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PubMed1985

Multi-score estimation of catecholamine fluorescence for clinical purposes.

Experience accumulated at multi-score semiquantitation of catecholamine fluorescence of glyoxylic acid-treated stretch preparations of human clinical specimens is presented. The methodology and criteria of quantitation are described in detail. For an example, comparison between 3 different methods for analyzing neural-bound noradrenaline in human myocardial tissue in various heart diseases (obtained during the course of cardiac surgery) is presented: Biochemical determination of tissue noradrenaline content multi-score estimation of catecholamine fluorescence of glyoxylic acid-treated stretch preparations microfluorimetric analysis of the same stretch preparations. The results show that the multi-score estimation method gives a reliable concept of the relative amounts of noradrenaline stored in the intrinsic adrenergic nerve net (corresponding closely to the individual and group differences observed at biochemical noradrenaline determination). In addition, possible regional differences, alterations in the structural integrity of the inbuilt intrinsic nerve net, and other structural changes (e.g. pathological catecholamine accumulations) are easily recognized, whereas biochemical estimation cannot give information on structural aspects, which may have important clinical repercussions. Microfluorimetry does not seem suitable for studies on human myocardial specimens for several reasons which are discussed. The method of multi-score estimation of catecholamine fluorescence described and discussed is recommended for other similar and related studies on human clinical materials.

Catecholamines↗
PubMed1996

Mn2+ can substitute for Ca2+ in causing catecholamine secretion but not for increasing tyrosine hydroxylase phosphorylation in bovine adrenal chromaffin cells.

The ability of the divalent cation manganese (Mn2+) to substitute for calcium (Ca2+) both in triggering catecholamine release and in stimulating catecholamine synthesis, as indicated by an increase in tyrosine hydroxylase (TOH) phosphorylation, has been determined in bovine adrenal medullary chromaffin cells maintained in tissue culture. Mn2+ was found to enter chromaffin cells through pathways activated by nicotinic receptor stimulation and potassium depolarisation, and via the Na1:Ca0 exchange mechanism in Na(+)-loaded cells. Like Ca2+, entry of Mn2+ through these pathways triggered immediate catecholamine release and, like Ca2+, maintained quantitatively comparable release at least up to 40 min. Unlike Ca2+, Mn2+ did not stimulate an increase in TOH phosphorylation in intact chromaffin cells, even over a prolonged time course, but Mn2+ did stimulate increased TOH phosphorylation in lysed cell preparations showing that its lack of effect in the intact cells was not due to inhibition of the specific phosphorylation pathway. In lysed cell preparations, Mn2+ stimulated also phosphorylation of a different spectrum of proteins to Ca2+, and of the same proteins to different extents. In particular, P80 (MARCKS protein) was more intensely phosphorylated in the presence of Mn2+ than in the presence of Ca2+. Since TOH phosphorylation always occurs when intracellular Ca2+ is increased, the absence of an increase with Mn2+ indicates that none of its intracellular effects could have occurred as a consequence of Mn2+ mobilisation of intracellular Ca2+. In summary, the data show that Mn2+ is a surrogate for Ca2+ in triggering and maintaining catecholamine release, but does not substitute for Ca2+ in stimulating TOH phosphorylation.

Adrenal Glands↗
PubMed1999

Mechanisms of bradykinin-induced catecholamine release in pithed spontaneously hypertensive rats.

Kinins have the potential to modulate the sympathetic system. However, the kinin receptor subtypes and secondary mediators involved in vivo are not fully characterized. Earlier studies failed to show complete inhibition by B1- or B2-antagonists of bradykinin-induced catecholamine release, and were impeded by direct stimulatory actions of those substances. Such effects may arise from the involvement of histamine, the release of which is known to be stimulated by bradykinin and kinin-receptor antagonists. The present study was designed to evaluate the significance of B2-receptors and histamine in the bradykinin-induced enhancement of plasma catecholamines in pithed spontaneously hypertensive rats. The effects of bradykinin, the B2-receptor antagonist HOE 140, histamine and the H1-receptor antagonist mepyramine were tested. Administration of histamine dose-dependently increased catecholamine release whereby a marked preference for adrenaline over noradrenaline was seen. The H1-receptor antagonist mepyramine (0.3 mg/kg) prevented this effect. Bradykinin (7.2 microg/kg) enhanced plasma adrenaline and noradrenaline. In doses > or = 10 microg/kg, HOE 140 completely suppressed the bradykinin-induced increase in plasma noradrenaline, while a slight stimulation of adrenaline that even persisted after a high dose of HOE 140 (100 microg/kg), was only abolished by additional administration of mepyramine (0.3 mg/kg). The H1-receptor antagonist at this dose did not influence the effectivity of bradykinin. It is concluded that the bradykinin-induced enhancement of catecholamine release during electrical stimulation is completely (noradrenaline) or predominantly (adrenaline) mediated by B2-receptors. A minor stimulating effect of bradykinin on plasma adrenaline is provoked independently of B2-receptors via histamine acting on H1-receptors.

Adrenergic beta-Antagonists↗
PubMed2002

The role of catecholamines in seizure susceptibility: new results using genetically engineered mice.

The catecholamines norepinephrine and dopamine are abundant in the CNS, and modulate neuronal excitability via G-protein-coupled receptor signaling. This review covers the history of research concerning the role of catecholamines in modulating seizure susceptibility in animal models of epilepsy. Traditionally, most work on this topic has been anatomical, pharmacological, or physiological in nature. However, the recent advances in transgenic and knockout mouse technology provide new tools to study catecholamines and their roles in seizure susceptibility. New results from genetically engineered mice with altered catecholamine signaling, as well as possibilities for future experiments, are discussed.

Animals↗
PubMed2003

Expression of mRNA for PACAP and its receptors in intra- and extra-adrenal human pheochromocytomas and their relationship to catecholamine synthesis.

PURPOSE: Pituitary adenylate cyclase-activating polypeptide (PACAP), a member of the secretin/glucagons/vasoactive intestinal peptide family, induces the expression of catecholamine-synthesizing enzymes in adrenal medullary cells. In addition, PACAP and its receptor have been detected in human pheochromocytoma tissues, though it is not yet known whether PACAP enhances the expression of genes encoding catecholamine-synthesizing enzymes. To address this question, we analyzed PACAP, PACAP receptor, and tyrosine hydroxylase (TH) and phenylethanolamine-N-methyltransferase (PNMT) mRNAs in pheochromocytomas. METHODS: The levels of the mRNA for PACAP and vasoactive intestinal peptide (VIP), and their receptors, and for TH and PNMT were measured by RT-PCR or real-time PCR analysis, and the concentrations of catecholamines were measured by HPLC in 24 intra-adrenal and six extra-adrenal pheochromocytomas. RESULTS: mRNA expression of PACAP and its receptor VPAC1R were detected in many pheochromocytomas (24/30 and 29/30, respectively), but mRNA expression of the PAC1R and VPAC2R receptor subtypes were detected in only one of six extra-adrenal pheochromocytomas. PACAP mRNA expression correlated with TH (p=0.0018) and PNMT (p=0.05) mRNA expression, as well as epinephrine (p=0.0342) levels in 16 intra-adrenal pheochromocytomas. CONCLUSION: Our findings support a possible role for PACAP in the regulation of expression of genes encoding catecholamine-synthesizing enzymes in intra-adrenal pheochromocytomas.

Adrenal Gland Neoplasms↗
PubMed2000

Footshock-induced changes in brain catecholamines and indoleamines are not mediated by CRF or ACTH.

Stressful treatments have long been associated with increased activity of brain catecholaminergic and serotonergic neurons. An intracerebroventricular (icv) injection of the corticotropin-releasing factor (CRF) also activates brain catecholaminergic neurons. Because brain CRF-containing neurons appear to be activated during stress, it is possible that CRF mediates the catecholaminergic activation. This hypothesis has been tested by assessing the responses in brain catecholamines and indoleamines to footshock in mice pretreated icv with a CRF receptor antagonist, and in mice lacking the gene for CRF (CRFko mice). Consistent with earlier results, icv administration of CRF increased catabolites of dopamine and norepinephrine, but failed to alter tryptophan concentrations or serotonin catabolism. A brief period of footshock increased plasma corticosterone and the concentrations of tryptophan and the catabolites of dopamine, norepinephrine and serotonin in several brain regions. Mice injected icv with 25 microg alpha-helical CRF(9-41) prior to footshock had neurochemical responses that were indistinguishable from controls injected with vehicle, while the increase in plasma corticosterone was slightly attenuated in some experiments. CRFko mice exhibited neurochemical responses to footshock that were indistinguishable from wild-type mice. However, whereas wild-type mice showed the expected increase in plasma corticosterone, there was no such increase in CRFko mice. Similarly, hypophysectomized mice also showed normal neurochemical responses to footshock, but no increase in plasma corticosterone. Hypophysectomy itself elevated brain tryptophan and catecholamine and serotonin metabolism. Treatment with ACTH icv or peripherally failed to induce any changes in cerebral catecholamines and indoleamines. These results suggest that CRF and its receptors, and ACTH and other pituitary hormones, are not involved in the catecholamine and serotonin responses to a brief period of footshock.

Adrenocorticotropic Hormone↗
PubMed1988

Blood pressure and both venous and urinary catecholamines after cerebral infarction.

Blood pressure, both venous and urinary catecholamines and plasma renin activity (PRA) were studied in 10 patients (6 men and 4 women, mean age 70 +/- 10 years) on the first three days after cerebral infarction. Blood pressure fell significantly (p less than 0.02) on the second and third day after stroke. There was a small but significant (p less than 0.01) decrease in plasma epinephrine concentration on the third day. The norepinephrine values remained constant on the three days. The PRA showed a significant (p less than 0.01) rise on the third day. No significant correlation was detected between the course of the blood pressure and the plasma catecholamines or PRA. When blood pressure was correlated with the urinary catecholamines, however, a significant correlation with epinephrine (r = 0.45; p less than 0.05) and with norepinephrine (r = 0.44; p less than 0.05) was found. We conclude that the changes in blood pressure after stroke are at least partly mediated by the changes in catecholamine production.

Aged↗
PubMed1997

Gene expression of catecholamine synthesizing enzymes and beta adrenoceptor subtypes during rat embryogenesis.

Timed-pregnant Sprague-Dawley rats were killed between gestational day (GD) 8 and 10, and embryos were explanted and separated into developmental stages according to a modified Theiler's system. Total RNA from each stage was isolated and subjected to reverse transcription-polymerase chain reaction (RT-PCR) assays to examine gene expression of catecholamine synthesizing enzymes and three subtypes of beta adrenoceptors. Expression of these genes was detected at much earlier stages than previously reported, and each enzyme and receptor subtype showed a different pattern of gene expression. For example, mRNA for tyrosine hydroxylase, the rate-limiting enzyme for catecholamine synthesis, was detected as early as stage 10a, late GD 8, before the neural crest cells appear (stage 12, mid GD 10). This contradicts the common belief that catecholamines are produced only in the cells of sympathoadrenal lineage which originate from the neural crest cells and the cells of central nervous system. Results from the present study indicate that catecholamine synthesis is not limited to the cells of sympathoadrenal lineage.

Animals↗
PubMed1997

Catecholamine enzymes and neuropeptides are expressed in fibres and somata in the intermediate gray matter in chronic spinal rats.

Spinal cord injury disrupts control of sympathetic preganglionic neurons because bulbospinal input has been lost and the remaining regulation is accomplished by spinal circuits consisting of dorsal root afferent and spinal neurons. Moreover, an initial retraction and regrowth of dendrites of preganglionic neurons in response to deafferentation creates the potential for remodelling of spinal circuits that control them. Although catecholamines and neuropeptide Y are found in descending inputs to the preganglionic neurons, their presence in spinal circuits has not been established. Spinal circuits controlling preganglionic neurons contain substance P but participation of these peptidergic neurons in remodelling responses has not been examined. Therefore, we compared immunoreactivity for the catecholamine-synthesizing enzyme dopamine beta-hydroxylase, for neuropeptide Y and for substance P in the intermediate gray matter of the spinal cord in control rats and in rats seven or fourteen days after transection at the fourth thoracic cord segment. Sympathetic preganglionic neurons were retrogradely labelled by intraperitoneal injection of the tracer FluoroGold. These experiments yielded three original findings. 1) At one and two weeks after cord transection, fibres and terminals immunoreactive for dopamine beta-hydroxylase and neuropeptide Y were consistently found in the intermediolateral cell column in segments caudal to the transection. The area of fibres and terminals containing these immunoreactivities was markedly reduced compared to control rats or to segments rostral to the transection in the spinal rats. 2) Immunoreactivity for substance P was increased after cord transection and the distribution of fibres immunoreactive for this peptide in segments caudal to the transection extended more widely through the intermediate gray matter. These reactions demonstrated a plastic reaction to cord transection by spinal neurons expressing substance P. 3) Dopamine beta-hydroxylase expression was up-regulated in somata within the intermediate gray matter of spinal segments caudal to the transection. The numbers of somata immunoreactive for this enzyme increased six-fold by 14 days after cord transection, compared to the few somata counted in control rats. In conclusion, the presence of a catecholamine synthesizing enzyme and neuropeptides in fibres surrounding sympathetic preganglionic neurons caudal to a cord transection suggests a source of catecholamines and these peptides within spinal circuits in the chronic spinal rat. The presence of dopamine beta-hydroxylase in a markedly greater number of neuronal somata after cord transection reflects significant up-regulation of gene expression and may indicate a switch by these neurons to an adrenergic phenotype, revealing a plastic response to injury within the spinal cord.

Animals↗
PubMed1998

Enkephalin neurons that project to the A7 catecholamine cell group are located in nuclei that modulate nociception: ventromedial medulla.

The location of methionine enkephalin neurons in the medulla oblongata that project to the dorsolateral pontine tegmentum was investigated using anterograde and retrograde tract tracing combined with immunocytochemical neurotransmitter identification. The results of these experiments demonstrate that enkephalinergic neurons from areas known to modulate nociception project to the region of the A7 catecholamine cell group in the dorsolateral pontine tegmentum. The medullary nuclei that contain these enkephalinergic neurons include the nucleus raphe magnus and the nucleus reticularis gigantocellularis pars alpha in the ventromedial medulla. While some of these enkephalinergic axons appose the somata and dendrites of A7 neurons, the majority of these axons appear to contact non-catecholamine neurons in the dorsolateral pontine tegmentum. Unidentified neurons located in the nucleus raphe magnus, the nucleus reticularis gigantocellularis pars alpha, and the nucleus reticularis gigantocellularis also project to the A7 area. Many of the neurons in the nucleus reticularis gigantocellularis pars alpha appear to contact both noradrenergic A7 neurons and non-catecholamine neurons in the dorsolateral pontine tegmentum, whereas most of those in the nucleus raphe magnus appear to contact non-catecholamine neurons. The anatomical findings described in this report and the results of preliminary behavioral studies provide evidence to support a model in which activation of the enkephalin-containing neurons in the ventromedial medulla facilitates nociception, while the non-enkephalin neurons mediate part of the antinociception produced by stimulating sites in the ventromedial medulla.

Animals↗
PubMed1988

Sensitive method for determination of picogram amounts of epinephrine and other catecholamines in microdissected samples of rat brain using liquid chromatography with electrochemical detection.

Liquid chromatography with high-sensitivity electrochemical detection has been employed to measure picogram amounts of epinephrine and other catecholamines in microdissected samples of the rat hypothalamus. Tissue catecholamines are purified by solvent extraction; this provides better selectivity and recovery than methods involving alumina. The solvent extraction technique has been modified in order to eliminate its major disadvantage, the presence of electroactive substances separating with catecholamines. Detection limits of below 1 pg allow for analysis of catecholamines including epinephrine in very small brain samples such as micropunches.

Animals↗
PubMed1986

Determination of free and total catecholamines and salsolinol in urine by ion-pair reversed-phase liquid chromatography with electrochemical detection after a one-step sample clean-up.

A simple method is presented for the routine determination of free and total catecholamines and salsolinol in urine. For the analysis of total catecholamines and salsolinol, the urine samples are first hydrolysed. The compounds are isolated by a one-step sample clean-up by cation-exchange chromatography and separated by ion-pair reversed-phase liquid chromatography and detected electrochemically. The method is suited for routine analysis. Pretreatment of ten samples for the high-performance liquid chromatographic analysis of free and total catecholamines and salsolinol is carried out in 4 h. A single analysis is completed in 30 min. The absolute losses of the compounds were less than 10%, except for epinephrine (20%). The detection limits were 0.9, 2.4, 4.8 and 6 nmol/l for norepinephrine, epinephrine, dopamine and salsolinol, respectively, in native urine. The values were twice as high for hydrolysed urine. The sample clean-up appears to be rather specific: apart from catecholamines and salsolinol, only those structurally related amines that contain a vicinal hydroxyl group are isolated.

Catecholamines↗
PubMed1981

Micro high-performance liquid chromatographic system with micro precolumn and dual electrochemical detector for direct injection analysis of catecholamines in body fluids.

A new micro high-performance liquid chromatographic system has been developed, which determines catecholamines from directly injected human urine without any sample pretreatment. The system consists of a mixing junction for adjusting the sample to pH 8.5, a micro alumina precolumn for enriching catecholamines in the sample, and a dual electrochemical detector for selectively detecting catecholamines based on their electrochemical reversibility. The system is able to operate with directly injected body fluids and to determine simultaneously all of the four catecholamines with high precision.

Catecholamines↗
PubMed1997

Determination of catecholamines and methoxycatecholamines excretion patterns in pig and rat urine by ion-exchange liquid chromatography with electrochemical detection.

A simplified liquid chromatographic method for the simultaneous determination of free or total catecholamines and methoxycatecholamines in rat and pig urine is presented. The extraction procedure involves a two-stage batch extraction, with successive adsorption on cation- (catecholamine elution) and anion-exchange columns (methoxycatecholamine elution). The column eluates are successively monitored by reversed-phase high-performance liquid chromatography (HPLC) with electrochemical detection. The proportion of conjugates for each compound was assessed in both species, through the comparison of concentrations with or without hydrolysis pretreatment. Conjugates were found to account for a small fraction of total catecholamines and methoxycatecholamines excretion (0 to 35%). The free fraction of each compound was highly correlated with the total amount. Furthermore, the hydrolysis procedure leads to partial degradation of metanephrine (25%) and to the production of compounds giving artefactual peaks. Thus, we do not recommend hydrolysis of rat and pig urines for catecholamine and methoxycatecholamine determination.

Animals↗
PubMed1997

Pulmonary and serum surfactant phospholipids and serum catecholamines in strangulation. An experimental study on rats.

Elevations of phospholipid and catecholamine concentrations in the blood are regarded as the vital reactions in asphyxial deaths, which leave few or no morphological signs in the body. These vital reactions were tested here, under strict experimental conditions, employing rapid asphyxia. Rats anaesthetized with barbiturate were strangled with a rope 2 mm thick tightened with a force of 29.4 N (3 kp). The main surfactant components, phosphatidyl choline and phosphatidyl ethanol amine, were measured in serum and lung samples, and catecholamines in the serum. The lungs were also investigated histologically. The serum phospholipid concentration in the strangulated rats was 1.36 +/- 0.32 g/l, versus 1.04 +/- 0.17 g/l in the controls (barbiturate intoxication), P < 0.001, but no change in their content was observed in the lungs (26.21 +/- 4.04 mg/g vs. 25.15 +/- 3.64 mg/g dry weight). Histologically, focal emphysema and tiny haemorrhages were seen in the lungs of both groups with similar frequency. Mean serum noradrenaline (NA) and adrenaline (A) concentrations were significantly higher in the strangulation group (NA = 5.4 +/- 2.6 ng/ml vs. 2.8 +/- 0.1 ng/ml, P < 0.001 and A = 6.0 +/- 3.4 ng/ml vs. 3.8 +/- 3.0 ng/ml, P < 0.05). The results support the notion that phospholipid and catecholamine concentrations are increased in the blood upon suffocation and could thus be taken as indicators of hypoxia. Further investigations into postmortem phospholipid change or stability are needed. There are reports that phospholipid concentration remain quite stable for two days post mortem, whereas catecholamine concentrations tend to rise quite soon after death.

Animals↗
PubMed2001

Catecholamine stress responses in arterialized blood.

Arterialized and venous blood was compared to determine if the arterialization procedure enhances the detection of stress-related changes in catecholamines. Lipid and hematologic measures were also compared for possible distortion by arterialization. Fifteen men completed two stressors. Indwelling venous catheters were placed retrograde in each hand, and the right hand was warmed to a constant temperature. Blood samples were taken simultaneously from both hands, and plasma catecholamines were determined. Arterialization increased baseline epinephrine; there were no effects of arterialization on catecholamines during stress, nor in lipid or hematologic measures during baseline or stress. Thus, arterialization of blood results in small increases in resting epinephrine levels, but does not obscure lipid measures. More importantly, arterialization of venous blood does not enhance the detection of stress-related changes in catecholamines.

Adult↗
PubMed2002

Sequential catecholamine and serotonin depletion in mirtazapine-treated depressed patients.

This study was aimed at determining whether patient- or antidepressant-related variables are most important to the mood response to serotonin (5-HT) or catecholamine depletion. Depressed patients treated with open-label mirtazapine (>or=6 wk) received two depletion tests (5-HT and catecholamine depletion) 1 wk apart. Both 5-HT and catecholamine depletion led to a partial return of depression in most patients. Antidepressant response to mirtazapine is dependent on its dual actions on norepinephrine and 5-HT neurotransmission. Mood response to tryptophan or catecholamine depletion is dependent on the pharmacological properties of the antidepressant being taken during depletion.

Adrenergic Uptake Inhibitors↗
PubMed2003

Modulation of frequency and duration of repetitive magnetic stimulation affects catecholamine levels and tyrosine hydroxylase activity in human neuroblastoma cells: implication for the antidepressant effect of rTMS.

Transcranial magnetic stimulation (TMS), which is produced by strong non-static magnetic fields, is a non-invasive means to stimulate the cerebral cortex. Studies from recent years show that TMS affects mood in healthy subjects and improves depressive symptoms in patients with major depression. However, the relationship between the clinical efficacy of TMS and stimulation parameters is still obscure. In the present study we have investigated the effects of different stimulation frequencies and number of treatments on catecholamine turnover in SH-SY5Y cell cultures. A single session of magnetic stimulation (1.7 T) caused a significant decrease in intracellular dopamine and L-DOPA and in noradrenaline (NE) release at a rate of 3 Hz for 10 s but increased NE release at a rate of 9 Hz. These alterations were associated with a reduction (47.8%) or an increase (48%) in tyrosine hydroxylase (TH) activity after 3 and 9 Hz magnetic stimulation, respectively. The latter may be related to the known sensitivity of TH to neuronal firing rates and NE concentrations. Higher stimulation frequencies (15, 20, 45 Hz) had no effect on catecholamine metabolism. Unlike 3 Hz acute treatment, chronic treatment (3 Hz, 11 sessions, for 4 d) had no effect on monoamines and TH activity was increased by 54.5% with no change in its protein level. The results of the present study demonstrate that in tissue culture system frequency and treatment duration of the magnetic stimulation are important factors in affecting catecholamine turnover. Considering the major role of catecholamine in the pathophysiology of depression, these findings may be of relevance to the application of rTMS in humans with major depression.

Blotting, Western↗