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PubMed1989

Ontogenesis of chromogranin A and B and catecholamines in rat adrenal medulla.

The ontogenesis of chromogranins A and B and catecholamines was investigated for rat adrenal medulla. The chromogranins, the major secretory peptides of chromaffin granules, were characterized by one- and two-dimensional immunoblotting. Chromogranin B appeared identical in fetal and postnatal adrenals. On the other hand a significant portion of chromogranin A immunoreactivity in fetal adrenals was present in a component which was identified as a proteoglycan form of chromogranin A. In adult adrenals this proteoglycan chromogranin A was different and much less prominent. Total chromogranins and catecholamines increased parallely from the 17th prenatal day to the adult stage. However in early periods of development chromaffin granules are likely to contain relatively higher catecholamine levels than adult granules. At the end of the gestational period both the ratio of adrenaline to noradrenaline and of chromogranin A vs B increases sharply. These results establish that from the 17th prenatal day onward fetal adrenal glands contain chromaffin granules which are filled with both the major secretory peptides and catecholamines. The relative composition of the secretory content (adrenaline vs noradrenaline and chromogranin A vs chromogranin B) changes at the end of the gestational period in parallel with the development of the corticosteroid-producing adrenal cortex.

Adrenal Medulla↗
PubMed1992

Role of catecholamines in the modafinil and amphetamine induced wakefulness, a comparative pharmacological study in the cat.

Seventeen adult cats were chronically implanted with electrodes for polygraphic recordings in order to assess the role of catecholamines in the arousal effects of oral administrations of modafinil, a presumed noradrenergic agonist, and amphetamine, a well-known catecholamine-releasing agent. Whereas both modafinil (1, 2.5 and 5 mg/kg) and amphetamine (0.25, 0.5 and 1 mg/kg) caused a significant and dose-dependent increase in wakefulness and brain temperature, amphetamine, but not modafinil, elicited marked signs of behavioral excitation. Pretreatments with alpha-methyl-DL-p-tyrosine methyl ester (50 mg/kg, i.p.), an inhibitor of catecholamine synthesis, almost completely prevented the effects of amphetamine (0.25 and 1 mg/kg), but only slightly reduced the duration of the waking effect of modafinil (2.5 and 5 mg/kg). Pretreatments with phentolamine (10 mg/kg, i.p.), prazosin (1.5 mg/kg, per os) and propranolol (5 mg/kg, i.p.), an alpha-, alpha 1- and beta-receptor antagonist, respectively, attenuated significantly the arousal effect of modafinil (1 mg/kg, the same as below) but not of amphetamine (0.25 mg/kg, the same as below). Intraperitoneal injections of haloperidol (0.5 mg/kg), a dopamine-receptor antagonist, blocked significantly the arousal of amphetamine but not of modafinil. The effects of both modafinil and amphetamine were enhanced by a pretreatment with yohimbine (1 mg/kg, i.p.), an alpha 2-receptor antagonist. These results suggest that the arousal effect of modafinil does not depend on the availability of the endogenous catecholamines but results from an enhancement of alpha 1- and beta-receptor activity and that the waking and behavioral effects of amphetamine may be mainly due to an increase in dopamine release.

Amphetamine↗
PubMed1994

Astrocytes and catalase prevent the toxicity of catecholamines to oligodendrocytes.

Metabolism of catecholamines can generate reactive free radical species, including hydrogen peroxide (H2O2), that are potentially harmful to cells. In this study, norepinephrine (NE) and epinephrine (EPI) were found to be toxic to oligodendrocyte (OL) cultures derived from adult rat brain. The catecholamine toxicity, reproduced by equimolar concentrations of H2O2, could be completely prevented by simultaneous treatment of OLs with the H2O2-decomposing enzyme catalase. These results implicate H2O2 produced by metabolism of NE and EPI as the toxic intermediate. Since OLs in vivo are not normally susceptible to the toxicity of catecholamine neurotransmitter molecules, we sought to examine the involvement of another cell type closely apposed to OL, that is astrocytes, as a protectant against catecholamine toxicity. When adult rat OLs were seeded onto a monolayer of neonatal rat astrocytes, the toxicity of NE, EPI and H2O2 to OLs was completely prevented; medium conditioned by astrocytes did not prevent the manifestation of H2O2 toxicity on OLs. We conclude that the OL-myelin complex is vulnerable to free radical-mediated damage, especially when the protective functions of astrocytes are impaired.

Animals↗
PubMed1984

Plasma levels of free and total catecholamines and two deaminated metabolites in man--rapid deconjugation by heat in acid.

We have described a procedure for deconjugation of plasma catecholamines, norepinephrine (NE), epinephrine (E) and dopamine (DA) and two catecholamine metabolites 3,4-dihydroxymandelic acid (DOMA) and 3,4-dihydroxyphenylglycol (DOPEG). Heat at 100 degrees C of the acidified specimen, pH 0.8, produced complete deconjugation of catecholamines in 7 minutes and of metabolites in 5-7 minutes. Subsequently all five products were simultaneously measured with a radioenzymatic assay. However, hydrolysis for 7 minutes produced approximately a loss of 5% in DA and E, 15% in NE and 50% in the metabolites. The percent of free compound in the plasma of 11 normotensive and healthy subjects was 23 +/- 16 for NE, 20 +/- 8 E, 0.8 +/- 1 DA, 20 +/- 7 DOMA and 42 +/- 12 for DOPEG. Similar results were obtained in a random specimen of six patients with primary hypertension. In a group of four patients with pheochromocytoma free levels of NE, DOPEG and DOMA were significantly greater than in the other two groups, whereas conjugates were not. The intravenous administration of NE or the activation of sympathetic nervous system by standing combined with exercise for 15 minutes did not produce a change in the levels of plasma conjugates. These findings suggest that short changes in plasma catecholamines are better reflected in the free than the conjugated part.

Catecholamines↗
PubMed1983

Effects of paraquat on plasma glucose, cortisol, catecholamines, and insulin in the beagle.

Paraquat is known to produce hyperglycemia in rodents, although the mechanisms responsible for the hyperglycemic effect of paraquat are not clearly understood. In this study we report the effects of paraquat (25 mg/kg iv) on plasma glucose, cortisol, catecholamines, and insulin in dogs. Paraquat caused a significant increase in plasma glucose level at all times of measurement except at 0.5 hr following paraquat administration. The cortisol levels after paraquat treatment were increased to 133, 305, 279, 418, 517, 672, and 567% above zero time control at 0.5, 1.5, 3, 6, 12, and 24 hr, and at death time respectively. The catecholamines at these times were increased to 42, 17, 72, 118, 138, 226, and 435% above the control. In contrast to cortisol and catecholamines, the plasma insulin levels after paraquat treatment were significantly decreased at 3, 6, 12, and 24 hr. These hormonal observations can explain, at least in part, the observed hyperglycemia, since all promote hyperglycemic states. For example, cortisol is gluconeogenic, catecholamines are glycogenolytic, and lower insulin levels result in depressed peripheral glucose utilization.

Animals↗
PubMed1979

Effect of catecholamines on oedema induced by inflammatory agents in the rat.

The effect of intracutaneous adrenaline and noradrenaline (5 X 10(-12) and 5 X 10(-11) mol) was examined on the oedema (Evans blue dye leakage) response of rats to several inflammatory agents. The catecholamines reduced the oedema response to all agents tested except prostaglandin E1 (PGE1) which was significantly potentiated by noradrenaline (5 X 10(-11) mol), and a combination of bradykinin 5 X 10(-11) mol with PGE1 5 X 10(-10) mol which was not significantly affected by any dose of catecholamine. Adrenaline was more effective than noradrenaline in reducing oedema produced by 5-hydroxytryptamine (5HT) and histamine and by agents which release these amines (compound 48/80, dextran and antigen challenge with egg albumin in sensitized rats), but noradrenaline was more potent against bradykinin-induced oedema. The inhibitory effect of catecholamines against oedema produced by histamine and 5HT was abolished by a combination of phentolamine and propranolol. It was concluded that the oedema-inhibiting effect of catecholamines is due to alpha- and beta-adrenoreceptor mediated actions.

Adrenergic alpha-Antagonists↗
PubMed1982

Interactions of catecholamine uptake inhibitors and norepinephrine on autonomic ganglia.

The effect of catecholamine uptake inhibitors on blockade by norepinephrine was observed in the isolated stellate ganglion of the hamster. The preganglionic nerve was stimulated, supramaximally, at 0.2 Hz and compound action potentials were recorded from the postganglionic nerve. Norepinephrine blocked ganglionic transmission. The sensitivity of the ganglion to norepinephrine was increased by the catecholamine uptake inhibitors, desipramine (3 X 10(-7) M), d-amphetamine (10(-6) and 10(-5) M) and tyramine (10(-4) M). Ouabain (10(-5) and 3 X 10(-5) M) did not change the sensitivity of the ganglion to norepinephrine. All the drugs reduced the uptake by the [3H]norepinephrine into the ganglion. The inhibition of [3H]norepinephrine uptake by the drugs could be correlated with the increase in sensitivity of the ganglion to norepinephrine. These results support the hypothesis that catecholamine uptake is important in terminating the actions of exogenously applied norepinephrine, and that inhibition of the catecholamine uptake increases the sensitivity of the ganglion to norepinephrine.

Animals↗
PubMed1986

Differential time course of protection by monoamine oxidase inhibition and uptake inhibition against MPTP neurotoxicity on central catecholamine neurons in mice.

Pretreatment with the monoamine oxidase inhibitor pargyline or the catecholamine uptake blocker nomifensine both protected central catecholamine neurons against MPTP-induced neurotoxicity as monitored by analyzing catecholamine levels and [3H]mazindol binding. Post-treatment with the inhibitors showed that the administration of nomifensine could be delayed longer than that of pargyline in order to achieve a protective effect. The results are compatible with the view that the monoamine oxidase-catalyzed conversion of MPTP to a toxic metabolite MPP+ occurs mainly extraneuronally. MPP+ is subsequently taken up and accumulated selectively in catecholamine neurons, initiating degeneration.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1992

Mechanism of blockade by flunarizine of bovine adrenal catecholamine release.

How flunarizine, a class IV Ca2+ antagonist, affects the secretion of catecholamines in response to nicotinic receptor activation (10-s pulses with 100 microM dimethylphenylpiperazinium, DMPP) or direct depolarization of chromaffin cells (10-s pulses with 100 mM K+ and 2.5 mM Ca2+, 100 K+/2.5 Ca2+) was studied in bovine adrenal glands perfused with an oxygenated Krebs-Tris solution at 37 degrees C at a rate of 20 ml/min. Experimental protocols aimed to test voltage and time dependence of the flunarizine blocking effects on secretion are described. The DMPP pulses released an average of 217 micrograms catecholamines and the K+ pulses, an average of 117 micrograms. These responses were blocked by flunarizine concentration dependently; IC50s were 3.7 microM for DMPP and 1.1 microM for K+. Under polarizing conditions (60-s perfusion with a solution containing 5.9 mM K+ and nominally zero Ca2+), a 10-s pulse with 100 K+/2.5 Ca2+ released 117 +/- 26 micrograms of catecholamines (n = 12). Under depolarizing conditions (60-s perfusion with 118 K+/0 Ca2+ prior to the Ca2+ pulse), the pulse with 118 K+/2.5 Ca2+ released 307 +/- 36 micrograms of catecholamines (n = 14). Flunarizine blocked these secretory responses equally and concentration dependently with an IC50 of 3.4 microM under polarizing conditions and of 3.8 microM under depolarizing conditions. Thus, blockade by flunarizine of secretion was apparently not voltage-dependent. The blockade was, however, clearly dependent on the time of exposure of the adrenal medullary tissue to flunarizine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗
PubMed1984

Effect of cardiotoxic concentrations of catecholamines on Na+-Ca2+ exchange in cardiac sarcolemmal vesicles.

The mechanism by which the administration of large doses of catecholamines produces myocardial necrosis in experimental animals and humans has not yet been ascertained. One of the consequences of such administration is the accumulation of high concentrations of Ca in the heart and it has therefore been suggested that this is the factor that leads to cell injury. The elevated intracellular Ca appears to be due in part to enhanced Ca influx resulting from catecholamine-induced opening of membrane Ca channels and in part to increased membrane permeability caused by membrane damage. It is not clear, however, why the myocardial cells are unable to extrude their extra load of Ca, at least initially, so as to maintain normal Ca concentrations. The effects of high concentrations of epinephrine and isoproterenol on Na+-Ca2+ exchange transport in isolated sarcolemmal vesicles prepared from hearts of Sprague-Dawley rats were determined. It was found that catecholamine concentrations of 10(-4) to 10(-2) M inhibited the exchange in a dose-related manner while choline, in the same concentrations, had no effect. It is therefore possible that cardiotoxic concentrations of catecholamines also interfere with Na+-Ca2+ exchange transport across the myocardial sarcolemma in vivo and thereby inhibit the efflux of intracellular Ca.

Animals↗
PubMed1989

Decreased catecholamine content in parkinsonian adrenal medullae.

Autopsy specimens of adrenal medullae from parkinsonian and nonparkinsonian patients were analyzed for free catecholamines by high-performance liquid chromatography with electrochemical detection. The total free catecholamine content (nanomoles free catecholamine per milligram protein) was significantly lower in the parkinsonian patients than in the control population when the values were corrected for age and time from death to organ harvest. It is not established whether this decreased catecholamine content in the adrenals of parkinsonian patients is a concomitant of the disease itself or whether it is secondary to drug therapies used to treat the symptoms of Parkinson's disease.

Adrenal Medulla↗
PubMed1990

Importance of catecholamine release for the functional action of intrastriatal implants of adrenal medullary cells: pharmacological analysis and in vivo electrochemistry.

The aim of the present experiments was to test whether adrenal chromaffin cells implanted into the striatum of rats could exert a functional effect through a release of catecholamines. A cell suspension obtained from bovine adrenal medulla was implanted unilaterally into the striatum. The striatal dopaminergic input was extensively destroyed beforehand to preclude the possibility of reinnervation of the striatum by endogenous dopaminergic neurons. The functional influence of the implant was tested through the measurement of drug-induced rotation, while catecholamine release was measured subsequently in the same animals by in vivo electrochemistry. Transplant survival, as shown by the immunohistochemical analysis performed at the end of the in vivo experiments, was highly variable. Surviving chromaffin cells maintained their endocrine morphology and no reinnervation of the host striatum could be detected. Rotation of the animals evoked by apomorphine (0.1 mg/kg, sc) or amphetamine (5.0 mg/kg, ip) following the lesion was left uninfluenced following transplantation, even when a large transplant was recovered. On the other hand, nicotine (0.5 mg/kg, sc) evoked a strong contraversive rotational response in the transplant-bearing animals. This response could not be ascribed to the central effect of substances released peripherally and entering the nervous system through the blood-brain barrier opened by the implantation procedure, as it could not be found in animals bearing implants of other peripheral endocrine tissue, viz, pituitary. The effect of nicotine was not blocked by the pretreatment of the animals with either the opiate antagonist naloxone (2.5 mg/kg, 10 min) or the dopamine receptor blocker pimozide (0.5 mg/kg, 1 h), although the latter pretreatment blocked the amphetamine-evoked rotation. No spontaneous catecholamine release could be detected from the implanted chromaffin cells by in vivo electrochemistry, while treatment with amphetamine or nicotine did evoke a release. The results suggest that the functional effects of such intrastriatal grafts of chromaffin cells, reported in previous studies, cannot be explained by the secretion from the grafted cells of catecholamines into the denervated striatum. On the other hand the results obtained following the pharmacological stimulation of these cells indicate that adrenal grafts can, under suitable conditions, influence the functioning of the host nervous system.

Adrenal Medulla↗
PubMed1992

Effects of adrenal medulla grafts on plasma catecholamines and rotational behavior.

The mechanisms by which adrenal medulla grafts influence the function of host brains in animal models of Parkinson's disease are unclear. To explore this issue, fragments of adrenal medulla or sciatic nerve were transplanted into the lateral ventricle of bilaterally adrenalectomized (ADX) or sham-ADX rats with unilateral 6-hydroxydopamine lesions of the substantia nigra. Additional control group received sham-transplantation surgery. Behavioral effects of these procedures were tested following administration of apomorphine, amphetamine, or nicotine. Plasma catecholamines were measured before and after transplantation surgery. In both ADX and sham-ADX rats, adrenal medulla grafts produced greater decreases in apomorphine-induced rotational behavior than did sciatic nerve grafts or sham-transplanted groups. Decreases in rotation were smaller in ADX than in sham-ADX animals, regardless of graft treatment. Plasma catecholamines increased after transplantation surgery in each of the sham-ADX groups, regardless of graft type. Increases in plasma dopamine concentrations were associated with decreases in rotational behavior. Five months after transplantation, grafted chromaffin cells demonstrated catecholamine fluorescence, tyrosine hydroxylase (TH) and chromogranin A immunoreactivities, and expression of TH mRNA. It is concluded that adrenal medulla grafts produce decreases in apomorphine-induced rotation through a combination of two independent effects. One is a specific effect of adrenal medulla grafts. The second is a nonspecific effect that requires an intact adrenal gland and may be related to increases in plasma catecholamine concentrations.

Adrenal Medulla↗
PubMed1983

The effect of N6-phenylisopropyladenosine on the regulation of fat cell hexose transport, glucose oxidation and fatty acid release by insulin and catecholamines.

N6-Phenylisopropyladenosine was employed in the absence of endogenous adenosine to explore the influence exerted by the R-site over the antagonistic interaction of insulin and catecholamines on several parameters of fat cell metabolism. When no hormones were present, N6-phenylisopropyladenosine had little or no effect; however, the nucleoside potentiated insulin inhibition of catecholamine-stimulated events, such as lipolysis, and, conversely, diminished or blocked catecholamine inhibition of insulin-stimulated processes, such as 2-deoxyglucose uptake, glucose oxidation and esterification, even under conditions where N6-phenylisopropyladenosine, alone, was ineffective in reversing catecholamine actions.

Adenosine↗
PubMed1984

Circadian variations of catecholamine levels in brain, heart, and plasma in the eel, Anguilla anguilla L., at three different times of year.

The amounts of catecholamine (dopamine, adrenaline, and noradrenaline) in the brain, heart, and plasma of the eel (Anguilla anguilla L.) during a 24-hr period and at three different times of year were determined by using a radioenzymatic method. Seasonal variations of catecholamine average values were found to be different when considering catecholamine levels in the same tissue (one exception: heart levels in May) or the same amine in different tissues. Circadian rhythms of catecholamine levels were evident only in the brain; the maximum amount generally occurred during the light phase. No correlation could be found between the 24-hr variations in the different tissues. The most important variations were phased with the dark-light cycle but were also dependent on the annual cycle.

Animals↗
PubMed1987

Catecholamine effect on cyclic adenosine 3':5'-monophosphate level in isolated catfish hepatocytes.

The effect of catecholamines (epinephrine, norepinephrine, isoproterenol, and phenylephrine) on cyclic adenosine 3':5'-monophosphate (cAMP) level in isolated catfish (Ictalurus melas) liver cells was studied in the presence or absence of alpha (phentolamine) and beta (propranolol)-receptor antagonists. All catecholamines increased the hepatocyte cAMP level: the rank of their potency was epinephrine = isoproterenol greater than norepinephrine greater than phenylephrine. Propranolol completely blocked the catecholamine effect; phentolamine was ineffective. Results confirm previous findings (L. Brighenti, A. C. Puviani, M. E. Gavioli, and C. Ottolenghi, 1987, Gen. Comp. Endocrinol. 66, 306-313) that epinephrine and norepinephrine act via beta-receptor activation. However, the comparison of the effects of isoproterenol and phenylephrine on cAMP with those on phosphorylase alpha and on glycogen breakdown suggests that a more complex mechanism is possibly involved in the catecholamine effect on catfish glycogenolysis.

Animals↗
PubMed1988

Interactive effects of catecholamines and hypercapnia on glucose production in isolated trout hepatocytes.

In response to added catecholamines, isolated trout (Salmo gairdneri) hepatocytes substantially increase the output of glucose into the surrounding medium. This effect is due to activation of glycogen breakdown concomitant with increases in gluconeogenesis and cell respiration. Each metabolic parameter is activated to a similar extent. In hormone-treated and untreated cells, glycogenolysis accounts for more than 97% of glucose production. Activation of glycogen phosphorylase is implicated in the degradation of cell glycogen, while increased flux through the gluconeogenic pathway from lactate is associated with inactivation of pyruvate kinase, possibly through enzyme phosphorylation as indicated by the activity ratio measured at low and saturating concentrations of phosphoenolpyruvate. From studies with specific adrenergic agonists and antagonists, we conclude that stimulation of glycogenolysis and gluconeogenesis in trout hepatocytes is consistent with a beta-adrenergic effect. Results are inconclusive with respect to catecholamine-mediated activation of cell respiration. None of the monitored cell acid-base variables (pH, PCO2, [HCO3-]) are implicated in the catecholamine-dependent changes in metabolic output of hepatocytes. Imposed hypercapnic conditions (increased medium PCO2 and decreased medium pH), which cause changes in cell acid-base parameters, result in a depression of lactate oxidation and gluconeogenesis, while the rate of glycogenolysis is not affected. In addition, the total amounts of glycogen phosphorylase and pyruvate kinase assayable are negatively affected by hypercapnic treatment of hepatocytes. Under hypercapnic conditions, cells are highly responsive to adrenergic agonists. It appears that--especially in the long term--the catecholamine-dependent activation of gluconeogenesis may compensate for the acid-base-dependent shortfall in glucose output by the liver.

Animals↗
PubMed1990

The source of circulating catecholamines in forced dived ducks.

Plasma catecholamines have been measured in chronically adrenalectomized (ADX) ducks, in chronically adrenal-denervated ducks (DNX), and in their respective shamoperated controls (SH-adx, SH-dnx) after 3 min forced submergence. The results showed that 100% of the plasma epinephrine (EP) and 70 to 80% of plasma norepinephrine (NE) released during the dive came from the adrenal glands. Only 20 to 30% of plasma NE came from the endings of the autonomic vascular sympathetic nerves which are strongly stimulated during diving. Adrenal catecholamines were released by nerve activation only; nonneural mechanisms did not play any role in their release. The action of adrenal catecholamines on the cardiovascular system during dives was investigated by measuring heart rate and arterial blood pressure in operated and sham-operated ducks. Cardiovascular adjustments, associated with 3 min of forced diving, were not affected by any differences in the levels of plasma catecholamines.

Adrenal Glands↗