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PubMed1985

Inhibitory effect of hyperosmolality on catecholamine secretion from the bovine adrenal medulla.

We examined the effect of hyperosmolality on exocytotic catecholamine secretion in isolated-perfused bovine adrenals, in both the absence and presence of Ca2+ in the extracellular medium. Exposure of adrenal glands to hyperosmotic media (600 mOsm/Kg H2O) for 20 minutes significantly decreased spontaneous catecholamine output, and was independent of extracellular Ca2+ concentration. Adrenal glands were exposed to a hyperosmotic Locke solution (600 mOsm/Kg H2O) for 10 minutes and then stimulated with acetylcholine. Hyperosmolality produced a significant, reversible inhibition of acetylcholine-evoked catecholamine secretion. As the osmotic strength of the perfusion fluid was increased, either by addition of sucrose or NaCl, there was a progressive reduction in the acetylcholine response. Hyperosmolality also decreased catecholamine release induced by 56 mM K+ and by removal of NaCl from the perfusion medium. Similar results were seen in glands exposed to a NaCl-free solution in the absence of extracellular Ca2+. These results suggest that inhibitory effects of hyperosmolality on stimulus-secretion coupling in the adrenal medulla are exerted after Ca2+ enters the chromaffin cells, and support one of the primary criteria of the chemiosmotic hypothesis.

Acetylcholine↗
PubMed1985

Ascorbic acid and catecholamine release from digitonin-treated chromaffin cells.

The subcellular localization of catecholamines and ascorbic acid in cultured bovine adrenal chromaffin cells was studied by permeabilizing the cells with digitonin, a steroid glycoside. Catecholamine release from permeabilized chromaffin cells was dependent on the free calcium concentration and the temperature of the incubation mixture. By contrast, [14C]ascorbic acid, preloaded into the cells, was released by digitonin treatment in a manner independent of the concentration of free calcium and with only moderate regard to the incubation temperature. The sensitivity of ascorbic acid release to digitonin treatment was identical to that of calcium-dependent catecholamine release. These results thus suggest that ascorbic acid preloaded into the cells may directly efflux from the cell cytoplasm as a result of the permeabilization of the plasma membrane. Dimethylepinephrine, a permanently positively charged catecholamine analog which is known to be excluded from vesicular fractions, was also released by digitonin treatment in a manner independent of calcium. The time course of dimethylepinephrine release was very similar to that of ascorbic acid release. Thus, newly accumulated ascorbic acid in chromaffin cells may be localized to a free pool in the cell cytoplasm rather than in a vesicular compartment.

Adrenal Medulla↗
PubMed1985

Effect of an opiate antagonist (naloxone) and an agonist/antagonist (nalbuphine) in primate hemorrhagic shock: relationship to catecholamine release.

Recent evidence has suggested a relationship between the endogenous opioid peptides and the pathophysiology of various shock states. In the present study, we investigated the relationship between the effectiveness of naloxone (an opiate antagonist) and nalbuphine (an opiate agonist/antagonist), and the changes in circulating levels of catecholamines in the nonhuman primate subjected to hemorrhagic shock. Plasma levels of catecholamines were measured using high-performance liquid chromatography (HPLC) during hemorrhagic shock in 15 female baboons. Plasma levels of both epinephrine and norepinephrine increased significantly during hemorrhagic shock (p less than 0.05), which correlated with an increase in heart rate. Bolus administration of naloxone (5 mg/kg) significantly increased both plasma epinephrine (p less than 0.01) and norepinephrine (p less than 0.05) over shock levels along with a transient but significant increase in cardiac output (p less than 0.05) and mean arterial pressure (p less than 0.05), and a significant decrease in heart rate (p less than 0.05). Improvements in hemodynamics were maintained with a constant infusion of naloxone (5 mg/kg/hr), which also caused a further significant increase in plasma epinephrine (p less than 0.01). Administration of a single bolus of the opiate agonist/antagonist nalbuphine (5 mg/kg) dramatically decreased cardiac output and mean arterial pressure and had no effect on circulating catecholamines. Our results suggest that (1) the beneficial action of high-dose naloxone in primate hemorrhagic shock may be attributable in part to a drug-induced increase in circulating endogenous catecholamines; and (2) the failure of high-dose nalbuphine to improve cardiovascular function may be related to its partial agonist (cardiodepressant) properties at higher doses.

Animals↗
PubMed1974

Use of plasma catecholamine values in diagnosing pheochromocytoma and neuroblastoma.

The diagnosis in two cases of neural crest tumours was confirmed by the measurement of concentration of plasma catecholamines. A histamine provocative test monitored by values of plasma catecholamines provided support for a diagnosis of pheochromocytoma in a patient with normal blood pressure and elevated values of urinary amines. In the second case the presence of a ganglioneuroblastoma secreting abnormal amounts of catecholamines was detected by plasma epinephrine and norepinephrine measurements when values of urinary free catecholamines were normal.

Adult↗
PubMed1979

Effects of acute and chronic administration of pentobarbital on catecholamine uptake in mouse brain synaptosomes.

The studies showed that pentobarbital at concentrations up to 10(-4) M failed to exhibit any effect on catecholamine uptakes in vitro. In mice treated both acutely and chronically with pentobarbital, there was a significant attenuation in both dopamine and norepinephrine uptakes into synaptosomal preparations. The decrease in both catecholamine uptakes during the course of the development of tolerance to pentobarbital was demonstrated to be time dependent. The ability of catecholamine uptake processes was restored by abrupt withdrawal of pentobarbital by the removal of pentobarbital pellet. It appears that both acute and chronic effects of pentobarbital on catecholamine uptakes may be associated with the development of tolerance to pentobarbital.

Animals↗
PubMed1977

[Effect of ionophore Brx537A on catecholamine liberation from chromaffin granules].

In the present paper the author studies the action of bromine analog of carboxil ionophore X-537A on the transport mechanism of catecholamines from isolated chromaffine granules. The transfer of catecholamines through artificial membranes was explained by the ability of ionophore and its bromine derivative to raise their permeability in organic solvents and to transfer them through the organic phase. A model for the action of Brx 537A on isolated granules was constructed. It was established that the ionophorex acted as a carrier, enhancing the transport of the protonated form of catecholamines, which in general diffuse slightly. The model transport system could explain the differences in releasing catecholamines and the favourable effect of cations in the transport through the membranes.

Adenosine Triphosphate↗
PubMedDate not supplied

[Catecholamine metabolism and mitochondrial enzyme activity].

Specific effects of various catecholamines as well as functional dependence of mitochondrial enzymes activity on catecholamine metabolism were studied. Dopamine activated cytochrome c oxidase in heart mitochondria and decreased this enzymatic activity in liver tissue. Noradrenaline and adrenaline activated cytochrome c oxidase in liver, brain and kidney tissues. The effect of dopamine on cytochrome c oxidase was prevented by activation of dopamine beta-hydroxylase. Increased activity of monoamine oxidase caused accumulation of catecholamine metabolites, which inhibited the succinate dehydrogenase activity in liver tissue and the cytochrome c oxidase activity in brain, kidney and liver tissues. In the catecholamine regulation of succinate dehydrogenase and ATPase activities in all the tissues studied as well as of cytochrome c oxidase activity in heart tissue the quinoid oxidation products were apparently involved.

Adenosine Triphosphatases↗
PubMed1984

Selective inhibition of cholinergic receptor-mediated 45Ca++ uptake and catecholamine secretion from adrenal chromaffin cells by taxol and vinblastine.

We have characterized the actions of taxol, a novel drug promoting microtubule formation, on 45Ca++ uptake and catecholamine release by isolated and cultured bovine adrenal chromaffin cells. The effects of taxol are compared with corresponding actions of vinblastine. We also have measured the effects of microtubule-active drugs on the dynamic pattern of release by means of column perifusion of isolated chromaffin cells. Taxol inhibits acetylcholine-stimulated catecholamine secretion (IC50: approximately 1 microM) and 45Ca++ uptake. The inhibitory effects of both taxol and vinblastine on secretion are rapid in onset (approximately 1 min) and reversible. Taxol and vinblastine (5 microM) exert little or no inhibitory effect on catecholamine secretion induced by 1) the nonreceptor mediated secretagogues K+, Ba++ or veratridine or by 2) the receptor-mediated secretagogues histamine or bradykinin. Similarly, taxol and vinblastine had no effect on K+-induced 45Ca++ uptake into chromaffin cells. The inhibitory effects of taxol and vinblastine during a secretory challenge are specific for cholinergic receptor-mediated 45Ca++ uptake and catecholamine release and prevent receptor-mediated membrane depolarization. These results do not support a role for microtubules either in the exocytosis event or in granule transport during an initial secretory challenge. The results would be consistent with either an interaction of microtubule protein with the acetylcholine receptor or a direct action of the drugs on the acetylcholine receptor.

Acetylcholine↗
PubMed1983

Plasma catecholamine and cardiovascular responses to morphine and D-ala2-d-leu5-enkephalin in conscious rats.

The effects of morphine and DADL on cardiovascular parameters and plasma catecholamine levels were studied in conscious unrestrained rats. Morphine 30 micrograms icv increased blood pressure over the 3 hr recording period, produced an initial bradycardia followed by a tachycardia and increased plasma epinephrine and norepinephrine levels 20- and 2-fold respectively. These responses were not altered by systemic naloxone 0.8 mg/kg ia or naloxone injected icv 110 micrograms. In adrenalectomized rats blood pressure, heart rate and plasma norepinephrine responses were not significantly altered. Lower doses of morphine 1, 3 and 10 micrograms icv produced dose-related increases in plasma catecholamines, in the absence of any signs of respiratory depression, which were antagonized by naloxone 110 micrograms icv. 1m Morphine 10 mg/kg produced effects similar to those of icv morphine and these were readily antagonized by naloxone 0.8 mg/kg ia. DADL 10 micrograms icv also produced effects similar to those of morphine but of a shorter duration, and these were also inhibited by naloxone 0.8 mg/kg ia. The results are consistent with an action of opiates on a specific opiate receptor in the brain mediating an increase in catecholamine release. The rise in blood pressure may in part be a consequence of the increase in circulating catecholamines.

Adrenalectomy↗
PubMed1978

Lack of effect of helium breathing on catecholamine levels in the adrenal vein blood of the rabbit.

Catecholamine levels were measured in the adrenal vein blood of the chloralose anesthetized rabbit during periods of helium-oxygen breathing (50% He-50% O2) and of air breathing. Blood samples were taken from the T-arm of a venous shunt made by cannulating the renal vein proximally to the orifice of the adrenal vein and connecting the distal end of the cannula to one in the femoral vein. Adrenal vein blood flow varied from 0.09-0.30 g/min in five animals, and catecholamine release from 10-92 ng/min. There were large differences between levels from animal to animal but no significant differences in any one animal between levels measured while breathing helium and levels measured while breathing air. The same held true for respiratory rate, blood pressure, heart rate, and percent change in blood pressure during a simulated valsalva maneuver. Although there were changes seen in catecholamine release during some of these experiments, they could not be related to an effect of gases breathed. It is concluded that if there was an effect of helium breathing on catecholamine release in these anesthetized rabbits it was masked by other conditions with stronger action on the sympatho-adrenal system.

Adrenal Glands↗
PubMed1984

Evaluation of free radical effects and catecholamine alterations in adriamycin cardiotoxicity.

With the goal of evaluating the potential roles of free radicals and catecholamines in the pathogenesis of acute and chronic Adriamycin (ADR) cardiotoxicity, evidence was sought for myocardial free radical toxicity and alterations in myocardial catecholamine levels after acute and chronic administration of ADR to rabbits. In acute studies, male New Zealand white rabbits received intravenous ADR, 1.1 or 5 mg/kg per day for 1 or 3 days or 10 mg/kg for 1 day and were sacrificed 3-72 hours later. Because the glutathione-glutathione peroxidase system is a major pathway for free radical detoxification, glutathione levels and glutathione peroxidase activity were measured. In the acute studies, ADR-treated rabbits exhibited significantly increased levels (up to 50%) of total and reduced glutathione, unchanged levels of oxidized glutathione, and a slight decrease in the percentage of oxidized glutathione. Major effects of dose and sacrifice interval were not observed. However, in animals receiving three injections of 5 mg/kg or one injection of 10 mg/kg ADR, myocytes exhibited fine vacuolization, due to lipid accumulation and dilatation of the sarcoplasmic reticulum, without evidence of coagulation necrosis. In the chronic study, rabbits received 1.1 mg/kg ADR twice weekly for up to 10 weeks. Levels of total and reduced glutathione were increased significantly by 23-36% after 9-12 and 16-20 injections without change in the percentage of oxidized glutathione. The mean percentage of myocytes with vacuolar-myofibrillar degeneration, the characteristic lesion of chronic ADR cardiotoxicity, was 0 after 5-7 injections, 3.3 after 9-12 injection, and 17.2 after 16-20 injections. Glutathione peroxidase activity was not reduced significantly in any group of acute or chronic ADR-treated animals. Tests for lipid peroxidation (malondialdehyde and ethane production) were negative in acute studies. Myocardial catecholamine levels were unchanged in acute and chronic ADR animals. Thus, the cardiac glutathione-glutathione peroxidase system is activated with ADR treatment at the onset of cellular damage, and cellular damage progresses without further alteration of this system, loss of glutathione peroxidase activity, or reduction in myocardial catecholamines in rabbit models of ADR cardiotoxicity. These findings suggest that free radical generation in the heart may contribute to ADR cardiotoxicity, but that other factors probably play a more important role in the pathogenesis of the myocardial damage.

Animals↗
PubMed1984

Carbamazepine decreases catecholamine turnover in the rat brain.

The anticonvulsant carbamazepine (100 mg/kg i.p.) increased the levels of 3-methoxy-4-hydroxyphenylglycol sulfate in the rat brain as well as its accumulation after inhibition of acid transport by probenecid. It did not interfere with 3-methoxy-4-hydroxyphenylglycol sulfation in vivo. However, this was not corroborated by the results of turnover studies. The depletion of brain norepinephrine after inhibition of tyrosine hydroxylase or dopamine (DA) beta-hydroxylase rather tended to be decreased and the accumulation of DA in the rat heart after DA beta-hydroxylase inhibition was diminished. Carbamazepine also reduced the depletion of striatal DA after tyrosine hydroxylase inhibition and the accumulation of striatal dopa after central decarboxylase inhibition, but did not affect the levels of the deaminated DA metabolites, homovanillic acid and 3,4-dihydroxyphenylacetic acid, even after pretreatment with probenecid. Therefore, carbamazepine seems to reduce catecholamine turnover in spite of its enhancing action on the firing of norepinephrine and DA neurons reported in the literature. These apparently paradoxical effects might be explained by an interference with the catecholamine storage mechanism. Two other anticonvulsants, diphenylhydantoin and phenobarbital, in doses approximately equieffective to that of carbamazepine with respect to their anticonvulsant action, showed similar although somewhat weaker effects on DA, but not on norepinephrine turnover. Within the catecholamine hypothesis of affective disorders, the reduction of catecholamine turnover by carbamazepine might explain the reported antimanic and antipsychotic effects in patients.

Animals↗
PubMed1984

Effects of upper abdominal sympathectomy on gastric acid, serum gastrin, and catecholamines in the rat gut.

Selective upper abdominal sympathectomy increased basal acid output in rats but was without effect on stimulated acid output, serum gastrin concentration, and gastric mucosal histidine decarboxylase activity. The sympathectomy was verified by fluorescence histochemistry and determination of tissue catecholamines. A drastic reduction in tissue noradrenaline, adrenaline, and dopamine levels occurred after sympathectomy, and fluorescence microscopy showed a complete loss of adrenergic nerve fibers. Vagotomy reduced catecholamine levels in the stomach wall by 50% but did not affect the catecholamine content in the pancreas and small bowel. Surprisingly, combined vagotomy and upper abdominal sympathectomy resulted in lower catecholamine levels than sympathectomy alone in extragastric but not in gastric tissues.

Animals↗
PubMed1978

[Changes in the myocardial catecholamines in experimental stress and during assisted circulation].

After two hours of immobilization stress in rats, the authors observed significantly decreased noradrenalin values in the myocardium, returning to normal values later. The concentration of adrenalin in the myocardium of rats showed a contrary behavior under stress conditions. Myocardiac catecholamin shifts in dogs with experimental stress induced by coronary occlusion were registered. After 120 minutes of mechanical circulatory support for the left-sided bypass system the catecholamin level in the left atrium decreased. On the other hand, catecholamin levels in the left ventricular myocardium, injured by experimental infarction, were unchanged after 120 minutes of assisted circulation. In correspondence with hemodynamic and metabolic findings, these results could support the method of assisted leftside bypass. Myocardial catecholamines seem to be another possible parameter for the assisted circulation.

Animals↗
PubMed1983

Catecholamines in diabetic retinopathy.

An attempt has been made to correlate the catecholamines and diabetic retinopathy. Plasma catecholamines and their urinary metabolite, vanillylmandelic acid, were measured in 53 cases of different stages of diabetic retinopathy and the results compared with the 30 cases of the control group. The study revealed a rise in total plasma catecholamines that was significant in the preretinopathic stage and highly significant in the early as well as in the late stages of diabetic retinopathy. Thus, catecholamines may play an important role in the pathogenesis of diabetic retinopathy by stimulating the counterregulatory hormones, namely growth hormone and glucagon.

Catecholamines↗
PubMed1983

[Metabolism of catecholamines in the clinical biochemistry of hypertension].

The object of this study was to review the state of methods of investigating the mmetabolism of catecholamines in the biochemical study of hypertension. A comparison between blood and urinary parameters would seem to show urinary metanephrine levels to be the most discriminating biochemical indicator of pheochromocytoma: this parameter is particularly valuable when pheochromocytoma is associated with normal blood pressure, a situation in which the circulating catecholamine levels are usually unchanged. Three recent aspects of this diagnosis, the development of which may provide new information, are discussed: differentiation between free and conjugated catecholamines, evaluation of platelet amines, the clonidine test. The study of the métabolism of catecholamines in non-tumoral hypertension is also considered but the problems in performing and interpreting these tests are much more difficult.

Adrenal Gland Neoplasms↗
PubMed1984

Plasma and urinary catecholamines and their metabolites in chronic renal failure.

The effect of chronic renal failure (CRF) on the plasma concentration and urinary excretion of catecholamines and their metabolites was studied in 14 patients with varying degrees of chronic renal failure who had creatinine clearances of 19 to 77 mL/min. The results were compared with those obtained in a group of age-matched normal controls. Plasma catecholamine concentrations were significantly higher in the CRF patients compared with age-matched normal controls (456.9 +/- 303.1 v 278.5 +/- 81.1 pg/mL). The urinary metanephrine (0.6 +/- 0.6 mg/g creatinine) and vanillylmandelic acid (VMA) (6.6 +/- 4.2 mg/g creatinine) were within the normal range. No significant correlations were found between creatinine clearance and urinary metanephrine and VMA excretion or with the plasma catecholamine concentrations. Our observations indicate that, despite the decrease in creatinine clearance, urinary VMA and metanephrine determinations are valid screening tests for pheochromocytoma in patients with compromised renal function. Plasma catecholamine concentrations, however, show moderate elevation with decreasing renal function.

Adult↗
PubMed1980

Effect of in vitro hemolysis on assay of plasma catecholamines and DOPA.

I analyzed for free and sulfate-conjugated catecholamines and DOPA (3,4-dihydroxyphenylalanine) in four aliquots of a single plasma pool with use of Upjohn's "Cat-A-Kit" (catecholamines radioenzymatic assay kit [3H]. One aliquot was a clear plasma control; the others were supplemented with different concentrations of lysed human erythrocytes, to investigate possible interference by hemolysis with analysis for norepinephrine, epinephrine, dopamine, or DOPA in plasma. I observed no statistically significant difference that could be attributed to the degree of hemolysis between control and treatment groups for DOPA or any catecholamine fraction. Hemolysis in plasma from improper collection or processing techniques apparently does not preclude accurate and precise quantitation of free or sulfate-conjugated catecholamines or DOPA with the Cat-A-Kit.

Blood Specimen Collection↗