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At least 1,135 records · Page 63Linked to original sources
PubMed1987

Dilution of plasma with Tris buffer increases measured catecholamines in plasma.

We investigated the effects of dilution of plasma samples on the measured concentrations of catecholamines. Diluting samples of human plasma 10-, 50-, and 100-fold with Tris buffer (100 mol/L, pH 8.6) improved analytical recovery of internal standards, suggesting that it decreases the commonly observed inhibition of methylation in radioenzymatic assays of catecholamines in plasma. However, the dilution is not associated with a proportional decrease in counted radioactivity. This extra amount of radioactivity, which is unlikely to be nonspecific in origin, accounts for a significant increase in the calculated catecholamine concentration. Tentatively, we suggest that Tris buffer releases both catecholamines and conjugated catecholamines bound to some unidentified low-molecular-mass component of plasma.

Dopamine↗
PubMed1987

Failure of chronic theophylline therapy to alter circulating catecholamines.

An increase in circulating adrenaline and noradrenaline has been reported following acute dosing with theophyllines. This effect on catecholamines has been proposed as a possible mechanism of action of theophyllines. In a double-blind placebo controlled trial we have studied the effects of 5 days oral theophylline therapy on circulating catecholamines and adrenaline clearance. There were no significant changes in circulating catecholamines or adrenaline clearance following theophylline. We also examined the effects of theophylline on the hypokalaemic and haemodynamic actions of adrenaline. Theophylline increased the hypokalaemia, tachycardia and rise in systolic blood pressure which occurs in response to intravenous infusion of doses of L-adrenaline (0.02-0.06 microgram kg-1 min-1). Our results suggest that chronic theophylline therapy does not significantly increase circulating catecholamines. Increased circulating catecholamine concentrations are thus not an explanation for the chronic actions of theophylline. We have demonstrated significant, potentially hazardous metabolic and haemodynamic interactions between theophylline and adrenaline.

Adult↗
PubMed1987

[Effect of stress and the antioxidant ionol on the biosynthesis of catecholamines and the content of dopamine in the heart and adrenal glands].

The effects of a synthetic antioxidant ionol (dibunol) on the biosynthesis and content of catecholamines in the heart and adrenal glands were studied. It was shown that in stress a mobilization of catecholamine reserve is combined with a considerable increase in dopamine concentration. In conditions of physiological rest, ionol did not affect the studied indices of adrenal catecholamine biosynthesis, while in the heart it enhanced the dopamine synthesis and content. With ionol administration, stress did not suppress but, on the contrary, increased the neuronal uptake and noradrenaline biosynthesis, catecholamine concentration remaining practically unchanged. Simultaneously, a manyfold increase in the biosynthesis along with a considerable increase in the concentration of dopamine developed in both organs. The data obtained suggest that ionol realizes its stress-defensive effect to a great extent due to the activation of catecholamine biosynthesis and to a concomitant increase in dopamine accumulation.

Adrenal Glands↗
PubMedDate not supplied

Relationships between thyroid hormone and catecholamines in experimental trauma.

The relationship between thyroid hormones (T4 and T3) and the catecholamines (adrenaline and noradrenaline) was studied as regards the possible value of administered T3 in the treatment of severely injured patients. Preparative surgery was performed on 36 pigs, 26 of which were then submitted to a standardized high-energy missile trauma to a hind leg. In 14 of the latter group, infusion of T3 was begun immediately before the trauma (n = 6), or after a delay of 8 h (n = 4) or 24 h (n = 4). A correlation was found between the disappearance rate of T3 and T4 and the catecholamine release, r = 0.79 (p less than 0.001) for adrenaline and 0.64 (p less than 0.01) for noradrenaline. T3 infusion started immediately before high-energy trauma resulted in raised serum levels of catecholamines, mainly noradrenaline, and was associated with a high mortality (4/6), and a clinical picture resembling thyrotoxic crisis. At 8 h the catecholamine-response to T3 administration was blunted and at 24 h post-trauma no influence on catecholamine levels could be determined. The high correlation between adrenaline release and disappearance rates of T3 and T4 after trauma suggests that adrenaline may in some way be connected to the fall in serum T3 and T4 concentrations following major trauma. The results further accord with the suggested role of T3 as a false neurotransmitter. Administration of T3 in the initial phase of the "low T3 state", presumably would not be of benefit for the severely injured patient.

Animals↗
PubMed1985

Effect of the rate of blood loss on the plasma catecholamine response.

In the present experiments the influence on the sympatho-adrenal system of the rate of haemorrhage-induced blood pressure fall in dogs was studied by measuring the plasma catecholamine response. Bleeding to a mean arterial pressure of 5.3 kPa in either 10 or 40 minutes caused an identical increase in the plasma catecholamine level. Similarly, there was no difference in bleeding volumes between the two groups. Within these limits the magnitude of the early catecholamine response was independent of the rate of the haemorrhage-induced decrease of blood pressure. The magnitude of the sympatho-adrenal response depended on the amount of lost blood. Bleeding for 80 minutes to the same pressure resulted in a considerably larger loss of blood and higher plasma catecholamine levels. No relationship was, however, found between the extent of the catecholamine response and the amount of the bleeding volume, probably due to some interaction with other control mechanisms.

Adrenal Glands↗
PubMed1979

Early mortality and temperature regulation in burned mice following administration of catecholamines and adrenergic receptor blocking drugs.

The effect of catecholamines and adrenergic receptor blocking drugs on mortality and body temperature was studied in mice subjected to burn, tourniquet, and endotoxin shock at an environmental temperature of 25 degrees C. Epinephrine and norepinephrine (0.5 mg/kg) injected intraperitoneally postburn increased shock mortality significantly (p less than 0.05); pretreatment with these catecholamines had no effect. Pretreatment of burn- and tourniquet-traumatized mice with propranolol (25 mg/kg) significantly decreased shock mortality, while pretreatment with dibenamine (25 mg/kg) significantly lowered early mortality after endotoxin. None of the catecholamines or their blocking drugs significantly prevented the characteristic immediate fall in core temperature after the three types of shock. At 6 days postburn, however, a combination of propranolol and dibenamine caused a marked fall in core temperature (p less than 0.05). These results indicate that beta-catecholamine agonists could play an important role in acute burn mortality and that both alpha- and beta-catecholamine agonists could significantly influence body temperature regulation and metabolic rate during the late postburn period.

Animals↗
PubMed1983

Effect of the centrally acting agent clonidine on circulating catecholamines at rest and during exercise. Comparison with the effects of beta-blocking agents.

To determine the amount of sympathetic outflow suppression due to the alpha 2-adrenergic receptor stimulating agent clonidine, its effect on heart rate, blood pressure, and on circulating plasma catecholamines was assessed in ten healthy subjects at rest and during submaximal ergometric exercise. Similar exercise studies were performed in eight healthy normotensive persons after beta-blockade using propanolol. In nine healthy subjects the effect of an acute intravenous (IV) intervention of clonidine on plasma catecholamines was compared with the results obtained after IV administration of the cardioselective beta-blocker metoprolol or of both drugs. Clonidine taken orally produced significantly reduced plasma levels of epinephrine and norepinephrine (p less than 0.01). During submaximal ergometric exercise, the sympatholytic effect of clonidine was relatively less marked than at rest (p less than 0.05). After beta-blockade, either orally with propanolol or IV with metoprolol, plasma catecholamines at rest did not change significantly; their plasma levels during exercise, however, exceeded those obtained after administration of placebo (p less than 0.05). Giving IV clonidine and metoprolol combined revealed no significant changes of plasma catecholamines at rest and during exercise; heart rate and blood pressure decreased significantly (p less than 0.001). Clonidine on the one hand and the beta-blocking agents on the other exhibit oppositely directed effects on plasma levels of catecholamines.

Adrenergic beta-Antagonists↗
PubMed1982

Osmotic pressures of solutions of ATP and catecholamines relating to storage in chromaffin granules.

The chromaffin granule, which is the catecholamine storage organelle of the adrenal medulla, contains at least 0.73 M ions, yet it is isotonic with 0.3 osM solutions. One hypothesis which accounts for this disparity is formation of a complex between major constituents of the granule: the catecholamines, the proteins, and the ATP. In this paper we show by vapor pressure osmometry, which affords a direct measure of colligative properties, that ATP-catecholamine mixtures form highly nonideal solutions. At 37 degrees C, solutions containing 0.6 M epinephrine and 0.15 M ATP show an effective osmotic pressure of only 0.25 osM. The existence of polymeric complexes is implied by the fact that the increase of osmotic pressure with increasing concentrations of ATP and catecholamine falls off substantially at concentrations approaching those in the chromaffin granules. Neither inorganic ions nor calcium chelators cause regain of ideal colligative behavior. Osmotic measurements on model compounds suggest that the primary interaction is between the phosphate and amino groups. There is also evidence that the effects are not wholly due to the formation of discrete complexes; factors of nonideal solution behavior also play a role in lowering the osmotic pressure. These observations show that the stability of the chromaffin granule in situ can be accounted for, perhaps entirely, by spontaneous interactions among nucleotides and catecholamines.

Adenosine Triphosphate↗
PubMed1983

Catecholamine secretion from digitonin-treated adrenal medullary chromaffin cells.

The plasma membrane of cultured chromaffin cells from bovine adrenal medulla was rendered leaky by incubation in low concentrations of digitonin. Digitonin (20 microM) induced Ca2+-dependent release of 10-20% of the catecholamine in the presence of 10 microM Ca2+ without addition of secretagogue. Half-maximal catecholamine release occurred at approximately 1 microM Ca2+ x Mg2+ could not substitute for Ca2+. Cells incubated with digitonin rapidly lost their ability to exclude trypan blue. Digitonin caused release of the cytosolic markers lactic dehydrogenase and phenylethanolamine-N-methyltransferase, but, in contrast to release of catecholamine, the release of the cytosolic proteins was inhibited by Ca2+. Soluble dopamine-beta-hydroxylase, a protein marker of granule contents, was released proportionally with catecholamine in a Ca2+ dependent manner. Catecholamine release was optimal in solutions containing MgATP. Hence, digitonin-treated cells, although they lose soluble cytosolic proteins and presumably low molecular weight cytosolic constituents, maintain the Ca2+-dependent reactions of exocytosis in the presence of MgATP. Digitonin-treated chromaffin cells may be a powerful system in which to study the biochemical mechanisms underlying exocytosis.

Adrenal Medulla↗
PubMed1982

[Plasma catecholamines and hemodynamics in patients with heart failure (author's transl)].

Plasma catecholamines and hemodynamic were assessed in 32 patients with heart failure of varying degrees due to coronary artery disease as well as in twelve healthy control subjects. The studies employed the use of a (Swan-Ganz) semi-floating, balloon-tipped, thermodilution catheter during supine bicycle ergometry at incremented workloads (except in four patients with overt symptoms at heart failure at rest). As compared with control subjects, the patients showed increases in radiologically-determined cardiac volumes, right atrial, right ventricular, pulmonary artery and pulmonary capillary wedge pressures proportionately expressing increasing degrees of severity and, accordingly, decreasing values of cardiac output and stroke volume as well as a severity-dependent tendency to increasingly rapid heart rates. Similarly, as compared with control subjects, catecholamine concentrations increased in proportion with the pathologic elevation of pressures and inversely proportional to the cardiac output. With respect to a given catecholamine concentration, the patients showed a severity-dependent decrease in cardiac output, as an expression of the degree of functional myocardial impairment, as well as a lower heart rate and higher total peripheral resistance (at the same catecholamine level). The heart rate reduction at the same catecholamine concentration may be due to a reduced adrenergic receptor sensitivity.

Blood Pressure↗
PubMed1975

Urinary catecholamines and their metabolites in diabetes.

Total, free, and conjugated urinary catecholamines and their metabolites are studied in diabetes before and after treatment. There are abnormalities in catecholamines metabolism and their metabolites caused by the diabetic condition. The 24 hour urinary excretion of the total catecholamines is significantly increased in diabetics. Epinephrine, as a free fraction, conjugated fraction, and, consequently, as a total metabolite, is significantly increased. No change in dopamine concentration is observed in diabetes although dopamine is known to inhibit insuline release. No sex difference is, however, observed in the diabetic patients with regards to the catecholamines excretion. After controlling the diabetic state, abnormalities in catecholamine metabolism and their metabolites are normalized.

Adult↗
PubMedDate not supplied

Adrenal catecholamine secretory responses in young and adult dogs.

To elucidate the secretory sensitivity of the adrenal medulla in young animals, a comparative study of the adrenal secretory reactivity in young and adult dogs was made. In the isolated perfused adrenal gland, acetylcholine, nicotine, muscarine (10(-6)-10(-4) M) and high K+ (15-45 mM) enhanced catecholamine release. The release of catecholamines, expressed per weight of adrenal gland and caused by cholinergic secretagogues, was significantly higher in young dogs than in adult dogs. The proportion of noradrenaline to adrenaline plus noradrenaline in the tissue was higher in young dogs. The proportion of noradrenaline in the effluent was higher by increasing the concentrations of the stimulants, up to a similar level of the tissue noradrenaline/noradrenaline+adrenaline ratio. In in vivo studies, the increase in catecholamine concentration, especially of noradrenaline, in the plasma of femoral arteries, induced by intravenous injection of nicotine, was higher in young dogs than in adult dogs. We also measured the catecholamine-synthesizing enzymes activities in the adrenal medulla. Tyrosine hydroxylase and phenylethanolamine-N-methyltransferase activities were lower in young dogs, but there was no difference in dopamine-beta-hydroxylase activity between young and adult dogs. These results may suggest that young dogs are more sensitive to cholinergic stimulation in spite of their low catecholamine-synthesizing enzyme activity.

Adrenal Medulla↗
PubMed1999

Comparison between uptake2 and rOCT1: effects of catecholamines, metanephrines and corticosterone.

Active and specialized transmembrane transport systems are responsible for the functional inactivation of catecholamines. Uptake2, the classical extraneuronal uptake system, and rOCT1, a recently cloned organic cation transporter, share a number of properties. The present study was undertaken to investigate putative differences between these two transporters that might clarify their relative physiological roles. Uptake of [3H]MPP+ ([3H]1-methyl-4-phenylpyridinium) by Caki-1 cells (to study uptake2) and by primary cultured rat hepatocytes (to study rOCT1) was kinetically and pharmacologically characterized. In both cell types, [3H]MPP+ was avidly taken up and accumulated. All compounds tested (catecholamines, metanephrines and corticosterone) inhibited [3H]MPP+ uptake, albeit with different potencies. In Caki-1 cells, the ranking order of inhibitory potency was: (-)isoprenaline > (-)adrenaline >> (-)noradrenaline > dopamine. Metanephrine and normetanephrine were equipotent. Corticosterone had an IC50 of 102 nM. In cultured hepatocytes, the ranking order of inhibitory potency was: (-)isoprenaline > dopamine > (-)adrenaline >> (-)noradrenaline. Metanephrine was about seven times more potent than normetanephrine. Corticosterone had an IC50 of 72 microM, being about 700-fold less potent in inhibiting rOCT1 than uptake2. The results showed that uptake2 and rOCT1 can be clearly distinguished on a functional basis. On the one hand, uptake2 prefers adrenaline among the endogenous catecholamines, whereas rOCT1 has similar affinity for adrenaline and dopamine. On the other hand, corticosterone and normetanephrine are significantly more potent in inhibiting uptake2 than rOCT1. The results are compatible with a possible physiological role of corticosteroids in the modulation of adrenaline effects in tissues equipped with uptake2, without significant interference with the hepatic and renal excretion of catecholamines.

1-Methyl-4-phenylpyridinium↗
PubMed1999

Transient depressive relapse induced by catecholamine depletion: potential phenotypic vulnerability marker?

BACKGROUND: Although state-related alterations in catecholamine function have been well-described in depressed subjects, enduring abnormalities have been less reliably identified. In our study, medication-free subjects with fully remitted major depression underwent a paradigm of catecholamine depletion, via use of the tyrosine hydroxylase inhibitor alpha-methylparatyrosine. METHOD: Subjects underwent 2 sets of testing conditions in a double-blind, random-ordered, crossover design, approximately 1 week apart. They underwent active catecholamine depletion (via oral administration of 5 g alpha-methylparatyrosine) or sedation-controlled, sham catecholamine depletion (via oral administration of 250 mg diphenhydramine hydrochloride), during a 2-day observation. Serial mood ratings and blood samples were obtained. RESULTS: Fourteen subjects completed the active testing condition; 13 completed sham testing. Subjects experienced marked, transient increases in core depressive and anxiety symptoms, as demonstrated by a mean 21-point increase on Hamilton Depression Rating Scale scores. Furthermore, 10 (71%) of 14 subjects fulfilled relapse criteria during active testing, whereas 1 (8%) of 13 subjects did so during sham testing. The severity of the depressive reaction correlated with baseline plasma cortisol levels (r = 0.59; P =.04). CONCLUSIONS: Euthymic, medication-free subjects with a history of major depression demonstrate significant depressive symptoms when undergoing testing with alpha-methylparatyrosine. This depressive reaction may represent a reliable marker for a history of depression. Further work is needed to clarify the significance of this finding.

Adult↗
PubMed1996

Immunocytochemical distribution of catecholamine-synthesizing neurons in the hypothalamus and pituitary gland of pigs: tyrosine hydroxylase and dopamine-beta-hydroxylase.

This study describes the distribution of catecholaminergic neurons in the hypothalamus and the pituitary gland of the domestic pig, Sus scrofa, an animal that is widely used as an experimental model of human physiology in addition to its worldwide agricultural importance. Hypothalamic catecholamine neurons were identified by immunocytochemical staining for the presence of the catecholamine synthesizing enzymes, tyrosine hydroxylase and dopamine-beta-hydroxylase. Tyrosine hydroxylase-immunoreactive perikarya were observed in the periventricular region throughout the extent of the third ventricle, the anterior and retrochiasmatic divisions of the supraoptic nucleus, the suprachiasmatic nucleus, the ventral and dorsolateral regions of the paraventricular nucleus and adjacent dorsal hypothalamus, the ventrolateral arcuate nucleus, and the posterior hypothalamus. Perikarya ranged from parvicellular (10-15 microns) to magnocellular (25-50 microns) and were of multiple shapes (rounded, fusiform, triangular, or multipolar) and generally had two to five processes with branched arborization. No dopamine-beta-hydroxylase immunoreactive perikarya were observed within the hypothalamus or in the adjacent basal forebrain structures. Both tyrosine hydroxylase- and dopamine-beta-hydroxylase-immunoreactive fibers and punctate varicosities were observed throughout areas containing tyrosine hydroxylase perikarya, but dopamine-beta-hydroxylase immunoreactivity was very sparse within the median eminence. Within the pituitary gland, only tyrosine hydroxylase fibers, and not dopamine-beta-hydroxylase immunoreactive fibers, were located throughout the neurohypophyseal tract and within the posterior pituitary in both pars intermedia and pars nervosa regions. Generally, the location and patterns of both catecholamine-synthesizing enzymes were similar to those reported for other mammalian species except for the absence of the A15 dorsal group and the very sparse dopamine-beta-hydroxylase immunoreactive fibers and varicosities in the median eminence in the pig. These findings provide an initial framework for elucidating behavioral and neuroendocrine species differences with regard to catecholamine neurotransmitters.

Animals↗
PubMed1999

Analysis of 9-fluorenylmethyloxycarbonyl derivatives of catecholamines by high performance liquid chromatography, liquid chromatography/mass spectrometry and tandem mass spectrometry.

9-Fluorenylmethyloxycarbonyl (FMOC) derivatives of catecholamines, including dopamine (DA; 3,4-dihydroxyphenethylamine), norepinephrine (NE; 2-amino-1-(3,4-dihydroxyphenyl)ethanol) and epinephrine (EPI; 1-phenyl-1-hydroxy-2-methylaminopropane) as well as 3, 4-dihydroxybenzylamine (DHBA) have been analyzed using high performance liquid chromatography coupled to fluorometric detection and atmospheric pressure chemical ionization mass spectrometry at low femtomole levels. Structures of the derivatives have also been characterized by liquid chromatography/atmospheric pressure chemical ionization mass spectrometry and electrospray/tandem mass spectrometry. Protonated molecules of FMOC-DA and FMOC-DHBA as well as [M + H - H(2)O](+) ions of FMOC-NE and FMOC-EPI appear in their conventional mass spectra, and abundant fragments characteristic of catecholamines dominated the spectra. Structurally diagnostic ions using several hundred femtomoles of the FMOC derivatives of catecholamine were observed. Collision-induced dissociation (CID) of electrospray-generated protonated molecules of FMOC-DA and FMOC-DHBA as well as [M + H - H(2)O](+) ions of FMOC-NE and FMOC-EPI produced diagnostic product ion spectra. Liquid chromatography/atmospheric pressure chemical ionization mass spectrometric analysis of the FMOC derivatives of catecholamines and DHBA should prove useful in the separation and characterization of these compounds from biological materials.

Animals↗
PubMed1996

Catecholamine metabolism and in vitro induction of premature cuticle melanization in wild type and pigmentation mutants of Drosophila melanogaster.

The major pathway leading to adult cuticle melanization in Drosophila melanogaster has been investigated by a combination of biochemical and genetic approaches. By comparing catecholamine pools in newly emerged flies and in frass (excreta) collected 1 to 4 days after eclosion from wild type with those obtained from several pigmentation mutants, the major flow of catecholamines through the pathway to an unidentified final catabolite was determined. We also demonstrate that incubation with dopamine in vitro induces premature melanization in wild type unpigmented pharate adults several hours before the developmentally programmed onset of melanization, supporting the hypothesis that the availability of catecholamines may be the limiting factor determining the onset of melanization and that the major enzymatic activities that act downstream of dopa decarboxylase in the pathway are deposited into the cuticle before pigmentation begins. In vitro melanization studies with various pigmentation mutants that are associated with critical enzymatic steps in Drosophila catecholamine metabolism are consistent with their proposed function and suggest a central role of N-beta-alanyldopamine in adult cuticle pigmentation.

Alleles↗
PubMed2001

Determination of catecholamines and their 3-O-methyl metabolites in mouse plasma.

The determination of catecholamines and their 3-O-methyl metabolites in a single mouse plasma is necessary to understand the role of the sympathetic nervous activity, while the inactivation of catecholamines by catechol-O-methyltransferase indicates the activity of blood pressure regulation in animals. Here we report the basal catecholamines and their 3-O-methyl metabolite concentrations obtained from 15 microL of mouse plasma utilizing semi-microcolumn high-performance liquid chromatography (HPLC)-peroxyoxalate chemiluminescence detection system. The concentrations were 6.63 +/- 1.37 pmol/mL plasma, 0.49 +/- 0.10 pmol/mL plasma, 5.25 +/- 2.30 pmol/mL plasma, 3.23 +/- 0.84 pmol/mL plasma, 0.44 +/- 0.11 pmol/mL plasma, and 3.39 +/- 1.67 pmol/mL plasma for norepinephrine, epinephrine, dopamine, normetanephrine, metanephrine and 3-methoxytyramine, respectively (n = 5-7). Further, when blood pressure was reduced by minoxidil, plasma catecholamines were found to be significantly increased by the baroreflex-mediated response in mouse.

Animals↗