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At least 811 records · Page 45Linked to original sources
PubMed1996

Modulation of brain catecholamine absorbing proteins by dopaminergic agents.

Catecholamine absorbing proteins (CATNAPs) are localized in the brain and thus far have no known biochemical and pharmacological characteristics consistent with other receptor proteins or metabolic enzymes in the central nervous system. The oxidative metabolism of catecholamines in the brain, especially the catabolism of dopamine and its conjugation with metabolic brain proteins, results in the production of highly toxic free radicals. Since such processes are implicated in the pathophysiology of various neurodegenerative diseases, including parkinsonism, and since CATNAPs bind catecholamines with high affinity, there is a need to further investigate if these novel proteins could play a protective role against these harmful catecholamine metabolites. In this study, we demonstrate the purification, pharmacological characterization and modulation of CATNAPs, as the first steps necessary to elucidate the function of these proteins in the brain. First, CATNAPs were identified from tissues using [3H]N-n-propylnorapomorphine (a specific dopamine receptor agonist) and [125I]6-hydroxy-5-iodo[N(N-2,4-dinitro-phenyl)- aminopropyl]1,2,3,4-tetrahydronaphthalene ([125I]DATN; a highly specific ligand synthesized in our laboratory). Three proteins, with molecular masses of 47, 40 and 26 kDa, were identified and purified, which allowed for the subsequent production of antibodies against each of these CATNAPs. The effects of in vivo chronic administration of several dopaminergic agents on CATNAPs were also examined by Western immunoblotting. L-3,4-Dihydroxyphenylalanine (L-DOPA) treatment in rats resulted in the increase of all of the three proteins, as compared to controls. Treatment in rats with the dopamine depleting agent, reserpine, produced a significant decrease in all of the three CATNAPs. In addition, the effects of direct administration of apomorphine, dopamine, epinephrine, isopropylnorepinephrine, norepinephrine, N-n-propylnorapomorphine and 6-hydroxydopamine on CATNAP levels in rats were examined. Interestingly, we observed an increase (as compared to control) of the 47, 40 and 26 kDa proteins in animals treated with dopamine, norepinephrine, N-n-propylnorapomorphine and apomorphine. In contrast, animals treated with 6-hydroxydopamine showed significant decreases in the levels of all three proteins. It is evident that as the concentration of catecholamines increases, there is a corresponding increase in the levels of CATNAPs in the brain. These results clearly demonstrate the pharmacological modulation of CATNAPs by dopaminergic agents and suggest their possible role in the cytoprotection against damage caused by free radicals generated by oxidative stress.

Adrenergic Uptake Inhibitors↗
PubMed1989

Simultaneous catecholamine histofluorescence and thymidine autoradiography of the sexually dimorphic nucleus of the preoptic area in the rat.

The sexually dimorphic nucleus of the preoptic area (SDN-POA) in the rat represents a morphological substrate in which the influence of gonadal hormones on the process of sexual differentiation of the brain can be seen. Since the medial preoptic area (MPO) is a region rich in catecholamine (CA) terminals, it is possible that catecholamines may play a role either in the differentiation of the perinatal SDN-POA or in the function of this nucleus in the adult. It is not known whether catecholamine terminals exist within the SDN-POA or whether they can directly influence the activity of SDN-POA neurons. The present study was conducted to determine the extent to which catecholamines innervate this nucleus and further to elucidate the possibility of a potential sexual dimorphism in the innervation pattern. In order to determine which of the neurons in the MPO are within the SDN-POA we have utilized the fact that the SDN-POA has a prolonged period of neurogenesis in comparison to other neurons of the MPO. Thus, tritiated thymidine-labeled neurons can be used as a detection criterion for the SDN-POA. To conduct this experiment, timed pregnant Sprague-Dawley females were given a single injection of [3H]thymidine on Day 18 of gestation. Pups were killed as adults and prepared for fluorescence histochemistry of monoamines. Sections adjacent to those examined for catecholamine fluorescence were treated for autoradiographic localization of [3H]thymidine. Fluorescence innervation patterns were plotted within the boundaries of the nucleus following its identification from Nissl sections as well as from adjacent autoradiograms simultaneously viewed in a comparator bridge microscope with dark-field illumination.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Phorbol ester stimulates catecholamine synthesis in isolated bovine adrenal medullary cells.

In isolated bovine adrenal medullary cells, the phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA), an activator of protein kinase C, stimulated [14C]catecholamine synthesis from [14C]tyrosine, but not from [14C]DOPA. This stimulatory effect of TPA on [14C]catecholamine synthesis was not dependent upon extracellular Ca2+, and TPA did not affect the uptake of 45Ca2+ or the release of catecholamine by the cells. TPA also did not affect the intracellular cyclic AMP (cAMP) level. 4 alpha-Phorbol 12, 13-didecanoate, which is not an activator of protein kinase C, did not stimulate the synthesis of [14C]catecholamine from [14C]tyrosine. The stimulatory effect of TPA on [14C]catecholamine synthesis was additive with that of carbamylcholine, but not with that of dibutyryl cAMP (DB-cAMP). From these results, it was suggested that protein kinase C is involved in the regulation of tyrosine hydroxylase activity and that this regulatory mechanism might be similar to that involving cAMP.

Adrenal Medulla↗
PubMed1983

Catecholamine effects on blood pressure and heart rate in the American bullfrog, Rana catesbeiana.

The effects of catecholamines and adrenergic blocking agents were studied in vivo on the blood pressure and heart rate of the unanaesthetized American bullfrog, Rana catesbeiana. Bullfrogs were chronically cannulated with a T cannula in the right sciatic artery. The mean systemic arterial blood pressure prior to the infusion of catecholamines was 18.5 +/- 1.5 mm Hg. Mean preinfusion heart rate was 30.9 +/- 2.0 beats/min. Epinephrine elicited the largest increase in blood pressure, with an accompanying decrease in heart rate. Norepinephrine and phenylephrine were less effective. Isoproterenol was the only catecholamine tested which elevated heart rate in a dose-dependent manner. It had no effect on blood pressure. The beta adrenergic antagonist, propranolol, blocked the increase in heart rate elicited by isoproterenol but had no effect on the blood pressure increases elicited by the other catecholamines. The alpha adrenergic antagonist, phentolamine, partially blocked the blood pressure increase by epinephrine, norepinephrine, and phenylephrine as well as the elevation of heart rate by isoproterenol. Atropine alone elevated heart rate 19 +/- 3 beats/min, and prevented slowing of the heart due to epinephrine, norepinephrine, and phenylephrine. Stimulatory effects of epinephrine on heart rate were observed only after atropine had been administered. Beta adrenergic receptors, therefore, appear to function in heart rate regulation; however, the predominant effect of catecholamines is reflex slowing of the heart due to stimulation of the vagus nerve. In contrast, the alpha receptor, stimulated by epinephrine, appears to be the main adrenergic receptor controlling blood pressure changes.

Animals↗
PubMed1990

Interaction of iron-bleomycin with catecholamines.

1. Catecholamines were found to reduce Fe(III)-bleomycin to the ferrous state. Aminochrome, an oxidation product of catecholamine, rapidly appears in the reaction solution. 2. The purple colour of Fe(III)-catecholamine is also detected in the reaction solution, suggesting that iron is transferred from bleomycin to catecholamine. 3. Gel filtration studies confirm that catecholamines are able to take up iron from the iron-drug complex.

Bleomycin↗
PubMed1979

Platelet aggregation in relationship to plasma catecholamines in patients with hypertension.

Plasma catecholamine concentration and platelet aggregation were studied in 22 patients with uncomplicated primary hypertension and 13 age-matched normotensive, healthy subjects at rest and in some during isometric handgrip exercise. The effect of norepinephrine (NE) infusion upon platelet aggregation was also examined. Plasma catecholamine concentration was slightly higher in the hypertensive than the normotensive group, but the difference was not significant. However, platelet aggregation to ADP was significantly greater in the hypertensive than the normotensive subjects. Exercise increased significantly both catecholamines and aggregation in both groups. Platelet aggregation was correlated with age (r = 0.62, P less than 0.01) and plasma NE (r = -0.34, P less than 0.05 for the total group of subjects). The infusion of NE increased significantly plasma NE and platelet aggregation and there was an inverse correlation between NE increase and threshold decrease (r = -0.69, P less than 0.05). Thus, plasma catecholamines and important determinants of platelet aggregation. However, in our study, uncomplicated primary hypertension was not associated with abnormal plasma catecholamine concentration. It is likely that the observed abnormal platelet aggregability to ADP represents a secondary phenomenon, possibly related to more advanced atherosclerotic vascular changes in hypertensive than normotensive subjects.

Adult↗
PubMed1985

Effect on human platelets of catecholamines at levels achieved in the circulation.

Epinephrine at concentrations varying between 3.3 and 12.5 nM had no effect on blood platelets when added alone, but augmented the in vitro platelet response to collagen and thrombin. Both aggregation and secretion responses were enhanced. Norepinephrine produced similar effects but was 50-60% less active than epinephrine. The minimum concentration of epinephrine or norepinephrine to achieve potentiation of platelet responses was even lower in the presence of 5-hydroxy- tryptamine. In contrast to the effects observed with higher concentrations of catecholamines, the synergistic interaction of these low concentrations of catecholamines with other agonists was not transient. The augmented response to catecholamines was mediated by platelet alpha 2-adrenoceptors. The response was inhibited by aspirin indicating that metabolism of arachidonic acid contributes to the synergy between low concentrations of catecholamines and other agonists. These studies show that the levels of the hormones epinephrine and norepinephrine obtained in circulating blood in humans, can be sufficient to enhance platelet responses. The action of catecholamines on platelets may be important in hemostasis and could provide an explanation for the association between certain risk factors and cardiovascular disease.

Adenosine Diphosphate↗
PubMed1982

Plasma free and sulfate conjugated catecholamine levels during acute physiological stimulation in man.

The responses of plasma free and sulfate-conjugated catecholamines to acute physiological stimulation was examined in normal male subjects. Catecholamines were measured with a sensitive radioenzymatic assay incorporating simultaneous hydrolysis of sulfate conjugates and O-methylation of free norepinephrine and epinephrine. Following 20 minutes recumbency after venepuncture 30 +/- 3% of norepinephrine and 16 +/- 5% of epinephrine was in thr free form. Free catecholamines generally increased during standing, cold immersion and isometric handgrip, but sulfates did not change. Bicycle ergometry markedly increased free catecholamines which rapidly returned to basal levels at the end of exercise. In contrast, sulfated norepinephrine decreased substantially with exercise in all subjects but returned to basal levels 3 minutes after stopping exercise. Epinephrine sulfate varied considerably between subjects but showed a similar, although smaller, fall with exercise. Thus, during physiological stimulation, which caused increases in free norepinephrine and epinephrine levels in plasma, the only consistent change in sulfated catecholamines was a marked fall in norepinephrine sulfate after bicycle exercise. This may indicate saturation of sulfotransferase activity, substrate inhibition or impaired tissue conjugation.

Adult↗
PubMed1983

Block by phencyclidine of acetylcholine and barium induced adrenal catecholamine secretion.

Activation of the sympathetic system by phencyclidine (PCP) should result in catecholamine release from the adrenals. However, adrenalectomy does not reduce PCP-induced hypertension. In an attempt to rectify this inconsistency, the direct effects of PCP on the bovine adrenal medulla were examined. At (3 X 10(-6) M), PCP reduced the acetylcholine-(ACh)-induced catecholamine release by 50%. Surprisingly, barium-induced secretion of catecholamines was also reduced by PCP. ACh-induced catecholamine release was not altered by 10(-3)M 4-aminopyridine (4 AP), the potassium channel blocker. Thus, calcium antagonist actions of PCP and consequent block of catecholamine secretion from adrenal medulla may explain the lack of effect of adrenalectomy on PCP-induced hypertension. Possible contributions of calcium and/or potassium channel blockade to other manifestations of PCP overdosage are discussed.

4-Aminopyridine↗
PubMed1986

Effect of aging and endurance training on tissue catecholamine response to strenuous exercise in Fischer 344 rats.

The purpose of the present investigation was to determine the catecholamine response in various tissues to a bout of strenuous exercise in young, adult, and old Fischer 344 rats. Further, to study the effect of endurance training on this response, animals from each age group underwent ten weeks of treadmill running at 75% of their functional capacity. On completion of the training program, all animals demonstrated significant increases (P less than 0.05) in VO2max and endurance capacity. At rest or immediately after an acute bout of strenuous exercise, animals were killed, and the heart, liver, kidney, and adrenals were removed for subsequent catecholamine analysis. Resting cardiac catecholamine levels declined significantly with age. In response to an acute exercise bout, epinephrine (E) levels in the heart were greatly reduced with age averaging 141.8, 62.3, and 21.7 ng/g for the 6-, 15-, and 27-month-old untrained group, respectively. The 15- and 27-month-old trained animals demonstrated significantly higher E levels (33% and 91%) than controls. A similar trend was found for norepinephrine (NE) content in the heart in response to acute exercise, with a marked reduction occurring with advancing age (904.6, 580.1, and 400.8 ng/g heart for 6-, 15-, and 27-month-old untrained groups, respectively). Again, training induced a greater NE response in the older trained animals compared to age-matched controls. In contrast, adrenal catecholamine levels showed a tendency to increase with age. It was concluded that when challenged with strenuous physical stress, cardiac catecholamine content is markedly diminished with age. Further, ten weeks of endurance training can attenuate this functional decline.

Adrenal Glands↗
PubMed1984

Hypothalamic opioid peptide regulation of catecholamine secretion.

We compared the plasma catecholamine responses to intracisternal beta-endorphin with those to two mu receptor agonists. Morphine was less potent and [D-Ala2, MePhe4, Gly5-ol]enkephalin (DAGO) was more potent in stimulating catecholamine secretion. Since the hypothalamic paraventricular nucleus (PVN) contains a high level of opioid binding sites and is important for sympathoadrenal regulation, we examined the effects on catecholamine secretion of DAGO infusion into the PVN. DAGO infused into the PVN produced dose-related increases in plasma catecholamine concentrations, with an effective dose as low as 10pmol. This DAGO effect was blocked by the prior systemic administration of naloxone, and DAGO was ineffective when infused into frontoparietal cortex. Thus, endogenous opioid peptides appear to increase central sympathetic outflow and catecholamine secretion by stimulating mu receptors in the PVN.

Animals↗
PubMed1994

Pertussis toxin pretreatment enhances catecholamine secretion induced by pituitary adenylate cyclase-activating polypeptide in cultured porcine adrenal medullary chromaffin cells: a possible role of the inositol lipid cascade.

We determined how pertussis toxin (PTX) pretreatment alters PACAP-induced catecholamine secretion in cultured porcine adrenal medullary cells. Pretreatment of these cells with PTX (1 ng/ml for 24 h or 10 ng/ml for 6 h) markedly enhanced PACAP-induced catecholamine secretion. PTX pretreatment also produced a small increase in basal secretion and secretion in response to nicotine and carbachol, but the effect of the PACAP-induced secretion was most striking. We examined the role of the phosphoinositol cascade in potentiating the PACAP-induced catecholamine secretion by PTX and found that PACAP-induced accumulation of inositol phosphates in PTX-pretreated cells was significantly greater than that in untreated cells. Furthermore, removal of extracellular Ca2+ and addition of Ca2+ channel blockers inhibited the catecholamine secretion induced by PACAP in PTX-pretreated cells. From these results, we speculate that a PTX-sensitive G-protein tonically inhibits phospholipase C. PTX enhances the PACAP-induced secretion of catecholamine by blocking the action of this inhibitory G-protein.

Adenylate Cyclase Toxin↗
PubMed1983

The adrenal chromaffin cell as a model to study the co-secretion of enkephalins and catecholamines.

The enkephalins, endogenous opioid pentapeptides first discovered in brain, are present in high concentrations in the adrenal medulla chromaffin cell. The enkephalins and other peptides containing enkephalin sequences are stored with catecholamines in the secretory organelles (chromaffin vesicles); these peptides are apparently incorporated into the vesicles at the time of their biosynthesis as opposed to later accumulation, as is the case with catecholamines. The enkephalins, catecholamines and other soluble components of the vesicle are co-secreted by the process of exocytosis. Regulatory mechanisms, apparently triggered by a critical catecholamine pool, control the synthesis of enkephalins. These mechanisms allow for rapid recovery of enkephalin content after secretion. These findings have been extended from the chromaffin cell to the ontogenically related sympathetic neurons and pheochromocytoma tumors. Secreted enkephalins and related peptides reach ubiquitous opiate receptors through the synaptic gap or the circulation and may modulate a number of important systemic functions. The co-storage and co-secretion of adrenomedullary opioid peptides and catecholamines is only one of a growing number of examples of co-existence of multiple messengers in single neuronal or endocrine cell types. Co-secreted multiple messengers may act in a co-ordinated fashion to produce integrated organismal responses.

Adrenal Glands↗
PubMed1989

Partial transection of the ipsilateral cervical spinal cord evokes a sustained increase in the adrenal section of catecholamines in the cat.

The importance of cervical spinal pathways on the adrenal secretion of catecholamines was assessed in chloralose-anesthetized cats. Partial transections of the upper cervical spinal cord were made ipsilateral (n = 21) or contralateral (n = 10) to the adrenal vein sampling catheter. Ipsilateral cuts evoked an immediate increase in the adrenal secretion of epinephrine that remained elevated at 60 min (+89.7 +/- 27.0 ng/min, P less than 0.001) and increased the epinephrine/norepinephrine secretory ratio from 1.99 +/- 0.4 to 5.02 +/- 0.6 by 60 min (P less than 0.01) indicating a preferential augmentation of the secretion of epinephrine. The magnitude of the increase in secretion of epinephrine was well correlated with the cross-sectional area of the ipsilateral cut (rs = 0.681, P less than 0.01). In contrast, partial transections of similar size made contralateral to the adrenal vein sample evoked significantly smaller increases in the adrenal secretion of epinephrine by 60 min (+12.7 +/- 4.8 ng/min) and were not correlated with the cross-sectional area of the cut. The region of transection common to those experiments that caused the greatest increase in the secretion of catecholamines included the deep laminae (laminae V-VII) within the central gray matter as well as a portion of the dorsal columns. Transections restricted to the dorsolateral and lateral funiculi caused small and inconsistent changes in the adrenal secretion of catecholamines. Ipsilateral and contralateral cuts evoked similar effects on peripheral concentrations of catecholamines, on plasma adrenocorticotropin and on plasma angiotensin II, suggesting that the facilitatory effect of ipsilateral cuts on the adrenal secretion of catecholamines was not the result of a humoral mechanism. Arterial pressure and heart rate increased equally by 1 min and returned to prestimulus values by 5 min after transections of the ipsilateral or of the contralateral cervical cord. Electrical stimulation of the ipsilateral cervical spinal cord, caudal to the level of transection, decreased the secretion of epinephrine and arterial pressure by 1 min (-30.5 +/- 9.0%. P less than 0.05) suggesting the presence of an active inhibitory mechanism that persisted after transection. The results indicated that transections of pathways ipsilateral, but not contralateral, to the adrenal medulla that traverse the upper cervical spinal cord evoke a persistent increase in the adrenal secretion of epinephrine, whereas other indices of neuroendocrine or autonomic function do not reflect this tonic influence.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Glands↗
PubMed1990

Alpha 2-adrenoceptor modulation of catecholamine and neuropeptide Y responses during haemorrhagic hypotension in anaesthetized dogs.

The acute effects of oxymetazoline, an alpha 2-adrenoceptor agonist, and idazoxan, an alpha 2-adrenoceptor antagonist, on the release of neuropeptide Y were evaluated during haemorrhage in pentobarbital-anaesthetized dogs. Plasma concentrations of neuropeptide Y and catecholamines (adrenaline, noradrenaline, and dopamine) were determined in samples simultaneously collected from aorta, portal vein, and adrenal veins. In control dogs, adrenal catecholamine output, aortic concentrations neuropeptide Y and catecholamines markedly increased during the hypotension period. However, adrenal neuropeptide Y output decreased significantly during this period. Portal venous noradrenaline and neuropeptide Y concentrations increased significantly. In dogs treated with idazoxan, catecholamine output from the adrenals increased to an extent similar to that observed in control dogs. However, the increase in noradrenaline and neuropeptide Y in aortic or portal venous blood during haemorrhage was significantly potentiated in the presence of idazoxan. Administration of oxymetazoline abolished this increase, but did not alter adrenal catecholamine or neuropeptide Y output. The present study demonstrates that neuropeptide Y is co-released with noradrenaline from sympathetic nerve fibers during haemorrhage. Since the release of neuropeptide Y appeared to follow a similar time course to that of noradrenaline release, the present observations suggest that haemorrhagic hypotension enhances both neuropeptide Y and noradrenaline release presumably through a common releasing mechanism. These results also indicate that, in peripheral sympathetic nerves but not in the adrenal gland, neuropeptide Y release is also modulated presynaptically by the inhibitory alpha 2-adrenoceptors in conjunction with the noradrenaline release.

Adrenergic alpha-Antagonists↗
PubMed1994

In search of a mechanism for receptor-mediated neurobehavioral teratogenesis by nicotine: catecholamine release by nicotine in immature rat brain regions.

Nicotine disrupts central nervous system development through interactions with nicotinic cholinergic receptors found in immature brain, leading to discoordination of target cell replication and differentiation. However, it is unclear whether the net result is achieved by nicotine's actions on its specific target cells, or indirectly through receptor-mediated release of other neurotransmitters, such as catecholamines, that possess neurotrophic properties. In the current study, developing rats (1, 7, 14 and 21 days old) were challenged acutely with nicotine (0.3 mg/kg) and the release of catecholamines was evaluated in vivo (AMPT method) in three brain regions that differ in nicotinic receptor concentrations. Nicotine did not stimulate catecholamine release at birth, but developed the capacity to do so in parallel with the ontogeny of nicotinic cholinergic receptors in the midbrain+brainstem and in the forebrain. In the cerebellum, which remains poor in nicotinic receptors, no response was obtained at any age. Superimposed on this general pattern, changes in sensitivity to nicotine were also seen that corresponded to ontogenetic changes in endogenous cholinergic tone, suggesting that receptor desensitization occurs normally during developmental stages in which neuronal activity is high. The absence of a catecholamine response to nicotine at birth in the rat indicates that neurobehavioral teratology associated with fetal nicotine exposure does not reflect secondary actions mediated through catecholamines. However, because brain development in the neonatal rat corresponds to fetal stages in man, the onset of these mechanisms may be relevant to human fetal exposure.

Aging↗
PubMed1990

Indomethacin prevents increased catecholamine turnover in rat brain following systemic endotoxin challenge.

1. Key features of the acute phase response to infection are replicated by systemic administrations of lipopolysaccharide and may be mediated via the production of lymphokines and cytokines, including interleukin-1. Inhibition of prostaglandin synthesis may attenuate certain features of the acute phase response. 2. In the present study, the effects of systemic administration of the lipopolysaccharide (LPS, 250 micrograms/rat) and interleukin-1 (IL-1, 10 micrograms/rat) on catecholamine metabolism in different brain regions were compared and the effects of indomethacin, a cyclooxygenase inhibitor was determined. 3. The ratio of metabolite to parent amine was used as an index of turnover of catecholamines. 4. In hypothalamus, both epinephrine and norepinephrine concentrations were decreased and their major metabolite, 3-methoxy,4-hydroxyphenylglycol (MHPG), was elevated at 4, 8 and 24 hr following LPS. The major metabolite of dopamine (homovanillic acid, HVA) was increased at 8 hours in striatum, hypothalamus and medulla. LPS increased dopamine turnover at 8 and 24 hr and norepinephrine turnover at 4, 8 and 24 hr. 5. In all regions examined, IL-1 produced effects similar to LPS on amine and metabolite contents and norepinephrine and dopamine turnover. 6. Significantly, co-administration of a single dose of indomethacin (50 mg/kg) completely blocked LPS-induced changes in hypothalamic catecholamines and metabolites and the increase in turnover at 4 and 8 hr. Furthermore, the effects of IL-1 on hypothalamic MHPG content and norepinephrine turnover were also blocked by indomethacin, although the effects of IL-1 on regional catecholamines and HVA content and turnover were either not modified or partially antagonized by indomethacin. 7. The present results suggest that in the rat, activation of noradrenergic, dopaminergic and epinephrine-containing neurons in hypothalamus, as well as dopaminergic neurons in other regions is associated with the acute phase response to endotoxin and that synthesis of prostaglandins plays a pivotal role in catecholamine responses in all brain regions examined.

Animals↗
PubMed1988

Potentiation of evoked adrenal catecholamine release by cyanide: possible role of calcium.

The effect of cyanide on release of catecholamines was evaluated in isolated bovine adrenal glands stimulated with 4 different agonists. Cyanide (0.1-1 mM) increased catecholamine release induced by barium or cadmium 2-3-fold. Acetylcholine or potassium induced secretion of adrenal catecholamines was also enhanced by cyanide, but only to the extent of 30-50%. These data suggest that cyanide acts by multiple mechanisms to enhance evoked catecholamine release. The above results may be partly explained by the fact that cyanide inhibited 45Ca efflux from stimulated bovine adrenals. Changes in plasma membrane permeability may be crucial in the alterations of ion flux and evoked catecholamine release caused by cyanide.

Acetylcholine↗