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PubMed2006

Recent advances in methods for the analysis of catecholamines and their metabolites.

Catecholamines, for example epinephrine, norepinephrine, and dopamine, are widely distributed and are important neurotransmitters and hormones in mammalian species. Several methods have been developed for analysis of catecholamines and related compounds. Determination of catecholamines in biological fluids has enabled us to clarify the physiological role played by these amines. Catecholamine levels in plasma and/or urine are also useful for diagnosis of several diseases, for example hypertension, pheochromocytoma, and neuroblastoma. This review covers reports from 2000 to the present of methods for the analysis of catecholamines and their metabolites.

Catecholamines↗
PubMed2004

Catecholamine-induced regulation in vitro and ex vivo of intralymphocyte ionized magnesium.

Despite the importance of the adrenergic activity and of the metabolism of magnesium in some important cardiovascular pathologies, very little is known about how intracellular ionized magnesium (Mgi2+) is regulated by catecholamines. We made an in-vitro study of the variations in the concentration of ionized magnesium in human lymphocytes using the fluorescent probe furaptra in response to different catecholamines. We also made an ex-vivo study of the changes in intracellular ionized magnesium in lymphocytes in 20 subjects with essential arterial hypertension, 10 treated with 120 mg/d of propranolol and 10 with placebo. Norepinephrine and isoproterenol significantly decrease Mgi2+ and this effect is blocked by beta-blockers but not by alpha-blockers. The EC50 of the effect of norepinephrine is within the range of concentrations physiologically present in plasma. The substitution of extracellular sodium with choline blocks the decrease in intracellular ionized magnesium induced by norepinephrine, which leads us to suppose that the magnesium-reducing effect of catecholamines is a result of the activation of a Na+-Mg2+ exchanger. We were not able to demonstrate any change in intracellular ionized magnesium after 1 and 17 days of active treatment in essential hypertensives. The impossibility of demonstrating ex vivo the mechanism of catecholamine-mediated regulation that is evident in vitro is perhaps due to our experimental conditions or to substances which in vivo inhibit the action of the catecholamines on magnesium, such as insulin and/or glucose.

Adrenergic alpha-Agonists↗
PubMed2006

Catecholamine secretion from rat foetal adrenal chromaffin cells and hypoxia sensitivity.

The adrenal medulla chromaffin cells (AMCs) secrete catecholamines in response to various types of stress. We examined the hypoxia-sensitivity of catecholamine secretion by rat foetal chromaffin cells in which the innervation by the splanchnic nerve is not established. The experiments were performed in primary cultured cells from two different ages of foetuses (F15 and F19). Membrane potential of AMCs was monitored with the patch clamp technique, and the catecholamine secretion was detected by amperometry. We found that: (1) AMCs from F19 foetuses showed hypoxia-induced catecholamine release. (2) This hypoxia-induced secretion is produced by membrane depolarization generated by an inhibition of Ca(2+)-activated K(+) current [I (K(Ca))] current. (3) Chromaffin precursor cells from F15 foetuses secrete catecholamine. The quantal release is calcium-dependent, but the size of the quantum is reduced. (4) In the precursor cells, a hypoxia-induced membrane hyperpolarization is originated by an ATP-sensitive K(+) current [I (K(ATP))] activation. (5) During the prenatal period, at F15, the percentage of the total outward current for I (K(ATP)) and I (K(Ca)) was 50 and 29.5%, respectively, whereas at F19, I (K(ATP)) is reduced to 14%, and I (K(Ca)) became 64% of the total current. We conclude that before birth, the age-dependent hypoxia response of chromaffin cells is modulated by the functional activity of K(ATP) and K(Ca) channels.

Adenosine Triphosphate↗
PubMed1997

Long-term exposure to ozone alters peripheral and central catecholamine activity in rats.

In addition to its noxious influence on lung airways, ozone inhalation can induce extrapulmonary neural dysfunctions the mechanisms of which are poorly understood. This study was intended to characterize the effects of long-term exposure to ozone (0.5 ppm, 5 days) on catecholamine activity in rat sympathetic efferents and brain areas of prime importance to adaptation to environmental stressors. Catecholamine activity was assessed by estimating the turnover rate of catecholamines and in vivo tyrosine hydroxylase activity in peripheral and central structures, i.e., heart, lungs, superior cervical ganglia, cerebral cortex, hypothalamus and striatum, A2 cell group within the nucleus tractus solitarius (NTS), and locus ceruleus (A6). Ozone inhibited norepinephrine turnover in heart (-48% of the control level) but not in lungs. Ozone failed to modify the tyrosine hydroxylase activity in superior cervical ganglia, and the catecholamine content in the adrenal glands. In the central nervous system, ozone inhibited tyrosine hydroxylase activity in noradrenergic brainstem cell groups, including the locus ceruleus (-62%) and the caudal A2 subset (-57%). Catecholamine turnover was decreased by ozone in the cortex (-49%) and striatum (-18%) but not in the hypothalamus. The data show that ozone can produce marked neural disturbances in structures involved in the integration of chemosensory inputs, arousal, and motor control.

Adrenal Glands↗
PubMed2002

Effects of sulfur containing amino acids on iron and nitric oxide stimulated catecholamine oxidation.

Taurine is a free amino acid found in high concentrations in tissues containing catecholamines. The ability of taurine and its metabolic precursors to inhibit or stimulate catecholamine oxidation and subsequent quinone formation was examined. Ferric chloride was used as the catalyzing agent to stimulate L-dopa or norepinephrine oxidation and NO donors were also examined for their actions to stimulate quinone formation. Taurine attenuated iron-stimulated quinone formation from catecholamines suggesting that it may function as an endogenous antioxidant. Several other sulfur-containing amino acids (homocysteic acid, cysteine sulfinic acid and SAM) were found to inhibit catecholamine oxidation. Among other amino acids tested, homocysteine had biphasic effects; attenuating L-dopa oxidation catalyzed by ferric chloride and potentiating norepinephrine's oxidation catalyzed by both ferric chloride and sodium nitroprusside (SNP). Homotaurine and homocysteine (1 or 10 mM) greatly stimulated SNP-induced norepinephrine oxidation. Homotaurine potentiated quinone formation in the presence of ferric iron and this effect was attenuated by desferroxamine. In order to exclude a possible NO/iron interaction in SNP's oxidizing action, SIN-1 chloride, a specific NO-donor, was tested as an oxidizing agent. The failure of desferroxamine or taurine to attenuate SIN-1 oxidation of norepinephrine suggests that peroxynitrite-mediated oxidation was likely the dominant mechanism. Our results show that endogenous sulfur containing amino acids, like taurine, could serve a protective role to reduce cellular damage associated with both NO and metal-stimulated catecholamine oxidation.

Amino Acids, Sulfur↗
PubMed1975

Metabolism of free fatty acids, glucose and catecholamines in acute myocardial infarction. Relation to myocardial ischemia and infarct size.

The myocardial metabolism of free fatty acids, glucose and catecholamines is reviewed in relation to current trends in the therapy of experimental myocardial infarction. Major modifications in the metabolism of free fatty acids, glucose and catecholamines have already been found after acute myocardial infarction in man, and animal experimental data suggest that such metabolic changes might play a role in the modification of infarct size and sometimes in the development of arrhythmias. However, animal experiments often represent extreme situations and the therapeutic use in man of agents to modify the metabolism of free fatty acids, glucose or catecholamines after myocardial infarction needs intensive investigation before general application. The sum total of the evidence from animal experiments suggests that increased circulating concentrations of free fatty acids and catecholamines, if sufficiently high, may be harmful rather than helpful to the outcome of acute myocardial infarction, and that increased provision of glucose (as glucose, insulin and potassium) may be beneficial. Reservations to these conclusions are that the concentrations used appear to be important factors in catecholamine and free fatty acid effects, and that the mechanism of action of glucose-insulin-potassium is more complex than originally thought.

Adenosine Triphosphate↗
PubMed1987

Stimulation by vasoactive intestinal polypeptide of catecholamine synthesis in isolated bovine adrenal chromaffin cells. Possible involvement of protein kinase C.

In isolated bovine adrenal medullary cells, vasoactive intestinal polypeptide (VIP) stimulated 14C-catecholamine synthesis from 14C-tyrosine, but not from 14C-DOPA. This stimulatory effect of VIP on 14C-catecholamine synthesis was not dependent upon extracellular Ca2+. VIP did not affect the intracellular cyclic AMP (cAMP) level. The stimulatory effect of VIP on 14C-catecholamine synthesis was additive with that of carbamylcholine, which was dependent upon extracellular Ca2+, but not with that of phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA), an activator of protein kinase C. Moreover, 1-(isoquinolinyl-sulfonyl)-2-methylpiperazine (H-7), an inhibitor of protein kinase C, inhibited not only TPA-stimulated, but also VIP-stimulated 14C-catecholamine synthesis from 14C-tyrosine. These results suggested that VIP stimulated catecholamine synthesis by activation of tyrosine hydroxylase and that protein kinase C was involved in this stimulatory mechanism.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1989

Inhibitory action of carvedilol, a novel alpha, beta-adrenoceptor antagonist, on catecholamine secretion and calcium influx in cultured bovine adrenal chromaffin cells.

The effect of carvediolol on the secretory function was studied using cultured bovine adrenal chromaffin cells. Carvedilol caused the concentration-dependent inhibition of catecholamine secretion evoked by carbamylcholine, high K+ or veratridine. The drug also caused the inhibition of radioactive calcium uptake stimulated by these secretagogues into the cells, and the inhibition of calcium uptake was observed in parallel with that of catecholamine secretion. The inhibitory action of carvedilol on catecholamine secretion was shown to be similar to that caused by a classical beta-adrenoceptor antagonist, propranolol. Furthermore, although the level of carbamylcholine-stimulated catecholamine secretion inhibited by diltiazem, a potent calcium channel antagonist, was significantly raised by elevating the calcium concentration in the reaction mixture, increasing the concentration of calcium ions in the mixture failed to induce any substantial influence on the secretion inhibited by carvedilol, as well as propranolol, under the same experimental conditions. These results seem to indicate that carvedilol may cause the inhibition of catecholamine secretion through its blocking action on calcium influx into the cells, and suggest the possibility that the inhibitory action of carvedilol on calcium influx is presumably based on its stabilizing action on the plasma membranes rather than its blocking action on the calcium channels in the chromaffin cell.

Adrenal Glands↗
PubMed1990

Role of Ca2+/phospholipid-dependent protein kinase in catecholamine secretion from bovine adrenal medullary chromaffin cells.

The role of Ca2+/phospholipid-dependent protein kinase (protein kinase C) in catecholamine secretion from bovine adrenal medullary chromaffin cells was examined using four protein kinase C inhibitors: polymyxin B, sphingosine, staurosporine, and 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7). For this purpose, digitonin-permeabilized chromaffin cells were used. Secretion of catecholamines from these cells was stimulated by the addition of micromolar amounts of exogenous free Ca2+. 12-O-Tetradecanoylphorbol-13-acetate (TPA) and arachidonic acid, activators of protein kinase C, enhanced the catecholamine secretion evoked by Ca2+. But phorbol-12, 13-diacetate, a phorbol ester analog that does not activate protein kinase C, had no effect on Ca2(+)-evoked secretion. Polymyxin B at a low concentration (1 microM) abolished the enhancement of secretion by TPA or arachidonic acid without affecting the secretion evoked by Ca2+. However, polymyxin B at higher concentrations (10-100 microM) greatly reduced Ca2+-evoked catecholamine secretion. Sphingosine 10 microM-1 mM), Staurosporine (100 nM-1 microM, and H-7 (100-500 microM) inhibited TPA- or arachidonic acid-enhanced secretion but not Ca2(+)-evoked secretion. In cells in which protein kinase C was down-regulated by TPA, specific binding of [3H]phorbol-12,13-dibutyrate to the cells almost disappeared and the enhancement of secretion by TPA was no longer observed, whereas Ca2(+)-evoked secretion was maintained. These results strongly suggest that protein kinase C is not essential for the Ca2(+)-dependent catecholamine secretion from bovine adrenal chromaffin cells, but acts instead as a modulator.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Involvement of phosphoinositide metabolism in GABA-induced catecholamine release from cultured bovine adrenal chromaffin cells.

The effects of GABA on catecholamine release and phosphoinositide metabolism were studied in cultured bovine adrenal chromaffin cells. GABA and muscimol, a specific agonist for the GABAA receptor, each evoked a gradual secretion of catecholamines from the cells in the presence of ouabain, an inhibitor of Na+, K(+)-ATPase. This release was inhibited by bicuculline, a specific antagonist for the GABAA receptor, or by picrotoxin, a blocker of GABA-gated Cl- channels, and was potentiated by diazepam or pentobarbital. GABA or muscimol induced a concentration-dependent formation of inositol phosphates. This accumulation of inositol phosphates was also inhibited by bicuculline, picrotoxin or removal of extracellular Ca2+, and also potentiated by diazepam and pentobarbital. Nicardipine suppressed GABA-induced catecholamine release in the presence of ouabain and accumulation of inositol phosphates, while verapamil, diltiazem, and omega-conotoxin failed to inhibit these responses to GABA. The phosphoinositide-specific phospholipase C inhibitor neomycin also inhibited both GABA-induced accumulation of inositol phosphates and stimulation of catecholamine release in the presence of ouabain. These results taken together indicate that GABA evoked catecholamine release from the chromaffin cells in the presence of ouabain by stimulation of phosphoinositide metabolism in a Ca2(+)-sensitive manner via activation of GABAA receptor-coupled Cl- channels.

Adrenal Medulla↗
PubMed1992

Prostaglandin E2-induced arachidonic acid release and catecholamine secretion from cultured bovine adrenal chromaffin cells.

We recently reported that prostaglandin E2 (PGE2) and arachidonic acid (AA) each induced a gradual secretion of catecholamines from cultured bovine adrenal chromaffin cells in the presence of ouabain by stimulation of phosphoinositide metabolism. In the present study, we examined the relationship between phospholipase A2 and C activation and catecholamine secretion by PGE2 in chromaffin cells. The phospholipase A2 inhibitors p-bromophenacyl bromide and mepacrine did not affect the basal and ouabain-induced release, but dose-dependently blocked PGE2-evoked phosphoinositide metabolism and the consequent catecholamine release at an IC50 value of 3 microM. PGE2 induced rapid hydrolysis of [3H]AA from prelabeled phospholipid pools: the release of [3H]AA could be detected at as early as 15 sec and reached a plateau after 1 min. While the phospholipase C inhibitor neomycin did not inhibit PGE2-induced AA release, phospholipase A2 inhibitors dose-dependently inhibited it at IC50 values comparable to those for catecholamine release. Pretreatment of intact cells with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate, but not with pertussis toxin, prevented AA release by PGE2. These results demonstrate that PGE2 activates phospholipase A2 as well as phospholipase C in a pertussis toxin-insensitive manner and suggest that the released arachidonic acid may be involved in PGE2-induced catecholamine release from chromaffin cells.

Adrenal Medulla↗
PubMed1994

Inhibition by ouabain of palytoxin-induced catecholamine secretion and calcium influx into cultured bovine adrenal chromaffin cells.

The effect of ouabain on palytoxin (PTX)-induced catecholamine secretion from cultured bovine adrenal chromaffin cells was examined in relation to its effect on calcium (Ca2+) influx into the cells. Ouabain showed concentration-dependent inhibition of catecholamine secretion induced by PTX. Ouabain also inhibited [45Ca]2+ influx induced by PTX, this inhibition being parallel with that of catecholamine secretion. The inhibitory effects of ouabain on PTX-induced catecholamine secretion and [45Ca]2+ influx were both overcome by increasing the concentrations of PTX, indicating that ouabain inhibited the actions of PTX in a competitive manner. These results suggest that the ouabain-sensitive (or-binding) site on the cell membrane might be the target site of action of PTX, which causes an increase in Ca2+ permeability and initiation of catecholamine secretion.

Acrylamides↗
PubMed1992

Lithium chloride stimulates catecholamine synthesis and secretion in cultured bovine adrenal medullary cells.

We examined the effects of lithium treatment on the synthesis and secretion of catecholamines in cultured bovine adrenal medullary cells. The treatment of cells with lithium (0.5-4 mmol/L) for 7 days caused an increase in basal and carbachol-stimulated synthesis of 14C-catecholamines from [14C]-tyrosine but not from [14C]-DOPA. Lithium treatment (4 mmol/L, 7 days) increased the activity of tyrosine hydroxylase in the cells. Lithium treatment (2-4 mmol/L, 7 days) also enhanced the secretion of catecholamines caused by carbachol, although the carbachol-induced influx of 45Ca2+ was reduced. Lithium (4 mmol/L, 7 days) potentiated the secretion of catecholamines evoked by the Ca2+ (1 mumol/L) from cells that were permeabilized by digitonin. The activity of protein kinase C in a soluble fraction was increased in lithium-treated cells (4 mmol/L, 7 days). These results demonstrate that lithium treatment increases the synthesis and secretion of catecholamines and the activity of protein kinase C in cultured adrenal medullary cells.

Adrenal Medulla↗
PubMed1979

Estrogen-induced efflux of endogenous catecholamines from the hypothalamus in vitro.

Short-term organ cultures of the intact hypothalamus were used to study the effects of various estrogenic compounds on catecholamine release. Estradiol-17 beta (0.1--20 microM) produced a concentration-dependent efflux of norepinephrine and dopamine while its biologically inactive enantiomer, estradiol-17 alpha, was ineffective at concentrations up to 20 microM. Diethylstilbestrol, a potent non-steroidal estrogen, was as effective as estradiol-17 beta in inducing catecholamine efflux. In contrast, weakly or non-estrogenic steroids such as estrone, estriol, and corticosterone were without effect. The time course of the estrogen-induced efflux of hypothalamic catecholamines was similar to that previously reported for the estrogen-induced accumulation of hypothalamic cAMP, providing further evidence for the involvement of catecholamines in this effect. Theses results suggest that estrogen may facilitate the release of catecholamines within the hypothalamus.

Animals↗
PubMed1981

Catecholamine synthesis regulation in hypothalamic synaptosomes.

In order to characterize the properties of synaptosomal catecholamine formation in a predominantly noradrenergic preparation, we have studied catecholamine synthesis in rat brain hypothalamic synaptosomes. Kinetic analysis revealed an apparent Km for tyrosine of 2.5 microM and an apparent Vmax of 2.1 nmol/h/g. In the hypothalamus, norepinephrine-induced synthesis inhibition was completely reversed by preincubation with desipramine, a blocker of catecholamine uptake into noradrenergic tissue. In contrast, desipramine was relatively ineffective in the predominantly dopaminergic striatum, indicating that most of the catecholamine synthesis observed in the hypothalamic synaptosomes was taking place in noradrenergic, as opposed to dopaminergic, terminals. Synthesis was stimulated approximately 30% in the hypothalamus by elevated (55 mM) potassium. This stimulation was markedly antagonized in a calcium-free buffer and by the addition of tetraethylammonium chloride. Phenylethylamine compounds could produce either stimulation (amphetamine) or inhibition (tyramine). The most effective synthesis stimulator was dibutyryl cyclic AMP (80% stimulation at 2 mM). Lowering the pH of the incubation buffer from 7.2 to 6.2 increased the basal rate but decreased the stimulatory response to elevated potassium. These data suggest that synaptosomal preparations from the hypothalamus offer a convenient system for studying drug effects on catecholamine synthesis in noradrenergic terminals.

Animals↗
PubMed1983

High-performance liquid chromatographic determination of urinary free catecholamines with electrochemical detection after prepurification on immobilized boric acid.

A reliable high-performance liquid chromatographic method is presented for the determination of the urinary free catecholamines noradrenaline, adrenaline and dopamine. Urine is purified on a column of immobilized boric acid. Catecholamines are separated by ion-pair reversed phase high-performance liquid chromatography and detected electrochemically. The method is suited for routine analysis. It allows the determination of urinary free catecholamines in concentrations as low as 1 microgram/1 for noradrenaline and adrenaline and 5 micrograms/1 for dopamine. A single analysis can be completed within 1 h. Routine analyses can be carried out in a series of 40 samples within 2 days. The within-assay and between-assay coefficients of variation of the analyses in urine were both 2.9% for noradrenaline, both 5.0% for adrenaline, and 1.9 and 2.1% for dopamine. The chromatographic properties of the immobilized boric acid were investigated. In particular, the elution pattern of a series of catecholamine metabolites and analogues was determined. Under the conditions used, only basic compounds containing both a vicinal hydroxyl configuration and a primary or secondary amino group adsorb and elute together with the free catecholamines.

Boric Acids↗
PubMed1985

Interference of labetalol metabolites in the determination of plasma catecholamines by HPLC with electrochemical detection.

The alpha and beta adrenoceptor blocking drug labetalol is a potent antihypertensive agent in widespread clinical use. Its interference in the classical chemical estimations of urinary catecholamines and their metabolites has been the subject of several reports. Factitiously raised values have been noted in both the fluorimetric catecholamine assay, and the standard spectrophotometric procedure for total (free and conjugated) metadrenalines. To avoid such drug interference, modification of these methods is required in the estimation of catecholamines and their o-methylated metabolites. Alternatively, VMA estimations or plasma/urinary catecholamine measurements by radioenzymatic assay may be used in patients on labetalol. Although high performance liquid chromatography coupled with electrochemical detection (HPLC-ECD) methods for estimation of plasma catecholamines are now in widespread use, the interference of labetalol in this method has not been reported. We now report that significant direct interference of labetalol in the HPLC-ECD assay does indeed occur, and can yield spuriously raised adrenaline levels.

Aluminum Oxide↗
PubMed1978

Analysis of feeding suppression produced by perifornical hypothalamic injection of catecholamines, amphetamines and mazindol.

The effects on feeding of perifornical hypothalamic injection of catecholamines, amphetamines and mazindol were examined in hungry rats. In pargyline-pretreated subjects, both dopamine and epinephrine significantly suppressed food intake, at doses as low as 31 ng for dopamine and 150 ng for epinephrine (the latter injected with an alpha-adrenoceptor blocker). This effect was reliably strengthened by inhibiting catecholamine deamination or presynaptic catecholamine uptake. Perifornical injections of amphetamine, mazindol, methamphetamine, and phenmetrazine also suppressed feeding. The magnitude of this effect in individual animals was positively correlated with the effect produced by catecholamine agonists. Moreover, this effect of mazindol was partially antagonized by perifornical injection of dopaminergic and beta-adrenoceptor blockers. The effects of amphetamine and epinephrine were abolished by these drugs, while dopamine's effect was selectively inhibited by the dopaminergic antagonist. Serotonergic antagonists produced no change. These findings lend support to the hypothesis that perifornical hypothalamic catecholamine neurons, through dopaminergic receptors and beta-adrenoceptors, are involved in inhibiting feeding behavior, as well as in mediating the anorexic action of the amphetamines and mazindol.

Amphetamines↗