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PubMed1999

Hepatic and gut clearance of catecholamines in the conscious dog.

Our aim was to assess hepatic and gut catecholamine clearance under normal and simulated stress conditions. Following a 90-minute saline infusion period, epinephrine ([EPI] 180 ng/kg x min) and norepinephrine ([NE] 500 ng/kg x min) were infused peripherally for 90 minutes into five 18-hour fasted, conscious dogs undergoing a pancreatic clamp (somatostatin plus basal insulin and glucagon). Arterial plasma levels of EPI and NE increased from 44 +/- 9 to 2,961 +/- 445 and 96 +/- 6 to 6,467 +/- 571 pg/mL, respectively (both P < .05). Portal vein plasma levels of EPI and NE increased from 23 +/- 8 to 1,311 +/- 173 and 79 +/- 10 to 3,477 +/- 380 pg/mL, respectively (both P < .05). Hepatic vein plasma levels of EPI and NE increased from 5 +/- 2 to 117 +/- 33 and 48 +/- 10 to 448 +/- 59 pg/mL, respectively (both P < .05). Net hepatic and gut EPI uptake increased from 0.5 +/- 0.1 to 30.0 +/- 3.0 and 0.4 +/- 0.1 to 26.3 +/- 4.0 ng/kg x min, respectively (both P < .05). Net hepatic and gut NE uptake increased from 1.5 +/- 0.4 to 74.7 +/- 8.4 and 0.8 +/- 0.2 to 57.9 +/- 7.6 ng/kg x min, respectively (both P < .05). Neither the net hepatic (0.86 +/- 0.05 to 0.93 +/- 0.02) nor gut (0.45 +/- 0.10 to 0.55 +/- 0.04) fractional extraction of EPI changed significantly during the simulated stress condition. Net hepatic and gut spillover of NE increased from 0.8 +/- 0.2 to 3.5 +/- 1.3 and 0.6 +/- 0.2 to 8.8 +/- 2.0 ng/kg x min, respectively, during catecholamine infusion (both P < .05). These results indicate that (1) approximately 30% of circulating catecholamines are cleared by the splanchnic bed (16% and 14% by the liver and gut, respectively); (2) the liver and gut remove a large proportion (approximately 86% to 93% and 45% to 55%, respectively) of the catecholamines delivered to them on first pass; and (3) high levels of plasma catecholamines increase NE spillover from both the liver and gut, suggesting that the percentage of NE released from the presynaptic neuron that escapes the synaptic cleft is increased in the presence of high circulating catecholamine levels.

Animals↗
PubMed1995

Hydrogen peroxide (H2O2) production by monoamine oxidase in rat tissues using endogenous catecholamines as substrates. A comparison of catalytic monoamine oxidase histochemistry and recently published catechol-O-methyltransferase immunohistochemistry.

Histochemical studies on hydrogen peroxide (H2O2) production by monoamine oxidase (MAOX) using xenobiotic (foreign) catecholamines such as tryptamine or tyramine as substrates may not reveal the true H2O2-production capacity of this enzyme and the potential co-localization and cooperation of MAOX with catechol-O-methyltransferase (COMT), the other catecholamine-degrading enzyme. Therefore, in the present study the catecholamine hormones adrenaline (epinephrine) and noradrenaline (norepinephrine) and the catecholamine neurotransmitter noradrenaline as well as the COMT metabolites metanephrine and normetanephrine, which are likely to be the more important MAOX substrates, were used for MAOX visualization in many rat tissues with a cerium-diaminobenzidine-H2O2-Co method. Adrenaline and noradrenaline were autooxidized by Ce3+ and could not be employed; with metanephrine or normetanephrine as substrates MAOX produced considerable amounts of H2O2 in many cells and tissues. Comparisons with immunohistochemical COMT-data for rats from the literature show that MAOX and COMT are co-localized or not. Therefore, different from our current knowledge in rats COMT and MAOX either co-operate in catecholamine degradation or they degrade the respective catecholamines alone.

Animals↗
PubMed1999

Reduced catecholamine response of lymphocytes from patients with rheumatoid arthritis.

Catecholamines modulate lymphocyte function via stimulation of beta2-adrenergic receptors (beta2R). Previous investigations revealed a decreased density of beta2R on peripheral blood mononuclear cells (PBMC) in patients with chronic rheumatic diseases. Aim of the present study was to determine the impact of this decrease on catecholamine response of PBMC from patients with rheumatoid arthritis (RA) in vitro. PBMC from 17 patients with RA and 12 healthy blood donors (HD) were investigated. Beta2R were determined by a radioligand binding assay. The effects of epinephrine (E) and norepinephrine (NE) on PBMC proliferation were studied using cells activated with pokeweed mitogen (PWM) and monoclonal anti-CD3-antibodies (OKT3), respectively. In parallel, alpha1- or beta-receptor antagonist were added to the culture to determine the specificity of the catecholaminergic effects. The results showed that depending on the stimulus and the catecholamine concentration employed E and NE exert inhibitory (OKT3) or stimulatory signals (PWM) on lymphocyte proliferation. Inhibitory effects could be abolished by adding beta-antagonist, while stimulatory signals were diminished after addition of alpha1- of beta-antagonist. Patients with RA showed a significantly reduced density of beta2R compared to HD paralleled by a significantly reduced influence of catecholamines on lymphocyte function. The study demonstrates the intricate relationship between PBMC reactivity and catecholamine effects that are mediated via alpha1- and beta-adrenergic receptors. In this respect the reduced catecholamine response of PBMC from RA patients may contribute to the pathogenic process of RA.

Adrenergic alpha-Antagonists↗
PubMed1997

Possible involvement of intracellular Ca2+ in hyposmosis-evoked catecholamine release from adrenal chromaffin cells.

The influence of hyposmotic conditions on catecholamine release was studied using cultured adrenal chromaffin cells. Incubation of the cells in hyposmotic solution led to the enhancement of catecholamine release in a manner dependent on the reduction of osmolarity. Hyposmosis-evoked catecholamine release was similarly observed in the presence or absence of extracellular Ca2+, and was not significantly affected by organic and inorganic Ca2+ entry blockers. These results indicated that the hyposmosis-evoked release might be associated with a rise in the intracellular Ca2+ concentration. Further studies showed that neither ryanodine nor thapsigargin caused any significant effect on hyposmosis-evoked catecholamine release, whereas pretreatment of chromaffin cells with carbonyl cyanide m-chlorophenyl hydrazone significantly enhanced the hyposmosis-evoked release. Catecholamine release evoked by exposure to hyposmotic medium is therefore thought to be mediated through intracellular Ca2+, which may be mainly sequestered by the mitochondrial pools. Neither caffeine- nor inositol 1,4,5-trisphosphate-sensitive Ca2+ pools seems likely to be involved in hyposmosis-evoked catecholamine release, although the Ca2+ pools that contribute to the elevation of intracellular Ca2+ observed under hyposmotic conditions are not yet completely identified.

Adrenal Medulla↗
PubMed1998

Vinblastine enhancement of hyposmosis-induced catecholamine release in cultured adrenal chromaffin cells: lack of relation to cell swelling and microtubule disruption.

Exposure of chromaffin cells to hyposmotic solution has been shown to cause catecholamine release through the elevation of intracellular Ca2+ level. While cell volume change observed under hyposmotic conditions has been shown to be accompanied by the movement of various ions and suggested to be associated with the reorganization of cytoskeletons. In the present study, the effects of cytoskeleton-disrupting agents on hyposmosis-induced catecholamine release were examined to investigate a possible relationship between catecholamine release and cell volume change under hyposmotic conditions. Hyposmosis-induced catecholamine release was enhanced by pre-treatment of the cells with a microtubule-disrupting agent vinblastine, but not significantly altered by a microfilament-disrupting agent cytochalasin B. Vinblastine also caused an additional increase in the intracellular Ca2+ but failed to affect the cell volume change under hyposmotic conditions. In contrast, the hyposmosis-induced release was not significantly altered by either colchicine, another microtubule-disrupting agent, or taxol, a microtubule-stabilizing agent. These results indicate that vinblastine enhances hyposmosis-induced catecholamine release through an additional increase in the intracellular Ca2+ and furthermore suggest that this effect of vinblastine on the hyposmosis-induced release is unassociated with the disruption of the microtubule system, providing evidence for a lack of the direct relationship between catecholamine release and the cell volume change observed under hyposmotic conditions.

Animals↗
PubMed2003

Effects of mental workload and caffeine on catecholamines and blood pressure compared to performance variations.

Caffeine is characterised as a central nervous system stimulant, also affecting metabolic and cardiovascular functions. A number of studies have demonstrated an effect of caffeine on the excretion of catecholamines and their metabolites. Urinary epinephrine and norepinephrine have been shown to increase after caffeine administration. Similar trends were observed in our study in adrenaline (ADR) and noradrenaline (NORADR) levels and additionally a dose dependent effect of caffeine. The effect of caffeine on cognitive performance, blood pressure, and catecholamines was tested under resting conditions and under mental workload. Each subject performed the test after oral administration of 1 cup and then 3 cups of coffee. Root mean square error (RMSE) for the tracking task was continuously monitored. Blood pressure was also recorded before and after each stage of the experiment. Catecholamines were collected and measured for three different conditions as: at rest, after mental stress alone, after one dose of caffeine under stress, and after triple dose of caffeine under stress. Comparison of the performance of each stage with the resting conditions revealed statistically significant differences between group of smokers/coffee drinkers compared with the other two groups of non-coffee drinkers/non-smokers and non-smokers/coffee drinkers. There was no statistically significant difference between the last two groups. There was an increase of urine adrenaline with 1 cup of coffee and statistically significant increase of urine noradrenaline. Both catecholamines were significantly increased with triple dose of caffeine. Mental workload increased catecholamines. There was a dose dependent effect of caffeine on catecholamines.

Adolescent↗
PubMed2001

Nitric oxide modulates evoked catecholamine release from canine adrenal medulla.

Nitric oxide has various actions, acting in a neurotransmitter-like role and also as a paracrine messenger between vascular endothelial and smooth muscle cells. This study was done to determine whether endogenous nitric oxide has a role in modulating evoked catecholamine release from the canine adrenal medulla. Isolated adrenal glands were perfused with Krebs-Ringer solution as a control, or with Krebs-Ringer solution containing either N(G)-monomethyl-L-arginine (L-NMMA; 3x10(-4) M) to non-selectively inhibit nitric oxide synthase or 7-nitroindazole (10(-4) M), a relatively selective inhibitor of neuronal nitric oxide synthase. Catecholamine release was evoked using the nicotinic cholinergic agonist 1,1-dimethyl-4-phenylpiperazinium iodine. From the collected perfusate epinephrine, norepinephrine, and dopamine were measured by high performance liquid chromatography. Previous studies have shown that in the presence of L-NMMA, basal releases of epinephrine, norepinephrine and dopamine are increased. 7-Nitroindazole had no effect on basal catecholamine release, suggesting that nitric oxide from an endothelial source was responsible for the inhibition of basal catecholamine release from the adrenal medulla. Epinephrine and norepinephrine releases were augmented when either of the nitric oxide synthase inhibitors was added during submaximal nicotinic stimulation, indicating that endogenous nitric oxide inhibited release of epinephrine and norepinephrine. Both neuronal and endothelial nitric oxide synthases appeared to be responsible for this inhibition. In summary, these studies suggest that nitric oxide, from both neuronal and endothelial sources, modulates evoked catecholamine release from canine adrenal medulla, while nitric oxide from an endothelial source is most likely responsible for modulation of catecholamine release under basal conditions.

Adrenal Medulla↗
PubMed1997

Study of salivary catecholamines using fully automated column-switching high-performance liquid chromatography.

Cortisol and catecholamines are major physiological markers of human stress. In order to establish a fully automated assay system for both cortisol and catecholamines in saliva, which can be sampled without imposing stress, the previously developed system for salivary cortisol [Okumura et al., J. Chromatogr. B, 670 (1995) 11] was modified. The practical sensitivity was around 0.1 pmol ml(-1) for norepinephrine and epinephrine and 0.5 pmol ml(-1) for dopamine. The established assay procedure provided R.S.D. values of 2 approximately 3% and recoveries of 96 approximately 104% at 0.5 pmol ml(-1). Measurement of salivary catecholamines in more than 300 samples taken from about 50 healthy volunteers indicated that the normal values of norepinephrine and dopamine were very low, about 0.1 pmol ml(-1) each. In contrast to cortisol, salivary catecholamine levels did not parallel those in plasma. Nevertheless, since levels of salivary catecholamines may reflect the sympathetic nerve activity in the salivary gland, they were assayed in volunteers making a scientific presentation before a large audience. Four out of eleven volunteers reported strong feelings of fear or anxiety, and their salivary catecholamine levels were about ten times higher than normal.

Adult↗
PubMed2000

The metabolism of plasma glucose and catecholamines in Alzheimer's disease.

Several lines of evidence suggest that the cholinergic system in the hippocampus plays a pivotal roll in regulating the peripheral metabolism of glucose and catecholamines. The injection of cholinergic stimulators including neostigmine, the acetylcholine esterase inhibitor, into the third ventricle or the hippocampus induces the elevation of glucose or catecholamines in plasma in rats. Under stress conditions, release of acetylcholine in the hippocampus increases, which coincides with the elevation of plasma glucose and catecholamines. Age-related reduction in responsivity of the cholinergic system in the hippocampus has been well documented. The intrahippocampal neostigmine injection induces significantly attenuated responses in plasma glucose and catecholamines in rats, the finding suggested that changes in cholinergic system activity in the hippocampus could result in alteration of the peripheral metabolism of glucose and catecholamines. In Alzheimer's disease (AD), the most common type of dementia, degeneration of the hippocampal cholinergic system is one of the most robust pathological features. Measurement of plasma catecholamines during a fasting state in the groups of AD subjects, vascular dementia subjects, and non-demented control subjects showed significantly lower plasma epinephrine levels in the AD subjects.

Acetylcholine↗
PubMed1995

Quantitation of catecholamines in uninflamed human dental pulp tissues by high-performance liquid chromatography.

The quantitation of catecholamines has yet to be reported in the human dental pulp. Various methods of chemical detection have shown the presence of catecholamines in pulpal tissue. Pulpal tissue was obtained from nonrestored, uninflamed teeth that needed to be extracted. The samples were collected, extracted, and analyzed by means of high-performance liquid chromatography with ultraviolet detection for levels of catecholamines (dopamine, epinephrine, and norepinephrine). As mediators of vasoconstriction, catecholamines play an important role in the control of intrapulpal pressure. This research describes a method for quantitation of catecholamines. Future studies investigating inflamed tissue can now be accomplished with the use of this analytic method. The results from this research indicate a baseline level of catecholamines in the uninflamed human dental pulp.

Catecholamines↗
PubMed2003

Regulation of nitric oxide production from macrophages by lipopolysaccharide and catecholamines.

Catecholamines are elaborated in stress responses to mediate vasoconstriction, and elevate systemic vascular resistance and blood pressure. They are elaborated in disorders such as sepsis, cocaine abuse, and cardiovascular disease. The aim of the study was to determine whether catecholamines affect nitric oxide (NO) production, as NO is a vasodilator and counteracts the harmful effects of catecholamines. RAW264.7 macrophage cells were cultured with lipopolysaccharide (LPS)+/-epinephrine, norepinephrine, and dopamine at 5x10(-6)M concentrations for 24h. Supernatants were harvested for measuring NO by spectrophotometry using the Greiss reagent and cells were harvested for detecting inducible NO synthase (iNOS) by Western blot. NO production in RAW 264.7 macrophages was increased significantly by addition of LPS (0.5-10ng/ml) in a dose-dependent fashion. The NO production induced by LPS was further enhanced by epinephrine and norepinephrine, and to a lesser extent by dopamine. These increases in NO correlated with expression of iNOS protein in these cells. The enhancing effect of iNOS synthesis by epinephrine and norepinephrine on LPS-induced macrophages was down regulated by beta-adrenoceptor antagonist, propranolol, and dexamethasone. The results suggest that catecholamines have a synergic effect on LPS in induction of iNOS synthesis and NO production, and this may mediate some of the vascular effects of infection. These data support a novel role for catecholamines in disorders such as septic shock and cocaine use, and indicate that beta-adrenoceptor antagonists and glucocorticoids may be used therapeutically for modulation of the catecholamine-NO axis in disease states.

Adrenergic beta-Antagonists↗
PubMed2002

Extraction and separation of urinary catecholamines as their diphenyl boronate complexes using C18 solid-phase extraction sorbent and high-performance liquid chromatography.

The clinical utility of a one-step extraction procedure based on the retention of a diphenyl boronate-catecholamine complex on a C18 solid-phase extraction sorbent was investigated for the measurement of urinary catecholamines. Although recoveries with the extraction procedure were optimal over a relatively broad pH range (7.5-9.5), analytical factors such as sample loading and elution flow-rates, wash step and elution conditions, the concentration of catecholamines in urine to be extracted and the type of C18 sorbent used for extraction were found to influence the efficiency of this procedure and would therefore need to be controlled for optimal recoveries. Under optimal conditions the recovery of noradrenaline, adrenaline and dopamine from spiked urine was high and reproducible (mean recoveries were >85% for all catecholamines). The effectiveness of sample clean-up step was demonstrated by reverse phase, ion pair high-performance liquid chromatography with electrochemical detection. The method described was found to be suitable for the routine measurement of catecholamines in urine in clinical biochemistry laboratories. It has a high sample extraction throughput (40/h) and has adequate precision (between batch CV<8%) and sensitivity (LOD<30 nmol/l; LOQ<65 nmol/l) for all the catecholamines measured. The method has acceptable accuracy, showing a mean bias of 6.6% for noradrenaline, 7.3% for adrenaline and 6.8% for dopamine from the mean value of laboratories (N=69) participating in an External Quality Assurance scheme for greater than 12 months.

Boron Compounds↗
PubMed1995

Simultaneous amperometric measurement of ascorbate and catecholamine secretion from individual bovine adrenal medullary cells.

Secretion of ascorbate and catecholamines from single bovine adrenal medullary cells has been detected with amperometry at carbon-fiber microelectrodes. Two carbon-fiber electrodes were employed. One was beveled, and voltammograms at this electrode showed overlap of the responses for ascorbate and the catecholamines. The other was beveled and electrochemically oxidized to shift the ascorbate oxidation wave to potentials more negative than that of the catecholamines. Thus, at an applied potential of 0.05 V vs SSCE, ascorbate was selectively oxidized at the treated electrode and both catecholamines and ascorbate were oxidized at an applied potential of 0.65 V at the untreated electrode. Exocytotic release from the cell was stimulated with K+, nicotine, and digitonin. Nicotine and K+ depolarize the cell membrane and elicit vesicular release. Digitonin is a detergent that reacts with cholesterol in the plasma membrane and causes the formation of pores. Ascorbate efflux from individual cells could be induced by digitonin but not by K+ or nicotine and was observed as a single peak with a full width at half-maximum of 4 s. In contrast, catecholamine release was observed as many rapid, sequential current spikes when the cell was exposed to either digitonin, K+, or nicotine. The two different types of release show that ascorbate and catecholamines are being released from two different cellular compartments. The calcium independence of the digitonin-induced ascorbate release provides additional evidence that ascorbate is released by a nonexocytotic process.

Adrenal Medulla↗
PubMed2002

Response times of carbon fiber microelectrodes to dynamic changes in catecholamine concentration.

The electrode response time and the measured concentrations during dynamic catecholamine changes were compared using constant potential amperometry and fast-scan cyclic voltammetry. The amperometric response to a rectangular pulse of catecholamine is more rectangular than the cyclic voltammetric response; however, the response times are very similar when, during cyclic voltammetry, the temporal lag due to adsorption and desorption of catecholamine to the electrode is removed by deconvolution. Deconvolution of cyclic voltammetry data was applied to stimulated dopamine release in vivo, allowing for modeling of release and uptake kinetics and to measure catecholamine release from single cells, resulting in better resolution of peaks from single vesicles. In vitro postcalibrations were performed to calculate concentrations of catecholamine measured with cyclic voltammetry and amperometry. The addition of 600 microM ascorbic acid to the postcalibration buffer, allowing a catalytic reaction to regenerate dopamine, resulted in similar calculated concentrations for stimulated release of dopamine using amperometry and cyclic voltammetry. Using deconvoluted cyclic voltammetry to remove the response time lag and adding ascorbic acid to the calibration buffer, the shape and concentration of dynamic catecholamine changes are very similar when measured with constant potential amperometry and cyclic voltammetry.

Animals↗
PubMed1997

Synergistic induction of DNA strand breakage caused by nitric oxide together with catecholamine: implications for neurodegenerative disease.

Oxidative damage in neuronal cells and DNA has been implicated in the pathogenesis of various neurodegenerative diseases. We have demonstrated that DNA strand breakage is induced synergistically when plasmid DNA is incubated in the presence of both an NO-releasing compound (diethylamine NONOate, spermine NONOate, sodium nitroprusside) and a catecholamine (e.g., L-DOPA, dopamine, etc.). Either an NO-releasing compound or a catecholamine alone induced much fewer strand breaks. Tyrosine and tyramine as well as O-methylated derivatives of DOPA and dopamines did not exert this synergistic effect in the presence of NO. The DNA strand breakage induced by NO plus dopamine was inhibited by carboxy-PTIO (a trapping agent of NO and possibly other radicals), superoxide dismutase, and antioxidants such as N-acetylcysteine and ascorbate but not by HO. scavengers such as dimethyl sulfoxide, ethanol, and D-mannitol. These results suggest that the free HO. is not involved; rather a new oxidant(s) formed by the reaction between NO and catecholamine could be responsible for causing the DNA strand breakage. We propose that one of the responsible compounds is peroxynitrite (ONOO-), which is a strong oxidant and nitrating agent formed by the reaction between NO and O2.-. NO has been shown to oxidize catecholamines to form quinone derivatives, which lead to the generation of O2.- by the quinone/hydroquinone redox system. O2.- then reacts rapidly with NO to form peroxynitrite. However, it is also possible that other compounds such as NOx generated from catecholamines and NO may cause DNA damage. Our results implicate a synergistic interaction of catecholamines formed in dopaminergic neurons and NO formed by microglia or astrocytes or the two compounds produced within the same neuronal cells to produce a potent oxidant(s) which could cause damage in cells and DNA, thus playing an important role in the pathogenesis of various neurodegenerative diseases.

Antioxidants↗
PubMed1982

The hypothalamo-neurohypophysial system of native Australian desert rodents. The catecholamine contents of the hypothalamus and posterior pituitary of Notomys alexis, Pseudomys australis and the laboratory rat.

The putative central catecholamine neurotransmitters, adrenaline, noradrenaline and dopamine, have been quantified by enzyme radiochemical methods in the hypothalamo-neurohypophysial system (HNS) of the xeric rodents, Notomys alexis and Pseudomys australis, using the laboratory rat for comparison. All three catecholamines were found (noradrenaline greater than dopamine greater than adrenaline) in the hypothalami of the three species. The hypothalami of the two xeric rodents contained some 5-10 times as much of each of the catecholamines (when expressed as ng per body weight) as the rat. The ratio of noradrenaline to dopamine was constant (3 X 8-4 X 2) between species. Posterior pituitary contents of the catecholamines were generally inconsistent within and between species, with only dopamine being invariably and consistently present. It was also found that, like the antidiuretic hormone content, the dopamine content of the neural lobe was significantly correlated with the body surface area of the animal. Withdrawal of drinking water or its replacement with 2 X 5% saline increased hypothalamic noradrenaline synthesis and dopamine utilisation. In the neural lobe, saline ingestion produced a significant increase in all three catecholamines, but with water deprivation only dopamine was increased (relative to body weight). The results of these studies are interpreted as indicating a possible role for catecholamine neurotransmitters, particularly dopamine, in the control of neurohypophysial hormone release in the HNS.

Animals↗
PubMed2002

Independent contribution of catecholamines to arrhythmogenesis during evolving infarction in the isolated rat heart.

Ventricular fibrillation (VF) in conscious rats with coronary artery ligation occurs in two phases, before (phase 1) and after (phase 2) 90 min of ischaemia respectively. The mechanisms of phase 2 VF are not established. Interestingly, phase 2 VF is absent in isolated (denervated) buffer-perfused rat hearts. We investigated whether catecholamine supplementation (to mimic sympathetic drive) was sufficient to restore phase 2 VF in such hearts. Isolated rat hearts (n=10 per group) underwent coronary ligation for 240 min. At 90 min, during a period of relative electrical stability, the perfusion solution was switched from standard (Krebs) to identical solution or Krebs containing catecholamines (313 nM noradrenaline and 75 nM adrenaline) with or without 10 microM trimazosin (an alpha(1)-adrenoceptor antagonist) or 10 microM atenolol (a beta(1)-adrenoceptor antagonist). Although in all groups the incidence of phase 1 VF was high (80 - 100%), the temporal distribution of VF was monophasic, i.e. only one heart in one group developed phase 2 VF (P=NS). Other ventricular arrhythmias (e.g., tachycardia; VT) exhibited a similar temporal distribution. Nevertheless, haemodynamic changes confirmed sympathomimetic effects of catecholamines, e.g., heart rate was increased from 278+/-7 beats min(-1) in controls to 335+/-8 beats min(-1) (P<0.05) by catecholamines, an effect that could be blocked by atenolol (285+/-7 beats min(-1)) but not by trimazosin (342+/-12 beats min(-1)). Coronary flow was correspondingly increased from 7.7+/-0.7 ml min(-1) g(-1) to 16.5+/-1.3 ml min(-1) g(-1) (P<0.05); this effect could be blocked by atenolol (8.1+/-0.6 ml min(-1) g(-1)) and was enhanced by trimazosin (20.7+/-2.4 ml min(-1) g(-1)). In conclusion, despite evidence of adequate alpha- and beta-adrenoceptor activation, catecholamine supplementation to isolated buffer-perfused rat hearts was insufficient to restore phase 2 VF. It therefore appears unlikely that catecholamines alone mediate phase 2 VF.

Adrenergic alpha-Antagonists↗
PubMed1996

Catecholamines are synthesized by mouse lymphocytes and regulate function of these cells by induction of apoptosis.

The immune and the nervous systems are anatomically closely related and interact with each other by molecules common to both systems, such as cytokines and neurotransmitters. The purpose of this study was to investigate the participation of catecholamines in the neuroimmunological network. The ability of immune cells to produce catecholamines was examined by a highly sensitive capillary electrophoresis assay, which permits detection of easily oxidized catecholamines in the zeptomole (10(-21)) range. In addition, the effects of catecholamines on in vitro proliferation, differentiation and apoptosis of lymphocytes were assessed. Mouse spleen cells and macrophages contained on average 7 x 10(-17) and 2 x 10(-17) mole dopamine per cell, respectively. In the former cell population also norepinephrine was found. Several mouse B- and T-cell hybridomas were also shown to contain endogenously produced dopamine in levels ranging from 7 x 10(-20) to 2 x 10(-18) mole dopamine per cell. In addition, one of the T-cell hybridomas proved to synthesize norepinephrine. The dopamine production of lymphocytes was blocked by the tyrosine hydroxylase inhibitor alpha-methyl-p-tyrosine, whereas incubation with the precursor L-DOPA increased the dopamine content. Incubation with L-DOPA, dopamine and norepinephrine dose-dependently suppressed mitogen induced proliferation and differentiation of mouse lymphocytes. Even short-time pretreatment of lymphocytes with L-DOPA and dopamine strongly suppressed lymphocyte proliferation and cytokine production. Incubation of lymphoid cells with L-DOPA, dopamine and norepinephrine dose-dependently induced apoptosis which, at least partly, explains the suppressive effects of catecholamines on lymphocyte function. Our results demonstrate that catecholamines: (i) are actively produced by lymphocytes and (ii) have the capacity to act as auto- and/or paracrine regulators of lymphocyte activity through induction of apoptosis.

Animals↗