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PubMed1982

Proportional secretion of opioid peptides and catecholamines from adrenal chromaffin cells in culture.

Bovine adrenal medullary chromaffin cells were used to study the relationship between opioid peptide and catecholamine secretion from the adrenal medulla. Stimulation of chromaffin cells by acetylcholine, nicotine, veratridine, barium, or Ionomycin produced secretion of opioid peptides and catecholamines which was proportional to the cellular content of these substances. Nicotine-evoked secretion of opioid peptides and catecholamines was dependent on extracellular calcium and was blocked by d-tubocurarine. Increased cellular content of opioid peptides and decreased catecholamine content induced by treatment of chromaffin cells with reserpine or tetrabenazine were reflected in the secretion of proportionally larger amounts of opioid peptides and smaller amounts of catecholamines when compared with secretion of these substances from untreated cells. Peptides of up to 25,000 daltons that express opiate activity only following digestion with enzymes, such s trypsin and carboxypeptidase B, also are secreted from chromaffin cells in the same proportion of their cellular content as are catecholamines and opioid peptides. Opioid peptides were secreted in proportion to total catecholamines but not in proportion to either epinephrine or norepinephrine alone, suggesting that the peptides are secreted from both epinephrine- and norepinephrine-containing cells in the cultures. The results are consistent with the co-storage of opioid peptides and opiate receptor-inactive peptides containing enkephalin sequences in chromaffin vesicles and with the all-or-none exocytotic secretion of chromaffin vesicles content in response to stimulation of the adrenal medulla.

Acetylcholine↗
PubMed1997

Urinary catecholamines and the diagnosis of phaeochromocytoma in Auckland.

AIM: To review the experience in Auckland with the use of urinary catecholamine measurements in the diagnosis of phaeochromocytoma. METHODS: Review of the test results of patients with proven phaeochromocytoma and retrospective analysis of the outcome of patients with increased 24-hour urinary excretion of the catecholamines noradrenaline, adrenaline and dopamine. RESULTS: Over six years the majority (16/18) of patients with proven phaeochromocytoma had raised urinary noradrenaline excretion either alone (3/16) or with raised adrenaline and/or dopamine (13/16). One phaeochromocytoma secreted adrenaline alone, none secreted dopamine alone and one had urinary catecholamine levels that were normal. Urinary adrenaline excretion was unexpectedly elevated in two patients with extra-adrenal phaeochromocytomas. Approximately 10% of 2590 24 hour urine specimens analysed over a 14 month period had an elevation of one or more catecholamine. Forty-six patients had urinary catecholamine excretion greater than twice the upper limit of normal. This group contained five of the six phaeochromocytomas diagnosed during this period. The other patients were normal (35/46, 76%) or were lost to follow up (6/46, 13%). CONCLUSIONS: In this series most patients with phaeochromocytoma (89%) had increases in the 24-hour urinary excretion of one or more than one catecholamine which exceeded twice the upper limit of normal for our laboratory with noradrenaline being most commonly affected. Increased catecholamine excretion was often seen in patients without phaeochromocytoma.

Adolescent↗
PubMed1984

Identification and characterization of the catecholamine transporter in bovine chromaffin granules using [3H]reserpine.

Characterization of the catecholamine transporter in chromaffin granule membranes has been hampered by the lack of a radioligand with high specific activity which binds selectively to the carrier with high affinity. We report here the identification of a high affinity binding site for [3H]reserpine on chromaffin granule membranes isolated from bovine adrenal gland which has the characteristics expected of the catecholamine transporter. [3H]Reserpine bound predominately to a high affinity site with a Kd for [3H]reserpine of 9 nM and a binding site density of 7.8 pmol/mg of protein. Comparison of the characteristics of the high affinity reserpine binding site to the characteristics of catecholamine transport indicated that (a) the Ki and rank order of potency for inhibition of [3H]reserpine binding by various biogenic amines was similar to their Ki for inhibition of catecholamine transport (b) both the inhibition of (-)-[3H]norepinephrine transport and inhibition of [3H]reserpine binding showed similar stereo-specificity, and (c) Kd for binding of reserpine to chromaffin granule membranes was similar to the Ki for reserpine inhibition of catecholamine transport. These results demonstrate that the high affinity binding site for [3H]reserpine on chromaffin granule membranes is associated with the catecholamine transporter.

Adrenal Medulla↗
PubMed1977

Catecholamine-induced muscle weakness.

Infusions of epinephrine or levarterenol bitartrate into a rabbit nerve-muscle preparation decreased the force of the evoked twitch of anterior tibial and gastrocnemius-soleus muscles. The adverse effect of the catecholamines was not directly on skeletal muscle. The alpha-receptor blocking drug phenoxybenzamine hydrochloride prevented the adverse effect of the catecholamines if it was given prior to catecholamine infusions and unmasked a weak augmentation of twitch tension. Taken with the finding of abnormal accumulation of catecholamine in human dystrophic muscles, the production of an experimental myopathy resembling human dystrophy by the monoamine oxidase inhibitor pargyline hydrochloride, and the finding of excessive levels of catecholamines in the tissues and urine of dystrophic animals, these experiments support the hypothesis that catecholamines could play a pathogenetic role in some dystrophic diseases of muscle.

Action Potentials↗
PubMed1998

Effects of tryptophan depletion vs catecholamine depletion in patients with seasonal affective disorder in remission with light therapy.

BACKGROUND: Although hypotheses about the therapeutic mechanism of action of light therapy have focused on serotonergic mechanisms, the potential role, if any, of catecholaminergic pathways has not been fully explored. METHODS: Sixteen patients with seasonal affective disorder who had responded to a standard regimen of daily 10000-lux light therapy were enrolled in a double-blind, placebo-controlled, randomized crossover study. We compared the effects of tryptophan depletion with catecholamine depletion and sham depletion. Ingestion of a tryptophan-free amino acid beverage plus amino acid capsules was used to deplete tryptophan. Administration of the tyrosine hydroxylase inhibitor alpha-methyl-paratyrosine was used to deplete catecholamines. Diphenhydramine hydrochloride was used as an active placebo during sham depletion. The effects of these interventions were evaluated with measures of depression, plasma tryptophan levels, and plasma catecholamine metabolites. RESULTS: Tryptophan depletion significantly decreased plasma total and free tryptophan levels. Catecholamine depletion significantly decreased plasma 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid levels. Both tryptophan depletion and catecholamine depletion, compared with sham depletion, induced a robust increase (P<.001, repeated-measures analysis of variance) in depressive symptoms as measured with the Hamilton Depression Rating Scale, Seasonal Affective Disorder Version. CONCLUSIONS: The beneficial effects of light therapy in the treatment of seasonal affective disorder are reversed by both tryptophan depletion and catecholamine depletion. These findings confirm previous work showing that serotonin plays an important role in the mechanism of action of light therapy and provide new evidence that brain catecholaminergic systems may also be involved.

Adult↗
PubMedDate not supplied

Chemiluminescent detection of catecholamines by generation of hydrogen peroxide with imidazole.

A novel detection method for catecholamines using imidazole was investigated using a chemiluminescence coupled flow injection system. Imidazole catalysed decomposition of catecholamines to generate hydrogen peroxide, then the hydrogen peroxide was detected by chemiluminescence. The optimal condition for generation of hydrogen peroxide from a catecholamine was to incubate the catecholamines (53 pmol) in an imidazole solution (50 mmol/L, pH 9.0, 1.0 mL) at 60 degrees C for 30 min. Peroxide-was detected by peroxyoxalate chemiluminescence, and the rank order of the light emission intensities was as follows; dopamine (100%) >epinephrine (78%) >L-DOPA (62%) >norepinephrine (58%) >deoxyepinephrine (51%) >isoproterenol (43%) >dihydroxybenzylamine (25%). The light intensities of the reaction mixtures (corresponding to 1.06 pmol catecholamines) varied depending on the chemiluminescence (CL) detection reaction, and the rank order of the light intensity was as follows; luminol CL catalysed with horseradish peroxidase (HRP) (371%) >peroxyoxalate chemiluminescence (100%) >luminol CL catalysed with ferrycyanide (62%) >lucigenin CL (15%) >pyrogallol CL (0.8%) >purpurogallin CL (0.4%) >luminol CL (0.3%). The luminol CL reaction catalysed by HRP is recommended for the detection of peroxide in this method for catecholamines.

Catecholamines↗
PubMed1975

The distribution of catecholamines within the inferior olivary complex of the cat and rhesus monkey.

Catecholamine histofluorescence was examined in the interior olivary complex of the cat and rhesus monkey. Species-specific patterns of catecholamine-containing varicosities were observed. In the rat, the highest concentration of catecholamine varicosities was seen within the dorsal lamella of the principal nucleus. In contrast, this same portion of the inferior olivary complex appeared void of catecholamine varicosities in the cat and rhesus monkey. In the cat, the highest concentration of varicosities occurred within the medial one-half of the dorsal accessory nucleus while few, if any, varicosities were seen in this portion of the complex in the rat and monkey. The lateral lamella of the principal nucleus contained the highest concentration seen in the rhesus monkey, a finding which contrasts to the minimal number of varicosities seen in this area in the rat and cat. Catecholamine-containing cell bodies, reported to exist in the rat, were not observed in cat and monkey. These data extend the previous observation of species-specific distribution in rodents to include members of the more phylogenetically advanced orders; Carnivora and Primata. Catecholamines were found primarily within those portions of the olivary complex reported to be involved in harmaline-induced tremor activity in the cat.

Age Factors↗
PubMedDate not supplied

The effect of peritoneovenous shunting on catecholamine metabolism in patients with hepatic ascites.

The elevated catecholamine levels in cirrhotic patients with ascites have been proposed to be due to sympathetic overactivity secondary either to reduced intravascular volume or to an underlying cardiovascular abnormality such as reduced pressor responsiveness. Furthermore, these elevated catecholamine levels have been proposed to be involved in the pathogenesis of salt and water retention. Therefore, the effect of peritoneovenous shunting on the circulating levels and renal excretion of catecholamines were studied in six patients with massive refractive ascites preoperative within the first 8 hr postoperative and by 2 weeks postoperative under metabolic conditions. The recirculation of ascites into the intravascular compartment resulted perioperatively in significant rises in cardiac output (p = 0.001), para-amino-hippurate clearance (p = 0.08), creatinine clearance, diuresis (p = 0.05) and natriuresis (p = 0.06). Systemic blood pressure remained unchanged while systemic vascular resistance decreased (p less than 0.05). Preoperative circulating levels of free catecholamine were highly elevated, and renal vein concentrations were about 25% higher than renal arterial levels. Perioperatively, there was little change in circulating catecholamine levels or distribution of renal blood flow although renal artery and vein concentrations tended to equalize. In contrast by 2 weeks postoperatively, free catecholamine levels had fallen to within the normal ranges: mean norepinephrine from 1,477.6 +/- 194.6 to 395 +/- 62.9 pg per ml (p less than 0.05); epinephrine from 276 +/- 74.2 to 65.7 +/- 15.0 pg per ml (p less than 0.02), and dopamine from 325.6 +/- 175.2 to 47.9 +/- 5.3 pg per ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Degeneration of the dendritic arbor as an index of neurotoxicity in identified catecholamine neurons in rat brain slices.

Although catecholamine neurons are vulnerable targets for neurotoxins and degenerative disease, few in vitro studies have investigated the mechanisms of neurodegeneration in these cells. We therefore developed a brain slice preparation for this purpose. Rats were killed by cervical dislocation and 400-microm-thick horizontal slices containing midbrain catecholamine neurons were incubated for 2 h in the presence or absence of kainic acid (KA, 50 microM). After fixation, the slices were recut by a technique that provided thin (40 microm) sections in the same plane as the parent slice. Catecholamine neurons in these coplanar sections were labeled by immunostaining for tyrosine hydroxylase (TH) coupled with diaminobenzidine. The topographical organization of the horizontal plane of the brain was retained in the coplanar sections, enabling precise identification of catecholamine neurons in the thin sections, by reference to an atlas in the horizontal plane. In this study we examined neurons in the substantia nigra (SN). A key feature of the immunostaining was that it revealed both the cell body and also the extensive dendritic projections of SN neurons in the horizontal plane. After treatment with KA, cell bodies remained intact but the dendrites were truncated or fragmented. The loss of dendrites is a sensitive and readily quantifiable indicator of damage. KA caused significant reductions in the proportion of SN neurons with intact dendrites and in the total length of the dendrites, measured using a computer program. The sensitive index of damage and the facility to clearly distinguish catecholamine groups that are topographically close yet functionally distinct are the principal features of the experimental approach that we have developed. The preparation offers major advantages for investigating the selective vulnerability or resistance of particular types of catecholamine neurons to damage.

Animals↗
PubMed2000

Differential vulnerabilities of substantia nigra catecholamine neurons to excitatory amino acid-induced degeneration in rat midbrain slices.

Although differential vulnerability in different regions of the central nervous system is a characteristic feature of neurodegenerative disorders in vivo, its cellular basis is not well understood. In the present study we investigated whether catecholamine neurons in different regions of the substantia nigra (SN) are differentially vulnerable to excitatory amino acid-induced damage in a midbrain slice preparation. Rats were anesthetized by halothane inhalation and killed, the brain was rapidly removed, and 300-microm-thick midbrain slices were cut horizontally on a vibratome. The slices were incubated at 35 degrees C for 2 h in saline buffer containing either kainic acid (KA) or N-methyl-d-aspartate (NMDA) (10-50 microM). They were then fixed and cut into 30-microm sections that were coplanar with the horizontal slice. Individual catecholamine neurons were identified in these thin sections using an antibody to tyrosine hydroxylase coupled to diaminobenzidine. Catecholaminergic neurons in the dorsal and ventral tiers of the SN were readily identified by reference to an atlas of the distribution of catecholamine neurons in the horizontal plane. Using dendritic degeneration as a sensitive index of damage, and submaximal concentrations of KA and NMDA, we found that catecholamine neurons in the dorsal tier were more vulnerable than those in the ventral tier. For example, KA (10 microM) caused a significant reduction in the proportion of neurons with dendrites in the dorsal tier (from 60 to 34%) without altering the dendritic arbor of ventral tier neurons. After treatment with 50 microM KA, only 11% of dorsal tier neurons retained any dendrites while 45% of ventral tier neurons retained their dendrites. These differences were statistically significant (P<0.001). A similar differential vulnerability was apparent in slices treated with NMDA; neurons in the dorsal tier lost dendrites before detectable damage in the ventral tier. An understanding of the comparative anatomical, neurochemical, and physiological properties of vulnerable (dorsal tier) and resistant (ventral tier) catecholamine neurons in rat SN may provide significant insights into the mechanisms and treatment of neurodegenerative disorders involving catecholamine neurons.

Animals↗
PubMed1996

Mechanisms of alterations in cardiac membrane Ca2+ transport due to excess catecholamines.

The occurrence of excessive catecholamine release is often associated with stress due to the lifestyle of Western societies. Contrary to the general thinking that excess catecholamines produce cardiotoxicity mainly via binding to adrenoceptors, there is increasing evidence that catecholamine-induced deleterious actions may also occur through oxidative mechanisms. In this overview it is shown that a high dose of isoproterenol induces a biphasic change in cardiac Ca2+ transport in the sarcolemma and in sarcoplasmic reticulum. Both sarcolemmal and sarcoplasmic reticular Ca2+-transport activities are initially increased to maintain Ca2+ homeostasis and then are impaired, which may be associated with the occurrence of intracellular Ca2+ overload. On the other hand, mitochondrial Ca2+-transport activities exhibited a delayed increase. Pretreatment with vitamin E partially prevented the deleterious changes in cardiac membranes as well as the depressed energetic status of the heart muscle cell. It is concluded that excess catecholamines affect Ca2+-transport mechanisms primarily via oxidation reactions involving free radical-mediated damage. Thus drug approaches that reduce circulating catecholamines and/or prevent their oxidation should prove beneficial. A combination therapy involving inhibitors of catecholamine release, blockers of adrenoceptors, and antioxidants may be indicated for stress-induced heart disease.

Adrenergic beta-Agonists↗
PubMed1987

The activity of the neuronal and extraneuronal catecholamine-metabolizing enzymes of the perfused rat heart.

In a comparative study the neuronal and extraneuronal metabolism of several 3H-catecholamines (all of which were tritiated in the C-7 position of the side chain only) was determined in isolated rat hearts perfused at a concentration of the 3H-amines of 50 nmol/l. While the neuronal MAO activity was determined after inhibition of extraneuronal uptake (100 mumol/l OMI) and COMT (10 mumol/l U-0521), the extraneuronal MAO activity was estimated after inhibition of neuronal uptake (30 mumol/l cocaine) and COMT. The extraneuronal COMT activity was determined under conditions of inhibition of both neuronal uptake and MAO (pretreatment with pargyline). Hearts were perfused with the 3H-catecholamines until the rate of appearance of the various 3H-metabolites in the venous effluent has reached a steady state. From these rates (vst-st) and the steady-state content of the unchanged 3H-catecholamines in the tissue (Si), the rate constants (Vmax/Km) for the unsaturated intracellular enzymes COMT (kCOMT) and MAO (kMAO) were calculated. The kCOMT values for all four catecholamines, (-)-noradrenaline, dopamine, (-)-adrenaline and (+/-)-isoprenaline exhibit a range from 0.24 to 0.78 min-1; the metabolism of the catecholamines by the COMT differs: (-)-noradrenaline = dopamine less than (-)-adrenaline less than (+/-)-isoprenaline. The extraneuronal MAO activity was low for all three catecholamines, (-)-adrenaline, (-)-noradrenaline and dopamine (range of kMAO from 0.05 to 0.28 min-1) and declined in the order.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effects of clonidine, dihydralazine and splanchnic nerve stimulation on the release of neuropeptide Y, MET-enkephalin and catecholamines from dog adrenal medulla.

Various neuropeptides are costored together with catecholamines in the adrenal medulla. The concurrent release (evaluated by adrenal vein plasma levels) of these neuropeptides [neuropeptide Y (NPY), met-enkephaline (ME)] and catecholamines [adrenaline (A) and noradrenaline (NA)] from the adrenal gland was examined in chloralose-anesthetized dogs after intravenous administration of clonidine (10 micrograms/kg) and dihydralazine (1 mg/kg). These results were compared to those obtained after the stimulation of the right splanchnic nerve at 1, 5 and 10 Hz frequencies. The increment in the release of catecholamines and neuropeptides was evaluated for dihydralazine and splanchnic nerve stimulation. Dihydralazine (at its maximal effect) induced a significant preferential increase in catecholamines (expressed as mean (SEM): NA: 17.3 (5.4) fold, A: 13.1 (2.6) fold) and ME (16.0 (7.1) fold) versus basal values. However, the significant increase in NPY-LI was only 2.0 (0.4) times the baseline. Splanchnic nerve stimulation induced a frequency-dependent increase in catecholamines and neuropeptides. When the stimulation frequency was increased from 1 Hz to 5 Hz, NA and A levels increased 17.9 (4.3) and 14.0 (2.2) fold, respectively and ME levels 14.1 (3.0) fold. By contrast, NPY-LI was increased only 2.3 (0.3) fold under the same conditions. Increasing the stimulation frequency from 5 Hz to 10 Hz resulted in similar elevations of NA, ME, and NPY-LI adrenal plasma levels (about 4 times) whereas A only increased twice. Clonidine decreased catecholamine and ME adrenal plasma levels (the maximal percent decrease when compared with control values was about 75%) whereas NPY adrenal plasma levels remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1983

[Behavior of free catecholamines in blood and urine of ambulance men and physicians during quick responses].

Free urine adrenaline, noradrenaline, (additional free plasma catecholamines in the physicians), and blood lactate were determined in 11 ambulance men and 5 physicians to assess stress during medical service. Stress was evaluated employing a stress index, based on difficulties in driving, traffic, severity of injuries or illness. Emergency cases with seriously injured subjects or reanimation were judged to have a 4-fold higher stress index than routine cases where strong physiological or psychological stress was absent. Urine catecholamines and stress indices were estimated in 3-h intervals. The calculations were based on the stress induced catecholamine concentrations minus the basal excretion during the same 3-h interval. Urine adrenaline and noradrenaline in ambulance men and physicians correlated directly with the stress index, as well as the plasma catecholamines of the physicians. Lactate levels showed similar behaviour and a descriptive direct correlation with the plasma catecholamines. Urine adrenaline increased more--dependent on the stress index--than urine noradrenaline. This over-proportional adrenaline response may be an indicator for the additional psychological stress in emergency cases. Therefore physicians showed--based on the same stress index--a tendency to higher urine adrenaline excretion and blood lactate levels than the ambulance men, which might be the consequence of the overall responsibility of the physicians. Because of the observed catecholamine responses during medical service, coronary insufficiency or hypertension might be contra-indications for participation in the medical service; regular clinical investigations including ergometric tests are advisable.

Adult↗
PubMed1984

Microfluorimetric quantitation of catecholamine turnover in the sympathetic neurons of rat.

The quantitative aspects of the formaldehyde-induced fluorescence and the turnover of catecholamines in the sympathetic neuronal perikaryon of different sympathetic ganglia were studied after a blockade of the amine synthesis with alpha-methyltyrosine. The concentration of catecholamines was determined by microfluorimetric quantitation method. The half-life of catecholamines in sympathetic neuronal perikarya was short and depended on the ganglion studied. The turnover rate of catecholamines in sympathetic neurons was highest in superior cervical and lowest in coeliac ganglion. Brightly fluorescent fibers were still seen five hours after the amine synthesis blockade, whereas almost all cell bodies had lost their fluorescence. Also small intensely fluorescent cells were still brightly fluorescent after the follow-up period. Microfluorimetrically determined turnover of catecholamines gave more detailed information about the turnover of catecholamines in sympathetic nervous system when compared to the biochemical methods used earlier.

Animals↗
PubMed1986

Inhibition of Na+-pump enhances carbachol-induced influx of 45Ca2+ and secretion of catecholamines by elevation of cellular accumulation of 22Na+ in cultured bovine adrenal medullary cells.

In bovine adrenal medullary cells, we reported that 22Na+ influx via nicotinic receptor-associated Na+ channels is involved in 45Ca2+ influx, a requisite for initiating the secretion of catecholamines (Wada et al. 1984, 1985 b). In the present study, we investigated whether the inhibition of Na+-pump modulates carbachol-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion in cultured bovine adrenal medullary cells. We also measured 86Rb+ uptake by the cells to estimate the activity of Na+,K+-ATPase. Ouabain and extracellular K+ deprivation remarkably potentiated carbachol-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion; this potentiation of carbachol-induced 45Ca2+ influx and catecholamine secretion was not observed in Na+ free medium. Carbachol increased the uptake of 86Rb+; this increase was inhibited by hexamethonium and d-tubocurarine. In Na+ free medium, carbachol failed to increase 86Rb+ uptake. Ouabain inhibited carbachol-induced 86Rb+ uptake in a concentration-dependent manner, as it increased the accumulation of cellular 22Na+. These results suggest that Na+ influx via nicotinic receptor-associated Na+ channels increases the activity of Na+,K+-ATPase and the inhibition of Na+,K+-ATPase augmented carbachol-induced Ca2+ influx and catecholamine secretion by potentiating cellular accumulation of Na+. It seems that nicotinic receptor-associated Na+ channels and Na+,K+-ATPase, both modulate the influx of Ca2+ and secretion of catecholamines by accommodating cellular concentration of Na+.

Adrenal Medulla↗
PubMed1985

Modulation by ouabain and diphenylhydantoin of veratridine-induced 22Na influx and its relation to 45Ca influx and the secretion of catecholamines in cultured bovine adrenal medullary cells.

The effects of ouabain and diphenylhydantoin on the secretion of catecholamines induced by veratridine were investigated in cultured bovine adrenal medullary cells with special reference to ion fluxes. Veratridine itself induced an influx of 22Na and 45Ca as well as secretion of catecholamines, which were antagonized by tetrodotoxin, a selective inhibitor of voltage dependent Na channels. The secretion of catecholamines caused by veratridine was not observed either in Na free or Ca free medium. Veratridine-induced influx of 45Ca did not occur in Na free medium, while veratridine-induced influx of 22Na occurred even in Ca free medium. Veratridine-induced influx of 22Na, 45Ca and secretion of catecholamines were all potentiated by ouabain, a potent inhibitor of Na,K-ATPase. Omission of K from the medium, a condition which suppresses the Na,K-ATPase activity, also augmented these cell responses caused by veratridine. On the contrary, diphenylhydantoin, which is known to decrease the intracellular concentration of Na, reduced the veratridine-induced influx of 22Na, 45Ca and secretion of catecholamines. The potentiating effects of ouabain on the veratridine-induced cell responses were all abolished by diphenylhydantoin. These findings imply that veratridine, ouabain and K removal as well as diphenylhydantoin modulate the intracellular accumulation of 22Na which is involved in the influx of 45Ca and the secretion of catecholamines.

Adrenal Medulla↗
PubMed1992

Training-overtraining: influence of a defined increase in training volume vs training intensity on performance, catecholamines and some metabolic parameters in experienced middle- and long-distance runners.

The influence of an increase in training volume (ITV; February 1989) vs intensity (ITI; February 1990) on performance, catecholamines, energy metabolism and serum lipids was examined in two studies on eight, and nine experienced middle- or long-distance runners; seven participated in both studies. During ITV, mean training volume was doubled from 85.9 km.week-1 (pretrial phase) to 174.6 km within 3 weeks. Some 96%-98% of the training was performed at 67 (SD 8)% of maximal performance. During ITI, speed-endurance, high-speed and interval runs increased within 3 weeks from 9 km.week-1 (pretrial phase) to 22.7 km.week-1 and the total training distance from 61.6 to 84.7 km.week-1. The ITV resulted in stagnation of running velocity at 4 mmol lactate concentration and a decrease in total running distance in the increment test. Heart rate, energy metabolic parameters, nocturnal urinary catecholamine excretion, low density, very low density lipoprotein-cholesterol and triglyceride concentrations decreased significantly; the exercise-related catecholamine plasma concentrations increased at an identical exercise intensity. The ITI produced an improvement in running velocity at 4 mmol lactate concentration and in total running distance in the increment test; heart rate, energy metabolic parameters, nocturnal catecholamine excretion, and serum lipids remained nearly constant, and the exercise-related plasma catecholamine concentrations decreased at an identical exercise intensity. The ITV-related changes in metabolism and catecholamines may have indicated an exhaustion syndrome in the majority of the athletes examined but this hypothesis has to be proven by future experimental studies.

Adult↗