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PubMed1988

Rapid antidepressant response to alprazolam in depressed patients with high catecholamine output and heterologous desensitization of platelet adenylate cyclase.

The present study examined the relationship between 24-hr urinary catecholamine (norepinephrine and epinephrine) output and measures of platelet adenylate cyclase (AC) activity in depressed patients (n = 17) and control subjects (n = 10). In both groups, significant inverse correlations were observed when 24-hr urinary catecholamine levels were examined in relation to measures of both receptor-mediated (prostaglandin D2 and alpha 2-adrenergic) and postreceptor-mediated (NaF) platelet AC enzyme activities, suggesting that circulating catecholamines may regulate platelet AC by heterologous (agonist-nonspecific) desensitization of the AC enzyme complex. Depressed patients who had favorable antidepressant responses to alprazolam had significantly higher pretreatment urinary catecholamine output and lower receptor-mediated platelet AC enzyme activities than control subjects, whereas the nonresponders did not. After 8 days of treatment with alprazolam, urinary catecholamine levels declined significantly. In responders, receptor-mediated measures of platelet AC activity increased significantly by day 8 to values comparable to those in control subjects; but similar changes were not observed in nonresponders. Prior to treatment, responders showed a strict linear relationship between receptor-mediated (prostaglandin D2) and postreceptor-mediated (NaF) stimulation of platelet AC activity through the stimulatory guanine nucleotide regulatory protein (Ns), whereas nonresponders did not. This suggests the presence of two distinct coupling interactions between platelet prostaglandin D2 receptors and the stimulatory guanine nucleotide regulatory protein in responders and nonresponders to the antidepressant effects of alprazolam prior to treatment. The authors propose that catecholamines, possibly acting through prostaglandins, may regulate platelet AC enzyme activity by heterologous desensitization occurring through postreceptor mechanisms.

Adenylyl Cyclases↗
PubMed1985

Tyrosine accelerates catecholamine synthesis in hemorrhaged hypotensive rats.

Tyrosine, the amino acid precursor of catecholamines, increases blood pressure (BP) in rats made hypotensive by hemorrhage. Since this amino acid also accelerates catecholamine synthesis in and release from frequently-firing neurons, we tested the hypothesis that tyrosine's pressor action resulted from this mechanism. Male Sprague-Dawley rats (500 g) were anesthetized with chloralose (50 mg/kg) and urethane (500 mg/kg) and tracheostomized. The carotid artery was cannulated allowing BP to be recorded continuously. Blood was removed until systolic BP fell to half of each animal's starting value; 45 min later, animals received tyrosine or other treatments in volumes of 1 ml/kg. Tyrosine (100 mg/kg) increased BP by 58%, while saline caused an insignificant increase. Pretreatment with carbidopa, which inhibits tyrosine's conversion to catecholamines, blocked the amino acid's effect. Tyrosine also failed to increase BP in rats made hypotensive with phentolamine, suggesting that it acts via catecholamine receptors. Adrenal epinephrine significantly (P less than 0.02) and splenic norepinephrine slightly (P less than 0.07) increased in rats receiving tyrosine after 1 h of hypotension when compared with tissue-catecholamine contents in similar rats. These observations show that tyrosine increases BP during hemorrhagic hypotension by accelerating catecholamine synthesis.

Adrenal Glands↗
PubMed1993

N-methyl-4-phenylpyridinium (MPP+) potentiates the killing of cultured hepatocytes by catecholamines.

The role of catecholamines in the toxicity of MPTP (N-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine) was explored. The killing of cultured hepatocytes by dopamine and 6-hydroxydopamine was enhanced following inhibition of glutathione reductase by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a manipulation known to sensitize such cells to an oxidative stress. The participation of activated oxygen species in the cell injury under such circumstances was shown by the ability of catalase and the ferric iron chelator deferoxamine to protect the hepatocytes. The toxicity of catecholamines was also potentiated by the mitochondrial site I (NADH dehydrogenase) inhibitor rotenone. MPP+ (N-methyl-4-phenyl-pyridinium), the putative toxic metabolite of MPTP is also a site I inhibitor. Incubation of hepatocytes with MPP+ similarly potentiated the toxicity of 6-hydroxydopamine, dopamine, and norepinephrine under conditions where MPP+ alone or catecholamines alone did not kill cells. Hepatocytes that had accumulated dopamine from the medium were killed by a subsequent exposure to MPP+ in the absence of a catecholamine in the medium. Hepatocytes that had not been pretreated with dopamine were not affected by the subsequent exposure to MPP+. These data indicated that catecholamines render hepatocytes more susceptible to the toxicity of MPP+ and suggest that the presence of catecholamines in specific neurons in the brain may be related to the selective neurotoxicity of MPTP.

1-Methyl-4-phenylpyridinium↗
PubMed1985

Development of cells containing catecholamines and somatostatin-like immunoreactivity in neural crest cultures: relationship of DNA synthesis to phenotypic expression.

The goal of our work is to understand the mechanisms which regulate the differentiation of embryonic neural crest cells into a number of adult cell types, including several classes of neurons. As one aspect of this analysis, the relationship between DNA synthesis and the ontogeny of cells with catecholamines and somatostatin-like immunoreactivity (SLI) in neural crest cell cultures has been investigated. Most of the precursors of the catecholamine- and SLI-positive cells carry out DNA synthesis. As these cells differentiate, their ability to carry out DNA synthesis declines. However, a small percentage of cells continue to synthesize DNA after they become catecholamine or SLI positive. There is no apparent difference between the temporal pattern of DNA synthesis in the precursors of catecholamine-positive cells with SLI and those without SLI. Thus, the time of withdrawal from the cell cycle does not distinguish the lineage of cells that are catecholamine and SLI positive from those that are catecholamine positive and SLI negative.

Animals↗
PubMed1985

Pharmacological interference with the neurotoxic action of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on central catecholamine neurons in the mouse.

The effect of pretreatment with various MAO and catecholamine uptake inhibitors on the MPTP-induced reduction of endogenous catecholamine levels and [3H]catecholamine uptake in mouse striatum and cerebral cortex associated with the neurotoxic action of MPTP on dopamine and noradrenaline neurons was investigated. Pargyline and deprenyl almost completely reversed the MPTP-induced reduction of these parameters in both regions while chlorgyline was without effect. Pretreatment with the dopamine uptake inhibitor amfolenic acid preferentially counteracted the depleting effect of MPTP on striatal dopamine levels. The noradrenaline uptake inhibitors desipramine, nortriptyline and LY 139603 all antagonized the MPTP-induced reduction of noradrenaline levels in cerebral cortex, while none of these inhibitors affected the action of MPTP on striatal dopamine. The results suggest that MAO-B and the catecholamine uptake system may be critically involved at certain steps in the neurotoxic action of MPTP on catecholamine neurons. The interaction with the uptake mechanism most likely explains the selective neurotoxic action of MPTP on catecholamine neurons.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1991

Mechanism of blockade by (+)isradipine of adrenal catecholamine release.

Cat adrenal glands were perfused at a high rate with various modified Krebs solutions containing different concentrations of K+ but no Ca2+. Catecholamine release was tested by applying brief Ca2+ pulses (10 s of a solution containing 120 mM K+ and 2.5 mM Ca2+). Under polarizing conditions (10 min perfusion with 1.4 mM K+ with no Ca2+), the total catecholamines released by the Ca2+ pulse amounted to 5 micrograms; in depolarizing conditions (10 min perfusion with a solution containing 70 mM K+ but no Ca2+), secretion was somewhat less (4-4.5 micrograms). (+)Isradipine, a 1,4-dihydropyridine Ca2+ channel blocker, did not affect the secretory response under polarizing conditions at 10(-8) M; at 10(-6) M, the secretory response was halved. When present under depolarizing conditions (70 mM K+ in 0 Ca2+), (+)isradipine (10(-8) M) blocked catecholamine release by 90%. In contrast, the inorganic Ca2+ channel blocker, Co2+, inhibited secretion equally well under polarizing or depolarizing conditions. Since 45Ca2+ uptake into adrenal medullary chromaffin cells was also inhibited by (+)isradipine (10(-8) M) in a voltage-dependent manner, it seems likely that blocking effects of the drug on catecholamine release are associated with inhibition of Ca2+ entry into cells through L-type Ca2+ channels. The association of (+)isradipine to its receptor is very rapid under polarizing conditions; dissociation is very slow in depolarized cells and very rapid upon polarization of such cells. Since chromaffin cells are being depolarized during stressful situations to secrete catecholamines into the circulation, (+)isradipine is likely to bind better to dihydropyridine receptors in this state; in this manner, the ensuing blockade of adrenal secretion could serve as a protective mechanism of cardiovascular tissues against massive increases in circulating catecholamines. If this suggestion is correct this mechanism could have additional therapeutic value in the treatment of hypertensive patients with (+)isradipine.

Adrenal Glands↗
PubMed1992

Effects of gentamicin on catecholamine levels in the striatum, hypothalamus, adrenal gland and vas deferens.

The effects of gentamicin, an aminoglycoside antibiotic, on changes in the catecholamine levels in the rat striatum, hypothalamus, adrenal medulla and vas deferens were studied. When rats were i.v. injected with gentamicin (1.0 mg/kg), the catecholamine content of all tissues increased 2-4 h after injection. The increases in catecholamine levels induced by gentamicin were about 1.4- to 2.3-fold those induced by saline. The effect of gentamicin was observed at 0.1 or 0.5 mg/kg, and was maximal at 2.0 mg/kg. The activity of tyrosine hydroxylase, a rate-limiting enzyme in catecholamine biosynthesis, was markedly increased in all four tissues of rats treated with gentamicin (1.0 mg/kg, 4 h). However, direct addition of gentamicin to the tyrosine hydroxylase assay medium did not affect tyrosine hydroxylase activity. These data indicate that gentamicin administration to rats increases the catecholamine content of both central and peripheral catecholamine-containing tissues. The results also suggest that the effect of gentamicin is due to an indirect activation of tyrosine hydroxylase.

Adrenal Medulla↗
PubMed1983

Effect of locally released catecholamines on lipolysis and injury of the hypoxic isolated rabbit heart.

The ability of endogenous myocardial catecholamines to stimulate lipolysis of endogenous triglycerides and the role of this process in the development of myocardial injury were studied in isolated, Langendorff-perfused rabbit heart preparations exposed to 3 h of hypoxic perfusion followed by 30 min of aerobic perfusion. Untreated hearts responded not only to hypoxia but also to reoxygenation with surges of noradrenaline outflow lasting 10 and 5 min, respectively. During hypoxia but not during reoxygenation a parallel surge of glycerol outflow was observed. Nicotinic acid (10(-5) M) prevented glycerol outflow during hypoxia but did not influence the outflow of noradrenaline during either hypoxia or reoxygenation. Neither noradrenaline nor glycerol were detected in the effluent from the hearts depleted of endogenous catecholamines by reserpine pretreatment. Those hearts also showed a smaller lactate dehydrogenase release during hypoxia (49% reduction) and no increase in lactate dehydrogenase release during reoxygenation. Similar reduction of lactate dehydrogenase release during hypoxia (52% reduction) was observed in the hearts treated with nicotinic acid. This drug, however, did not prevent the reoxygenation-induced lactate dehydrogenase release. The effects of reserpinization and nicotinic acid treatment on lactate dehydrogenase release were not additive. It is concluded that hypoxia is a stimulus for lipolysis in the isolated rabbit heart and most probably this process is catecholamine dependent. At least part of the deleterious effect of endogenous catecholamines on hypoxic myocardium might be attributed to catecholamine-stimulated lipolysis of endogenous triglycerides. The latter, however, does not seem to contribute to deleterious effects of endogenous catecholamines during reoxygenation.

Animals↗
PubMed1991

Respiratory function of catecholamines during the late period of avian development.

To study the function of catecholamines in the late period of avian embryogenesis, the time course of plasma catecholamines, the release of catecholamines by hypoxia and finally the effect of adrenergic agents on blood parameters and on circulation were recorded. The experiments reveal a temporary increase in plasma adrenaline and noradrenaline shortly before internal pipping occurs. On the other hand a premature increase of plasma catecholamines is induced by hypoxia. Furthermore, treating the embryo with adrenergic agents such as adrenaline, noradrenaline and phenylephrine resulted in changes of blood gas parameters: increase of PO2, O2-saturation and negative base excess, decrease of PCO2 and HCO3-. In addition, exogenous adrenaline and noradrenaline released an increase in the blood flow and an enhanced hemoglobin content in the chorioallantoic membrane, but not in the kidneys. Finally, adrenaline caused a decrease of 2,3 DPG and an increase of lactate in the plasma. The data indicate that hypoxia, which is formed normally towards the end of embryogenesis, induces an increased secretion of catecholamines which in turn improves the blood gas status. In this way the embryo is protected from deleterious hypoxic damages. This conclusion has been derived from experiments, in which the release of catecholamines was blocked under hypoxia. Under these conditions a significant increase in the mortality rate was observed.

2,3-Diphosphoglycerate↗
PubMed1983

Role of tyrosine in the acute effects of ethanol on rat brain catecholamine synthesis.

Acute ethanol administration exerts multiple effects on rat brain catecholamine synthesis, associated with corresponding changes in cerebral tyrosine concentration. Catecholamine synthesis is enhanced at 1 hr by an increased availability of circulating tyrosine to the brain after inhibition of liver tyrosine aminotransferase activity. Tyrosine hydroxylation in vivo and tyrosine hydroxylase activity measured in vitro are also enhanced at 1 hr. Catecholamine synthesis is inhibited at 2-4 hr when tyrosine availability to the brain is decreased because of an enhancement of liver tyrosine aminotransferase activity. Serum neutral amino acid concentrations are decreased at 5 hr. This is followed 1 hr later by normalization of cerebral catecholamine synthesis. By 8 hr after ethanol administration, the latter becomes enhanced because of increased cerebral uptake of tyrosine. Catecholamine synthesis is inhibited at 12 hr because of enhanced transamination of brain tyrosine. Tyrosine metabolism finally returns to normal at 16 hr after ethanol administration. These results are discussed in relation to previous work with ethanol, and to central and peripheral mechanisms of regulation of brain catecholamine synthesis.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Determination of catecholamines in rat tissues by high-performance liquid chromatography using a precolumn fluorescence labeling method.

A high-performance liquid chromatographic method using solid-phase dansylation on alumina for precolumn fluorescence label has been developed for the determination of catecholamines (norepinephrine, epinephrine, and dopamine) in various rat tissues. After alumina treatment of the tissue homogenate, catecholamines adsorbed on the alumina were dansylated by solid-phase reaction. Both the excess reagent and fluorescent degradation products produced during dansylation were washed out from the alumina. Dansylated catecholamines were eluted from the alumina and separated by reversed-phase high-performance liquid chromatography. The four catecholamine derivatives, including the internal standard, were separated within 17 min, and no major interfering peak could be detected on any chromatograms. The calibration graph showed a good linearity in a range of 10 to 500 pmol for each catecholamine per sample. This method was applied to different rat tissues, and both the recovery and the reproducibility for all samples proved to be satisfactory. The present study provides a simple, sensitive, and selective method useful for routine pharmacological experiments of the determination of catecholamines.

Animals↗
PubMed1994

Interference by pH and Ca2+ ions during measurements of catecholamine release in slices of rat amygdala with fast-scan cyclic voltammetry.

Fast-scan cyclic voltammetry (FSCV) at carbon-fiber microelectrodes was used to investigate catecholamine release and uptake induced by local electrical stimulation of rat brain slices containing the basolateral amygdaloid nucleus. The amygdala contains less catecholamine than the striatum, and the observed release is proportionately smaller. Stimulus trains of long duration were required to obtain a well-resolved concentration change in the basolateral amygdala. Voltammetric detection of catecholamines under these conditions was complicated by interference from two extracellular ions, H+ and Ca2+. Ion-selective microelectrodes were used in conjunction with carbon-fiber microelectrodes to monitor pH and Ca2+. The magnitude of the pH changes was correlated with stimulation length and followed the pattern of a brief alkaline shift followed by a longer acidic shift. Extracellular Ca2+ concentration decreased during stimulation and returned fairly rapidly to baseline after the stimulation was over. Because it was not possible to account for all of the ionic interferences using information in the voltammograms, other strategies were employed. Exposure of amygdala slices to L-DOPA or DA increased electrically evoked release of catecholamine, but the effect was transient, and uptake rates decreased during continued exposure to these agents. The most successful approach to remove the interferences was to subtract the response obtained after exposure of the slice to the catecholamine depleter, Ro 4-1284. This agent eliminates the catecholamine response but does not appear to alter the ionic changes.

Amygdala↗
PubMed1988

Enhancement of peptidergic synaptic transmission by catecholamines in the bullfrog sympathetic ganglion.

Extracellular recordings were made from postganglionic branches or ganglion cells of the 9th or 10th ganglia of the paravertebral sympathetic chain of the bullfrog in vitro. Tetanic preganglionic stimulation, applied to nerve fibers between the 7th and 8th ganglia, elicited cholinergic (muscarinic) and non-cholinergic synaptic responses in nicotinized preparations. These were an early after-discharge (EAD) and a late after-discharge (LAD), respectively. Brief application (3-10 min) of catecholamines augmented the LAD and this augmentation continued for 90-120 min after catecholamine withdrawal. In contrast, these catecholamines did not significantly augment the EAD. The catecholamine effects were concentration-dependent within the range 1-100 microM, and the order of the potency was isoprenaline greater than adrenaline greater than noradrenaline greater than dopamine = phenylephrine. The catecholamine-induced augmentation was blocked by propranolol (0.1-1 microM) and pindolol (1-10 microM), but not by phentolamine (up to 10 microM). The catecholamine-evoked augmentation of the LAD could be mimicked by dibutyryl cyclic adenosine 3',5'-monophosphate (dbc-AMP) at 1-50 microM. However, similar concentrations of cyclic adenosine 3',5'-monophosphate (c-AMP), cyclic guanosine 3',5'-monophosphate (c-GMP) and dibutyryl c-GMP (dbc-GMP) had no effect. None of cyclic nucleotides appreciably augmented the EAD. Methylxanthines, 3-isobutyl-1-methylxanthine and caffeine, facilitated the LAD and potentiated the isoprenaline-induced augmentation of the LAD. The excitatory actions of luteinizing hormone releasing hormone (LHRH) were also enhanced by (-)-isoprenaline and dbc-AMP. The former was prevented by propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1995

Pericardial repair depresses canine cardiac catecholamines and met-enkephalin.

Decreased cardiac catecholamines were observed following incision and repair of the pericardium in sham-operated vs. unoperated control dogs. Animals were assigned to five groups: unoperated, sham-operated intact pericardia, open pericardia, sutured pericardia and complete ventricular sympathectomy. Hearts were collected four weeks after surgery. Sympathectomy decreased catecholamine content when compared to all other groups. Hearts with open/sutured pericardia contained significantly less catecholamines than controls. When the pericardium was intact or left open following incision, cardiac catecholamines were unchanged compared to unoperated controls. Since opioid peptides are colocalized with catecholamines, we measured met-enkephalin and met-enkephalin-arg-phe, proenkephalin A peptide products, in parallel samples. Similar to norepinephrine, met-enkephalin was decreased following both sympathectomy and pericardial repair. However, met-enkephalin-arg-phe, which may be more associated with the myocardium than its innervation, was not changed by any treatment. The sutured pericardium more than the stress of surgery apparently alters the tissue catecholamines and enkephalin. This may have resulted from the mechanical friction at the site of repair. Epinephrine and met-enkephalin contents in sympathectomized hearts were significantly lower than unoperated controls but were not significantly different from the intermediate values observed in the sutured group. The functional consequences of these changes on neuroendocrine status are unclear and will require further evaluation. The results also emphasize the need for careful attention to proper controls for surgical studies.

Animals↗
PubMedDate not supplied

Fetal adrenal VIP: distribution and effect on medullary catecholamine secretion.

Vasoactive intestinal peptide (VIP) was found in the adrenal gland of ovine fetuses at 130-135 days gestation and was shown to stimulate catecholamine secretion. VIP was demonstrated by immunocytochemistry using the indirect antibody-enzyme method. VIP-immunoreactive nerve fibers were observed in the capsule, zona glomerulosa and inner layer of the cortex as well as in the medulla; furthermore small clusters of VIP-containing cell bodies were found at the corticomedullary border. To study the direct effect of VIP on catecholamine release, fetal adrenal medulla was dispersed into single cells and incubated in vitro with VIP for 6 hours. Catecholamine release into the medium was measured at 1, 3 and 6 hours. At 6 hours of incubation, VIP stimulated total catecholamine release from fetal adrenomedullary cells in a dose-dependent manner at concentrations ranging from 10(-8) to 10(-4) M. The release of norepinephrine and epinephrine, but not dopamine, was significantly enhanced. The presence of VIP in the fetal adrenal cortex and medulla, and the ability of VIP to stimulate catecholamine release from fetal adrenomedullary cells in vitro suggest that VIP may be an important modulator of medullary catecholamine secretion during fetal life.

Adrenal Glands↗
PubMed1996

Correlation between secretagogue-induced Ca2+ influx, intracellular Ca2+ levels and secretion of catecholamines in cultured adrenal chromaffin cells.

Catecholamine secretion induced by various secretagogues in cultured bovine chromaffin cells has been correlated with Ca2+ influx and intracellular Ca2+ concentrations. Nicotine and high K+ caused prompt secretion of catecholamines from cells. Coincidently, both secretagogues evoked 45[Ca2+] influx with a parallel increase in free intracellular Ca2+ concentration, as determined by Quin 2 fluorescence. However, the rate of return of Ca2+ level to baseline after nicotine stimulation was more rapid than after K+ stimulation. In comparison, stimulation with veratridine produced a slow and prolonged Ca2+ influx accompanied by lower levels of intracellular Ca2+ than those observed after nicotine or K+ stimulation. Yet, during 15 min of stimulation, veratridine induced a substantial catecholamine release, which was larger than that obtained after nicotine or K+ stimulations. The Ca2+ ionophore A23187 (1 microM) induced a pronounced increase in intracellular Ca2+ levels, but did not evoke any significant catecholamine release. Finally, addition of the Ca2+ channel blocker verapamil following stimulation, at a time when intracellular Ca2+ concentration was at its peak level, did not affect the rate of decline in intracellular free Ca2+ concentration but promptly blocked Ca2+ uptake and catecholamine secretion. These findings suggest that the rate of Ca2+ influx, rather than the absolute level of intracellular Ca2+ concentration, determines the rate and extent of catecholamine release.

Aminoquinolines↗
PubMed1991

Palytoxin: a potent stimulator of catecholamine release from cultured bovine adrenal chromaffin cells.

The effect of palytoxin (PTX), a potent marine toxin, on catecholamine release from cultured bovine adrenal chromaffin cells was examined. PTX at concentrations of over 10(-9) M induced catecholamine release dose-dependently. About 40-50% of the total cellular catecholamine was released during 20-min incubation with 3 x 10(-8) M PTX. PTX-induced catecholamine release was dependent on both extracellular Na+ and Ca2+, and was inhibited by organic and inorganic Ca2+ channel blockers, but not by tetrodotoxin. PTX-induced increase in 45Ca2+ influx into the cells, which was associated with catecholamine release, was also inhibited by these Ca2+ channel blockers. These results indicated that PTX-induced catecholamine release was mediated by activation of Na(+)-dependent, tetrodotoxin (TTX) insensitive voltage-dependent Ca2+ channels.

Acrylamides↗
PubMed1976

Catecholamine secretion by isolated adrenal cells.

Isolated adrenal cells were prepared by collagenase digestion of guinea pig adrenal glands. Acetylcholine stimulates the secretion of catecholamines by these isolated adrenal cells. Acetylcholine-stimulated catecholamine secretion is inhibited by cholinergic blocking agents (atropine and hexamethonium) and by local anaesthetics (tetracaine), and is dependent upon the concentration of Ca2+ in the incubation medium. In the presence of Ca2+, catecholamine secretion is also stimulated by two divalent cation ionophores, A23187 and X-537A. Cyclic nucleotides and 5'-nucleotides cause a small, non-specific stimulation of catecholamine secretion. These results indicate that isolated adrenal cells are a useful system in which to study catecholamine secretion, and support the hypothesis that increased Ca2+ entry into chromaffin cells is a sufficient stimulus for catecholamine secretion.

Acetylcholine↗