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PubMed1986

[Catecholamines in the cardiovascular expression of pheochromocytoma. II--Study of free urinary catecholamines in 14 pheochromocytomas. Classification of pheochromocytomas according to type of secretion].

Studies were conducted in 14 patients with pheochromocytoma over a 3-year period. Circumstances of detection of these tumors varied greatly and were sometimes misleading, hypertension being an inconstant finding in the clinical history and was not always the predominant feature. Biologic exploration involved assay of excretion of free urinary noradrenaline (NA), adrenaline (AD) and dopamine (DA) using a HPLC technique as well as assay of total methoxy derivatives and urinary vanilmandelic acid. Validity of each assay in the diagnosis of pheochromocytoma could be evaluated and only the total free methoxy derivatives gave false negative results. Hormonal secretion of pheochromocytoma is often mixed, but sometimes predominant or exclusive for a single catecholamine. Relative increases of the different catecholamines, evaluated from the ratios DA/NA and DA/NA + AD, are an important factor since a relation exists between blood pressure induced symptomatology and equilibrium between hypotensive hormone (DA) and pressor amines (NA + AD); 3 types of pheochromocytoma can be described: NA-induced with paroxysmal or permanent hypertension but without typical metabolic and cardiac disorders, and with a very reduced DA/NA + AD ratio during hypertensive crises; AD-induced without permanent hypertension but with a mainly orthostatic hypotension and episodes of cardiovascular collapse following hypertensive attacks and with an AD/NA ratio greater than 1; finally the DA-induced lesion in which hypertension is never associated and manifestations are misleading and atypical with an elevated DA/NA + AD ratio.

Adrenal Gland Neoplasms↗

PubMedDate not supplied

Antagonism between pineal peptides and catecholamines. II. The action of a pineal peptide extract on the process of endogenous catecholamines secretion-excretion.

To determine the processes of adrenaline and noradrenaline secretion-excretion in rats and rabbits with/without associated insulin lente administration (20 U.I./kg rat b.w. and 6 U.I./kg rabbit b.w.), the authors used a pineal peptide extract that has now become available under the trade name of "Crinofizin". Under conditions of natural light, environmental temperature of 18-20 degrees C and fed ad libitum, Crinofizin did not cause significant alterations in the rat 24 hrs urinary excretion of catecholamines. Administration of insulin induced a more than two-fold increase in the two catecholamines both in the rabbit and the rat. Administration of Crinofizin one hour before insulin prevented totally or partially these effects of insulin. The drug acted as a blocking agent in the processes of endogenous adrenaline and noradrenaline secretion-excretion under hormonal stimulation, but not under basal conditions.

Adrenal Cortex Hormones↗

PubMed1981

[Metabolism of myocardial catecholamines and plasma catecholamine levels in patients with chronic aortic regurgitation (author's transl)].

In 17 patients suffering from severe chronic aortic regurgitation (class III N.Y.H.A.), during aortic valve replacement right atrial biopsies were taken. In these samples myocardial content of norepinephrine, normetanephrine, epinephrine and dopamine were determined. 2-4 days before valve replacement, plasma catecholamines were measured at rest and during isometric exercise. 15 patients with atrial septum defect (foramen secundum) served as controls. In patients with aortic regurgitation demonstrating no clinical signs of cardiac failure, myocardial content of norepinephrine, normetanephrine and epinephrine was significantly reduced compared to tissue content of patients with atrial septum defect. Right atrial content of dopamine did not reveal any difference between the two groups. In all patients, plasma catecholamines at rest were within normal limits. During isometric exercise, however, the increase of plasma norepinephrine in patients with aortic regurgitation was significantly higher compared to the control group. It is concluded from these data that patients with aortic regurgitation, demonstrating an exaggerated increase in sympathetic activity during exercise, probably show a decrease in myocardial norepinephrine tissue content. Therefore, clinical demonstration of hyperadrenergic response during exercise represents a simple metabolic parameter indicating alteration in myocardial metabolism in patients with chronic aortic incompetence. Since decision for aortic valve replacement should be done before irreversible damage of myocardium has established, it is supposed that assessment of sympathetic activity, at rest and during exercise, may reveal practical clinical importance.

Adult↗

PubMed1999

Is the use of catecholamine before ischemic arrest safe? Effect of catecholamine on rat heart ischemia/reperfusion injury.

Using an isolated working heart model, we studied the effects of dopamine, adrenaline, or noradrenaline pretreatment on ischemia/reperfusion injury. Hearts from Wistar rats were perfused in the first 20-minute working mode, 15 minutes in Langendorff mode, and in the second 20-minute working mode. Hearts were treated with dopamine (0.52 and 2.60 mmol/L), adrenaline (16 and 80 nmol/L), or noradrenaline (16 and 80 nmol/L) during the second working perfusion, then arrested with St. Thomas' Hospital cardioplegic solution and subjected to global ischemia (37 degrees C or 20 degrees C). During reperfusion, recoveries of cardiac function and creatine kinase leakage were measured. At 37 degrees C, dopamine and adrenaline had a harmful effect at both doses; noradrenaline was harmful at a high dose but beneficial at a low dose. At 20 degrees C, adrenaline, dopamine, and noradrenaline had a harmful effect at high doses but no harmful effect at low doses. To determine the role of beta adrenergic stimulation before ischemia, a dose-response study was undertaken with isoprotelenol and milrinone at 37 degrees C. Combined pretreatment with isoprotelenol and milrinone accelerated ischemia/reperfusion injury dose-dependently. Preischemic beta adrenergic stimulation thus plays a significant role in the deleterious effect of catecholamine pretreatment at high doses. At low doses, however, the effect of the inotropic agent could be changed depending on ischemic temperature. Our results suggest that catecholamine should not be given at high doses before ischemia, regardless of temperature during ischemia.

Adrenergic beta-Agonists↗

PubMed2002

V-1, a catecholamine biosynthesis regulatory protein, positively controls catecholamine secretion in PC12D cells.

Stably transfected PC12D cell lines overexpressing a catecholamine biosynthesis regulatory protein, V-1, were used to examine the functional role of V-1 in catecholamine secretion. High K(+)-induced dopamine secretion in V-1 overexpressing clones was shown to be markedly potentiated compared with control clones carried with a vector alone. As assayed intracellular calcium concentration ([Ca(2+)](i)) using fura-PE3, V-1 overexpression was observed to enhance high K(+)-elicited [Ca(2+)](i) elevation. Electron microscopic analysis revealed an increase in dense-cored vesicle formation by V-1 overexpression. These results suggest that the enhancement of high K(+)-induced dopamine secretion by V-1 overexpression results from the potentiation of high K(+)-induced [Ca(2+)](i) elevation and the increase in the number of dense-cored vesicles.

Animals↗

PubMed1975

Effects of catecholamines on rat myocardial metabolism. I. Influence of catecholamines on energy-rich nucleotides and phosphorylated fraction contents.

1. The influence of catecholamines (adrenaline and noradrenaline) on energy metabolism of the rat myocardium has been studied by incubating slices of this tissue with these hormones and by following the levels of the different phosphorylated fractions and adenylic nucleotides. 2. Similar effects are obtained with both hormones, adrenaline being more effective. 3. Catecholamines decrease significantly the total amount of phosphate while Pi content increases during the first 10 minutes of incubation; labile and residual phosphate contents increase at the beginning of incubation and decrease to the initial values afterwards. 4. ATP and ADP levels decrease significantly with both hormones; however, the effect of noradrenalin on the ATP level needs a longer time of incubation. The ATP/ADP ratios decrease after 5 minutes incubation and the total adenylic nucleotide content is severely decreased (35 per cent with adrenalin, after 20 minutes incubation). 5. Similar results have been obtained with other tissues; these results can explain the decrease of aerobic metabolism we observed under the same conditions.

Adenosine Diphosphate↗

PubMed2000

Behaviorally-evoked plasma catecholamine response and 24-hour excretion of urinary catecholamines among cardiac and vascular reactors.

Individuals differ in the cardiac and vascular processes that underlie blood pressure elevations evoked by environmental stimuli; such differences may reflect variability in sympathoadrenal response. We separated 108 healthy, young-adult males into those with predominant elevations in either cardiac output or peripheral resistance when exposed to psychological challenges. We then asked if they differed on other measures of cardiovascular response, concomitant plasma catecholamine reactions or 24-h urinary excretion of catecholamines. Cardiac reactors, relative to vascular reactors, showed reduced cardiac pre-ejection period, a smaller reduction in stroke volume, and elevated plasma epinephrine response and 24-h urinary epinephrine excretion. Vascular reactors, relative to cardiac reactors, responded to mental stress with more elevated diastolic blood pressure, a rise in peripheral resistance and pulse wave velocity, and a greater reduction in stroke volume. Vascular reactors, however, did not show plasma norepinephrine response or 24-h urinary norepinephrine excretion that was greater than cardiac reactors. The results provide partial support for the hypothesis that variability in sympathoadrenal activity contributes to individual differences in cardiac and vascular reactivity, and extend prior observations by demonstrating covariation of behaviorally-elicited cardiac reactivity with the 24-h excretion of epinephrine.

Adolescent↗

PubMed1987

Differential effects of nerve growth factor and ciliary neuronotrophic factor on catecholamine storage and catecholamine synthesizing enzymes of cultured rat chromaffin cells.

The effects of nerve growth factor (NGF) and ciliary neuronotrophic factor (CNTF) on catecholamine content and in vitro activities of tyrosine hydroxylase (TH) and phenylethanolamine N-methyltransferase (PNMT) were studied in adrenal chromaffin cells cultured from 8-day-old rats. Both NGF and CNTF enhanced chromaffin cell survival and partially prevented losses of adrenaline during the 4-day culture period in a dose-dependent manner. CNTF was more potent, although cellular levels of adrenaline and noradrenaline were not maintained. NGF did not add to the effect of CNTF. The effect of CNTF on catecholamine storage was not accompanied by changes in the activities of TH and PNMT. In contrast, NGF induced TH but not PNMT activity. These data indicate differences between the mechanisms by which NGF and CNTF affect adrenal chromaffin cells.

Adrenal Medulla↗

PubMed1989

Effects of acute insulin deficiency on catecholamine and indoleamine content and catecholamine turnover in microdissected hypothalamic nuclei in streptozotocin-diabetic rats.

The effects of streptozotocin-induced diabetes on catecholamine and indoleamine concentrations and catecholamine turnover rates in individual microdissected hypothalamic nuclei known, or believed, to be involved in the control of neuroendocrine function, were examined in control, insulin-treated diabetic and acutely insulin-withdrawn diabetic female rats. Streptozotocin-induced diabetes and acute insulin deficiency were demonstrated to result in increased concentrations of epinephrine in the suprachiasmatic nucleus, decreased turnover of epinephrine in the arcuate nucleus and decreased turnover of dopamine in the ventromedial nucleus was found to be increased in the insulin-treated diabetic animals. These data indicate that experimental diabetes and acute insulin deficiency result in the rapid onset of detectable alterations in epinephrine and dopamine activity in specific hypothalamic nuclei. These diabetes-induced changes may cause, or contribute to, the development of secondary neuroendocrine abnormalities known to occur in the diabetic condition.

Amines↗

PubMed1981

Use of 6-hydroxydopamine to deplete brain catecholamines in the rhesus monkey: effects on urinary catecholamine metabolites and behavior.

The purpose of this study was to determine: 1) whether 6-hydroxydopamine (6-OHDA), previously shown to deplete brain catecholamines (CA) in rodents, depletes brain CA in rhesus monkeys; 2) whether depletion of brain CA produces changes in behavior; and, 3) whether urinary output of 3-methoxy-4-hydroxyphenylglycol (MHPG) reflects brain norepinephrine (NE) depletions. Repeated intracerebroventricular (ICV) injection of 6-OHDA (N = 20; 15.5-73.3 mg/subject) produced chronic changes in social behavior and, at higher dosages, reduced output of urinary MHPG. However, 4 weeks after the last ICV 6-OHDA injection, urinary MHPG excretion returned to baseline values and whole brain CA content was not reliably different from control. A single treatment with 6-OHDA microinjected into the substantia nigra (SN) (N = 12; 120-240 microgram/subject) produced chronic whole brain depletions of brain CA without depleting serotonin. Reductions in brain CA were associated with a specific set of motor behaviors, aphagia, and adipsia. SN 6-OHDA produced greater brain NE depletions than ICV 6-OHDA, but urinary MHPG output was not reduced. SN 6-OHDA treated subjects showed chronic changes in social behavior and were more sensitive to the operant response rate decreasing effects of alpha-methyl-para-tyrosine (AMPT) than control subjects. Subjects with the largest depletions of brain dopamine (DA) (greater than 90%) were hypokinetic, rigid, and had a distal limb tremor. These results show that SN but not ICV injection of 6-OHDA can deplete brain CA in the rhesus monkey. The most prominent behavioral changes were characterized by disturbances in motor function. Urinary MPHG output does not reflect depletions of brain NE in this species.

Animals↗

PubMed1992

Relationship between arterial and peripheral venous catecholamine plasma catecholamine concentrations during infusion of noradrenaline and adrenaline in healthy volunteers.

Noradrenaline and adrenaline were infused IV at 5 different rates (0.01-0.2 micrograms.kg.min-1) for 30 min to volunteers. The plasma catecholamine concentrations were determined by HPLC and electro-chemical detection. At the highest infusion rate, the arterial and venous plasma concentrations of noradrenaline increased from 1.18 to 44.1 nmol.l-1 and from 1.14 to 31.9 nmol.l-1, respectively, and of adrenaline from 0.29 to 23.9 nmol.l-1 and from 0.28 to 19.3 nmol.l-1, respectively. The peripheral venous plasma concentration of noradrenaline averaged 76% of the arterial concentration, and of adrenaline it was 73%. There was a linear relationship between the peripheral venous and arterial plasma noradrenaline and adrenaline concentrations at therapeutic doses.

Adult↗

PubMed1985

Long-term application of some catecholamines elevates levels of other catecholamines in rats.

Male Sprague-Dawley rats were treated during 20 h with subcutaneously implanted tablets (controlled release systems) containing either adrenaline (A), noradrenaline (NA), isoprenaline (ISO) or just placebos. Levels of the exogenously administered catecholamines (CA) in plasma and liver homogenate were significantly higher than in controls throughout the test time. During NA application endogeneous A and dopamine (DA) plasma values rose considerably, while ISO application enhanced endogenous NA and A levels. Adrenaline application increased NA and DA plasma levels. Several possibilities for this phenomenon are discussed, and it is concluded that previous papers dealing with observations of long term action of CA's should be reevaluated unless the influence of the artificially given CA on the elevation of endogenous CA's has been already taken into consideration.

Animals↗

PubMed1998

Circulating neuropeptide Y (NPY) and catecholamines in rat under resting and stress conditions. Arguments for extra-adrenal origin of NPY, adrenal and extra-adrenal sources of catecholamines.

Neuropeptide Y (NPY) is found in cell bodies of neurons in the brain and co-localized with noradrenaline (NA) in sympathetic nerves as well as with NA and adrenaline (A) in the adrenal chromaffin cells. The purpose of the present work is to determine whether NPY and catecholamines found in the plasma of the rat under resting and stress conditions (ether inhalation, restraint) arise from the adrenals or from extra-adrenal sites. We used adrenalectomized (adx) rats and sham-adx ones. Adrenalectomy increased plasma adrenocorticotrophic hormone (ACTH) levels but decreased drastically circulating corticosterone (B) and A (-97%). However, resting NA was slightly but not significantly decreased and NPY not affected. Ether inhalation (3 min) increased plasma levels of ACTH, B, NA and A in sham-adx rats, ACTH, NA and, weakly, A in adx ones. Restraint (30 min) increased B, NA and A in sham-adx rats, NA and, poorly, A, in adx ones. In contrast, plasma levels of NPY were not significantly affected by these stress conditions. The present data suggest that NA found in rat plasma at rest and during ether or restraint stress could arise from both adrenal medulla and noradrenergic nerve endings while A arises mainly from the adrenergic chromaffin cells of the adrenals. In contrast, NPY found in the circulation, at rest and under stress conditions, is not derived from the adrenals but emanates mainly from an extra-adrenal source.

Adrenal Glands↗

PubMed1978

Brain catecholamines and catecholamine-synthesizing enzymes in renovascular hypertension in the rat.

1. Noradrenaline content of several rat brain stem and hypothalamic nuclei falls transiently at 72 h after initiation of renovascular hypertension (one-kidney Goldblatt model). 2. Tyrosine hydroxylase activity is significantly reduced in posterior, paraventricular and periventricular nuclei of hypothalamus at this time but returns to control value by 7 days. 3. Treatment with hydrallazine, 5 mg/kg intraperitoneally, twice daily or methaoxamine, 5 mg/kg, three times daily for 3 days respectively raises and lowers the noradrenaline content of brain nuclei, suggesting that short-term changes in noradrenaline may be secondary to afferent baroreceptor input. 4. At later times after the development of renovascular hypertension (7 and 28 days) activity of phenylethanolamine-N-methyl transferase is increased in the nucleus of the solitary tract and the locus coeruleus. 5. Brain catecholamines may participate both early in the development and later in the maintenance of renovascular hypertension.

Animals↗

PubMed1981

Presence of conjugated catecholamines in rat brain: a new method of analysis of catecholamine sulfates.

A new method of measuring catecholamine (CA) sulfate permitted us to detect its presence in rat brain for the first time. The procedure consisted of separating the CA sulfate from the free CA by alumina adsorption followed by passage through Dowex, and measuring the CA sulfate by a radioenzymatic assay in the presence of a sulfatase. This method permitted demonstration of the presence of dopamine sulfate, and occasionally, of norepinephrine and epinephrine sulfate in the hypothalamus, striatum, and hippocampus of rat brain.

Animals↗

PubMed1991

Plasma catecholamine levels in SART-stressed rats and effects of drugs on stress-induced alteration in plasma and brain catecholamine levels.

1. Plasma catecholamine (CA) levels were examined in rats exposed to SART (specific alternation of rhythm in temperature) stress, a repeated cold stress. Effects of neurotropin, a sedative analgesic, and alprazolam, an anxiolytic, on the changes in plasma and brain CA levels were then studied. 2. SART stress induced remarkable increases in plasma levels of noradrenaline (NA) and dopamine (DA). The plasma adrenaline (Adr) level also increased significantly, but the extent was smaller than that of NA or DA. 3. Repeated treatments with neurotropin reduced the stress-induced increases in plasma and brain NA and DA levels significantly and dose-dependently. 4. Repeated treatments with alprazolam markedly reduced all increases in plasma and brain CA levels. 5. The above findings suggest that SART-stressed animals are in an increasing state of sympathetic neuronal activity and in a slightly increasing state of adrenal function. Neurotropin is also suggested to have modulating effects on autonomic imbalance in both catecholaminergic and cholinergic nerves.

Alprazolam↗

PubMed1974

Effect of selective destruction of central and peripheral catecholamine-containing neurones with 6-hydroxydopamine on catecholamine excretion in the rat.

1 The contribution of various tissues to some of the pools of catecholamine metabolites in urine has been estimated by measuring the excretion of these compounds by rats given DOPA-free diets and intravenous, intraventricular, or intracisternal 6-hydroxydopamine.2 Destruction of peripheral sympathetic neurones by repeated intravenous doses of 6-hydroxydopamine led to a 34% decrease in noradrenaline excretion, and a 38% decrease in 4-hydroxy-3-methoxyphenylglycol sulphate excretion. Depletion of brain noradrenaline (by 67%), after intracisternal 6-hydroxydopamine, was unassociated with changes in the excretion of noradrenaline or of 4-hydroxy-3-methoxyphenylglycol sulphate. This suggests that these compounds in rat urine are derived mainly from peripheral tissues.3 Depletion of brain dopamine (by 80%) by intraventricular 6-hydroxydopamine was associated with a 27% decrease in the excretion of homovanillic acid. Destruction of peripheral sympathetic neurones with intravenous 6-hydroxydopamine led to a 25% decrease in homovanillic acid excretion. The data suggest that the homovanillic acid in rat urine derives partially from brain dopamine and partially from dopamine released from or metabolized within sympathetic neurones.4 Neither depletion of brain dopamine, nor destruction of sympathetic neurones, caused alterations in the excretion of dopamine or dihydroxyphenylacetic acid.

Animals↗

PubMed1996

Catecholamine content and in vitro catecholamine synthesis in peripheral human lymphocytes.

We studied the catecholamine (CA) content in peripheral human lymphocytes and the ability of these cells to synthesize CA in vitro. CA were separated by high performance liquid chromatography (HPLC) and determined in the supernatant by electrochemical detection as well as being determined after ultrasonic cell disruption in mononuclear leukocytes, adherent cells (monocytes/macrophages), total lymphocytes, and B- and T-cell enriched fractions. T lymphocytes contained L-Dopa and norepinephrine (NE), whereas B lymphocytes contained only L-Dopa. Lymphocytes seem to be able to synthesize NE from both L-tyrosine and L-Dopa added to the incubation medium in concentrations similar to the peripheral venous plasma (i.e. 5 x 10(-5) m and 10(-8) m, respectively). The addition of D-Dopa did not increase intracellular NE. alpha-methyl-p-L-tyrosine, benserazide, disulfiram, and fusaric acid (which are inhibitors of the enzymatic pathway) all decreased the synthesis of NE. After the addition of [3H]-L-Dopa (10(-8) m and 10(-7) m) to the incubation medium, [3H]-NE and [3H]-dopamine appeared. By increasing the concentration of L-Dopa in the medium (< 10(-6) m), CA were detected in the supernatant as well. These data show that peripheral human T lymphocytes contain and are able to synthesize CA from normal precursors in physiologic concentrations, i.e. a CA synthetic pathway is shown in nonneural cells. These data seem to support the hypothesis of autocrine and paracrine loops in the regulation of lymphocyte activity in lymphocytes taken from human cerebrospinal fluid (as suggested by other authors).

Adult↗