradrenaline and only four studies showed significant increases in plasma or urinary adrenaline. By contrast, six out of eight studies on MSNA showed increased sympathetic nerve activity to the leg. An increased clearance of plasma catecholamines during hypoxia may be a possible explanation. Furthermore, many of the studies had limitations in a number of subjects and catecholamine assays used. Emotional aspects of the study protocols, which could contribute to the increase in adrenaline, was only assessed by sham runs in one chamber study. However, 13 out of 14 reviewed field studies on subjects staying for more than 1 week at high altitude, reported increased plasma or urinary excretion of noradrenaline which may be compatible with increased sympathetic activity. Adrenaline changed to a lesser degree. Out of seven studies on more short-term (4 h to 3 days) exposure to high altitude, only one demonstrated significantly increased plasma noradrenaline. In this study, however, several subjects had been exposed to high altitude less than 1 week before the experiment. In a new study on 12 climbers reported in this paper, a temporary reduction in plasma catecholamines was found 2 days after arrival at 4200 m. There was a steady increase towards normal levels after 1 week. Plasma vasopressin (AVP) increased suggesting a compensatory mechanism. Both plasma noradrenaline and adrenaline were positively correlated with oxygen saturation in these subjects. Thus, in previously unacclimatized subjects, short-term exposure to high altitude does not increase plasma catecholamines, rather plasma levels decreased. In addition to increased clearance, there is some evidence of reduced synthesis of catecholamines during short-term hypoxia. The oxygen sensitivity of tyrosine hydroxylase (TH) activity, may be one possible mechanism.

Acclimatization↗
PubMed1997

The effect of enteric bacterial toxins on the catecholamine levels of the rabbit.

The rabbit catecholamine responses to bacterial toxins commonly found in Sudden Infant Death Syndrome (SIDS) victims were studied as part of a proposed animal model for SIDS. Six bacterial toxins commonly isolated from SIDS baby feces and a comparison endotoxin were injected intravenously (i.v.) and intraluminarily (i.l.) to determine their effects on catecholamine levels. I.v. injected toxins clearly altered catecholamine levels causing sharp rises in adrenaline and noradrenaline levels and at critical toxin concentrations sudden death ensued. Clostridium perfringens enterotoxin and alpha-toxin, Clostridium difficile enterotoxin (A) and cytotoxin (B), Escherichia coli STa toxin and staphylococcal enterotoxin B caused rises in catecholamine levels similar to that caused by E. coli endotoxin. Control rabbits showed very little or no obvious change in catecholamine levels. Clostridium difficile enterotoxin (A) and cytotoxin (B) injected i.v. exhibited synergy. Toxins injected into the duodenum, jejunum, ileum, cecum and large intestine caused behavioural changes ranging from reduced appetite and diarrhea to, in rare cases, death. Changes in the catecholamine levels of these animals however were not significantly different from those of the control animals. The results are discussed in relation to the possible effect of certain conditions (physiological, viral infections and environmental) which increase toxin permeability and allow absorption of these toxins, possibly resulting in sudden infant death.

Animals↗
PubMed1974

A cyclic adenosine monophosphate link in the catecholamine enhancement of transmitter release at the neuromuscular junction.

The frequency of miniature endplate potentials (mepps) in rat diaphragms was markedly increased by epinephrine and norepinephrine in preparations exposed to 15 mM K(+). The effect was rapid in onset but gradually declined during continued exposure to the catecholamines. N(6), O(2')-dibutyryl adenosine 3',5'-monophosphate (dibutyryl-cAMP) also caused transient frequency increases resembling in time-course those observed with catecholamines. Contrary to previous reports, catecholamines and dibutyryl-cAMP had little effect on mepp frequency in preparations not treated with K(+). Sustained increases with theophylline and decreases with adenosine were found in both K(+)-treated and untreated preparations. Analysis of the data obtained with catecholamines showed the intensity of the response to be a function of nerve terminal polarization. The inability of catecholamines and dibutyryl-cAMP to affect mepp frequency of untreated preparations argues against an obligatory role for cAMP in the neurosecretory mechanism. The findings are consistent with an action of catecholamines and cAMP in the regulation of transmitter release at fatigued preparations.

Animals↗
PubMed2005

Beta2-adrenergic receptors mediate the differential effects of catecholamines on cytokine production of PBMC.

We determined characteristics of beta2-adrenergic receptors (beta2R) on peripheral blood mononuclear cells (PBMC) and cytokine production after mitogenic stimulation and coincubation with catecholamines. PBMCs were stimulated with interleukin-2 (IL-2), tetanus toxoid (TT), anti-CD3 antibody, or phytohemagglutinin (PHA). The cytokines interferon-gamma (IFN-gamma), IL-4, and IL-6 were determined by ELISA following coincubation with high-dose (10(-5) M) and low-dose (10(-9) M) epinephrine (EPI) and norepinephrine (NE). Intracellular IFN-gamma and IL-4 were studied by FACS analysis. The beta2R density was investigated using a radioligand binding assay. The stimuli induced various cytokine profiles in PBMCs. Synthesis of IFN-gamma was induced by all mitogens and could be suppressed by catecholamines (26%-85% reduction). In PHA-stimulated PBMCs, IL-4 synthesis was decreased by high-dose catecholamines (24%-28% reduction). Adding a beta-blocking agent attenuated most catecholamine effects. A highly significant negative correlation between the density of beta2R with IFN-gamma and IL-6 levels of PHA-activated PBMCs (r = -0.88 to -0.96, p < 0.01-< 0.001) was observed. The results indicate that the density of beta2R on PBMC plays a role in mediating the differential catecholamine effects on cytokine production of PBMC. Furthermore, changes in cytokine expression induced by catecholamines favor Th2 responses.

Cyclic AMP↗
PubMed1991

Catecholamine release and arrhythmias in acute myocardial ischaemia.

Increased sympathetic activity is assumed to contribute substantially to the occurrence of malignant arrhythmias in patients with coronary heart disease, since the rate of sudden cardiac death is significantly reduced by beta-adrenoceptor blockade, but not by antiarrhythmic agents such as flecainide or encainide. During acute myocardial ischaemia, adrenergic stimulation of the ischaemic myocardium is independent of plasma catecholamines. Rather, it is caused by the combination of excessively high local noradrenaline concentrations and an enhanced responsiveness of the myocyte to catecholamines. Myocardial ischaemia of 15 min duration results in a 100-fold increase in catecholamine concentrations within the extracellular space of the ischaemic zone, a two-fold increase in functionally coupled alpha-adrenoceptors, and a 30% increase in beta-adrenoceptors. Within the first 10 min of ischaemia, the myocardium is protected from excessive catecholamine release. Ischaemia-associated metabolic alterations, such as extracellular potassium accumulation, acidosis, and especially the accumulation of adenosine reduce the transmitter release caused by central sympathetic activation. Furthermore, the functional neuronal amine reuptake (uptake1) prevents excessive local accumulation of noradrenaline. With progression of ischaemia to more than 10 min, local nonexocytotic catecholamine release becomes predominant. This release is independent of central sympathetic nerve activity, availability of extracellular calcium, activation of both neuronal calcium channels and protein kinase C, and it is not accompanied by the release of sympathetic cotransmitters such as neuropeptide Y. It has been demonstrated to be nonexocytotic and to be caused by a carrier-mediated transport of noradrenaline from the sympathetic nerve ending into the synaptic cleft. This release is not modulated through presynaptic receptors. It is, however, suppressed by blockers of uptake1 and by inhibitors of sodium-proton exchange. Depletion of cardiac catecholamine stores by chronic surgical or chemical sympathectomy effectively suppresses malignant arrhythmias induced by experimental coronary ligature. Accordingly, inhibitors of nonexocytotic noradrenaline release, such as uptake1 blocking agents or sodium-proton exchange inhibitors, effectively reduce the occurrence of ischaemia-associated ventricular fibrillation, emphasizing the relevance of nonexocytotic release mechanisms in myocardial ischaemia.

Animals↗
PubMed1991

Detailed examination of the mechanism and site of action of progesterone and corticosteroids in the regulation of gonadotropin secretion: hypothalamic gonadotropin-releasing hormone and catecholamine involvement.

Progesterone and certain corticosteroids, such as deoxycorticosterone (DOC) and triamcinolone acetonide (TA), can stimulate gonadotropin surges in rats. The mechanism of these steroids could involve a pituitary or hypothalamic site of action, or both. Progesterone and TA did not alter the ability of GnRH to release LH or FSH either before, during, or after the gonadotropin surge induced by these steroids in estrogen-primed ovariectomized female rats. Furthermore, progesterone, TA and DOC were unable to induce a gonadotropin surge in short-term estrogen-primed castrated male rats. These results suggested a hypothalamic rather than a pituitary site of action of progesterone and corticosteroids in the release of gonadotropins. Since progestin and corticosteroid receptors are present in catecholamine neurons, a role for catecholamine neurotransmission in progesterone and corticosteroid-induced surges of LH and FSH in estrogen-primed ovariectomized rats was examined. Catecholamine synthesis inhibitors and specific alpha 1 (prazosin), alpha 2 (yohimbine), and beta (propranolol) receptor antagonists were used to determine the role of catecholamine neurotransmission in the steroid-induced surges of LH and FSH. Both of the catecholamine synthesis inhibitors, alpha-methyl-p-tyrosine HCl (alpha-MPT), a tyrosine hydroxylase inhibitor, and sodium diethyldithiocarbamate (DDC), an inhibitor of dopamine-beta-hydroxylase, attenuated the ability of progesterone, TA, and DOC to induce LH surges when administered 3 h and 1 h, respectively, before the steroid. DDC also suppressed the ability of progesterone, TA, and DOC to induce FSH surges. Rats treated with alpha-MPT had lower mean FSH values than did steroid controls, but the effect was not significant. Both the alpha 1 and alpha 2 adrenergic antagonists, prazosin and yohimbine, significantly suppressed the ability of progesterone, TA, and DOC to induce LH and FSH surges. In contrast, the beta adrenergic receptor blocker, propranolol, had no effect upon the ability of progesterone, TA, or DOC to facilitate LH and FSH secretion. Finally, the stimulatory effect of progesterone and TA upon LH and FSH release was found to be blocked by prior treatment with a GnRH antagonist, further suggesting hypothalamic involvement. In conclusion, this study provides evidence that the stimulation of gonadotropin release by progesterone and corticosteroids is mediated through a common mechanism, and that this mechanism involves the release of GnRH, most likely through catecholaminergic stimulation. Furthermore, catecholamine neurotransmission, through alpha 1 and alpha 2 but not beta receptor sites, is required for the expression of progesterone and corticosteroid-induced surges of LH and FSH in estrogen-primed ovariectomized rats.

Adrenal Cortex Hormones↗
PubMed1994

Effect of continuous venovenous hemofiltration with dialysis on hormone and catecholamine clearance in critically ill patients with acute renal failure.

OBJECTIVES: To measure the effect of continuous venovenous hemofiltration with dialysis on cardiovascular stability in the critically ill patients and to assess the extraction of a number of hormones and catecholamines by continuous venovenous hemofiltration with dialysis. DESIGN: Prospective, clinical study. SETTING: Intensive care unit of a tertiary medical center. PATIENTS: Twenty critically ill patients with acute renal failure. INTERVENTIONS: Timed collections of serum and ultradiafiltrate in patients receiving continuous venovenous hemofiltration with dialysis, with measurements of their catecholamine and hormonal content and calculation of continuous venovenous hemofiltration with dialysis clearances and daily extractions. Correlation of changes in catecholamines with prospectively collected hemodynamic data during the first 24 hrs of continuous venovenous hemofiltration with dialysis therapy. MEASUREMENTS AND MAIN RESULTS: No significant changes in dopamine, epinephrine, and norepinephrine requirements or plasma concentrations were seen during the first 24 hrs of continuous venovenous hemofiltration with dialysis. Overall daily losses of catecholamines in the ultradiafiltrate were small (dopamine 404 micrograms; epinephrine 32 micrograms; norepinephrine 29 micrograms). Hemodynamic variables remained stable during this period of continuous venovenous hemofiltration with dialysis therapy. All studied hormones were detected in the ultradiafiltrate, but their mean daily extractions were very small (aldosterone 0.37 micrograms; parathyroid hormone 53.4 pmol; cortisol 4.8 mg; T4 and T3 [trace amounts]; thyroid-stimulating hormone 2.6 mU; testosterone [trace amounts]). CONCLUSIONS: In critically ill patients with acute renal failure, continuous venovenous hemofiltration with dialysis results in minimal losses of catecholamines and is associated with cardiovascular stability. It causes only minor losses of several hormones. These losses are unlikely to be clinically important. Thus, blood purification achieved by continuous venovenous hemofiltration with dialysis does not produce significant catecholamine or hormonal losses and is associated with hemodynamic stability.

Acute Kidney Injury↗
PubMed1998

Human immune cells mediate catecholamine secretion from adrenal chromaffin cells.

OBJECTIVES: To determine the ability of human mononuclear cells to produce factors that cause catecholamine secretion from adrenomedullary chromaffin cells; to determine conditions that stimulate mononuclear cells to produce such factors; and to compare these results with catecholamine secretion in response to the cytokines interleukin (IL)-1 and IL-2. DESIGN: Randomized, controlled, prospective study using in vitro conditions. SETTING: University research laboratory. SUBJECTS: Human mononuclear cells and porcine chromaffin cells. INTERVENTIONS: Circulating human mononuclear cells were isolated and cultured overnight in RPMI media. Cell-free media from these cultures (conditioned media) were then tested for the ability to cause epinephrine secretion from porcine chromaffin cells. Mononuclear cells were stimulated with phytohemagglutinin or by mixing cells from two different individuals while suppression was tested with dexamethasone. Catecholamine secretion in response to IL-1 and IL-2 (50 and 500 units/well, respectively), or nicotinic agonist dimethylphenylpiperazinium (10 microM, which mimics the action of acetylcholine), was tested for comparison. MEASUREMENTS AND MAIN RESULTS: Isolated porcine chromaffin cells had stable catecholamine content at the time of secretion measurements, and catecholamine release from cells into the media was measured using electrochemical detection after high-performance liquid chromatography separation. Catecholamine secretion was expressed as a percentage of the total cellular content. Epinephrine secretion due to human conditioned media was 6.9 +/- 1.0% compared with 1.4 +/- 0.6% for control media (p < .05) and 14.6 +/- 3.3% for dimethylphenylpiperazinium (p < .05). Epinephrine secretion with conditioned media from mixed cells (mixed leukocyte reaction) was 16.6 +/- 1.2%, which was higher than the epinephrine secretion caused by media from a single donor (6.9% +/- 1.0, p < .001). Pretreatment with dexamethasone inhibited the formation of bioactive products from mixed mononuclear cell preparations. Cytokines IL-1 and IL-2 did not stimulate chromaffin cell epinephrine secretion above background release with control media incubation. In all cases, norepinephrine secretion was similar to that of epinephrine, and results are included in all figures. CONCLUSIONS: Factors released from human immune cells can mediate epinephrine and norepinephrine release from adrenomedullary cells through a nonneural mechanism. Such immune cell factor release can be modulated by immunostimulation and steroid suppression. Release of such factors in vivo may contribute to increased circulating epinephrine in response to infectious challenge and may be an important factor in the critically ill patient.

Animals↗
PubMed1982

On the mechanism of the involvement of monoamine oxidase in catecholamine-stimulated prostaglandin biosynthesis in particulate fraction of rat brain homogenates: role of hydrogen peroxide.

The mechanism of involvement of monoamine oxidase (MAO) in catecholamine-stimulated prostaglandin (PG) biosynthesis was studied in the particulate fraction of rat brain homogenates. High concentrations of either noradrenaline (NA) or dopamine (DA) stimulated effectively PGF2 alpha formation. The same amount of 2-phenylethylamine (PEA) acted similarly, provided that it was administered together with a catecholamine analogue or metabolite possessing the 3,4-dihydroxyphenyl nucleus--3,4-dihydroxyphenylalanine (DOPA), 3,4-dihydroxyphenylacetic acid (DOPAC), 3,4-dihydroxyphenylglycol (DOPEG), 3,4-dihydroxyphenylacetaldehyde (DOPAL), or alpha-methylnoradrenaline (alpha-met-NA)--or with SnCl2. In the absence of PEA, these compounds were ineffective with regard to stimulation of PGF2 alpha formation. Catalase, pargyline, or indomethacin abolished completely PGF2 alpha formation elicited either by catecholamines or by PEA plus a 3,4-dihydroxyphenyl compound or SnCl2. With regard to the stimulation of PGF2 alpha formation in the presence of alpha-met-NA, PEA could be replaced by H2O2 generated by the glucose oxidase(GOD)-glucose system. The effect of H2O2 was inhibited by indomethacin or catalase, but pargyline was ineffective. It is assumed that catecholamines play a dual role in the activation of PG biosynthesis in brain tissue. During the enzymatic decomposition of catecholamines MAO produces H2O2, which stimulates endoperoxide synthesis. Simultaneously, catecholamines as hydrogen donors promote the nonenzymatic transformation of endoperoxides into PGF2 alpha. The possible physiological importance of these findings is discussed.

Animals↗
PubMed1987

Plasma catecholamine levels in preterm infants. Effect of birth asphyxia and Apgar score.

Catecholamine levels were measured in cord arterial blood from preterm infants. Relatively lower catecholamine levels were found in the preterm infants than in term infants, although no significant correlation was found between noradrenaline and adrenaline levels and either gestational age or birthweight. Significantly higher catecholamine levels were found after labour. Preterm females had significantly higher catecholamine levels than boys after asphyxia and tended also to have higher catecholamine levels without asphyxia, although not significant. Catecholamine levels were also significantly elevated in those infants with a low Apgar score (less than 7 at 5 min) and those who were acidotic (cord arterial pH less than 7.25). A good correlation was found between a low Apgar score and the presence of acidosis.

Apgar Score↗
PubMed1992

Effects of a postnatal exposure to cigarette smoke on hypothalamic catecholamine nerve terminal systems and on neuroendocrine function in the postnatal and adult male rat. Evidence for long-term modulation of anterior pituitary function.

The purpose of this paper was to study the possible long-term effects of postnatal exposure to cigarette smoke. Male Sprague-Dawley rats were exposed to the smoke from 2 cigarettes (Kentucky reference IR-1 type) every morning from day 1 after birth for a period of 5, 10 or 20 days. The rats were decapitated 24 hours (5, 10 and 20 days of exposure), 1 week (20 days of exposure) or 7 months (20 days of exposure) after the last exposure. Using the Falck-Hillarp methodology in combination with quantitative histofluorimetry catecholamine levels and changes in catecholamine utilization (alpha MT-induced CA fluorescence disappearance) in discrete hypothalamic catecholamine nerve terminal systems were analysed. Serum prolactin, LH, TSH and corticosterone levels were determined by means of radioimmunoassay procedures. In the postnatal period serum LH levels were significantly increased 24 hours after a 10 and 20 day exposure to cigarette smoke. In adult life after a 20-day postnatal exposure to cigarette smoke a highly significant increase was observed in serum prolactin levels, which were unaltered by this exposure when measured in the postnatal period. Twenty-four hours following a 20-day postnatal exposure, catecholamine utilization was increased in the medial palisade zone of the median eminence and substantially reduced in the parvocellular and magnocellular parts of the paraventricular hypothalamic nucleus. One week and 7 months following a 20-day postnatal exposure to cigarette smoke no alterations were observed in catecholamine levels or utilization in various hypothalamic areas including the median eminence. All the above changes were observed in the presence of an unaltered development of body weight. The results indicate that marked but temporary increases in LH secretion occur 24 hours after a postnatal exposure to cigarette smoke, while increase in prolactin secretion only develop in adult life, when the maturational processes of the brain and/or the anterior pituitary gland are completed. Changes in catecholamine levels and utilization are found in discrete hypothalamic nerve terminal networks but do not play a major role in mediating the above changes in anterior pituitary function and are probably the result of a withdrawal phenomenon.

Animals↗