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PubMed1988

Can plasma catecholamine levels be a useful index of sympathetic nervous system activity?

The hemodynamic responses of the sympathetic nervous system to the Valsalva maneuver were related to changes in circulating levels of catecholamines, aldosterone and plasma renin activity. Fourteen healthy normotensives (aged 27 +/- 8 years) took part. A catheter was inserted in the forearm then the subject was rested quietly (supine) for 30 mins. The Valsalva maneuver was performed (duration 40 s, intrathoracic pressure 40 mmHg) with continuous recording of supine heart rate. Blood was sampled before the maneuver (basal state) and at the bradycardic post maneuver phase for measurement of plasma noradrenaline, adrenaline, renin activity and aldosterone. In six subjects the procedure was repeated for durations of 10, 20, 30 and 40 s with a 30-min rest between each maneuver. Plasma catecholamines increased consistently (P less than 0.001) from pre- to post bradycardic phases of the maneuver. No changes in plasma renin activity or aldosterone were observed. The maximum tachycardia observed during each maneuver and the increments in catecholamine concentrations were each linearly related to the duration of straining but there was no overall correlation between the tachycardia and catecholamine concentrations. In conclusion under controlled conditions, plasma catecholamine concentrations can be useful indices of the stimulation of the sympathetic nervous system; the Valsalva maneuver does not appear to affect significantly the peripheral renin-angiotensin system; and the heart rate response to the Valsalva maneuver does not appear to be mediated solely by the sympathetic nervous system.

Adult↗
PubMed1988

Results for 74 substances tested for interference with determination of plasma catecholamines by "high-performance" liquid chromatography with electrochemical detection.

Various catecholamine metabolites, catecholamine-related compounds, catechols, drugs, amines, and other nitrogen compounds were injected onto an HPLC system ("ClinRep Catecholamine-Plasma" assay kit with a reversed-phase C18 column) used for measuring catecholamines. None of the 74 substances tested co-eluted with any of the catecholamines--norepinephrine, epinephrine, or dopamine--or with the internal standard, 3,4-dihydroxybenzylamine.

Catecholamines↗
PubMedDate not supplied

Effects of muscarinic pharmacophores on the cholinergic regulation of catecholamine secretion from perfused adrenal glands.

The effects of the muscarinic antagonists, atropine, aprophen, azaprophen and pirenzepine, on catecholamine secretion stimulated by acetylcholine (ACh) and nicotine were studied using perfused and isolated guinea-pig adrenal glands. Sequential 2-min infusions of ACh (10(-5)M) at 15-min intervals evoked repetitive catecholamine secretory responses for at least 1 hr. This dose of ACh produced a predominantly muscarinic receptor-mediated catecholamine secretory response, which was inhibited by all muscarinic antagonists used. The order of potency was atropine greater than azaprophen greater than pirenzepine greater than aprophen, with IC50 values of 1.0 x 10(-9), 3.8 x 10(-9), 7.0 x 10(-8) and 1.3 x 10(-6) M, respectively. In comparison, repeated 1-min infusions of nicotine (2 x 10(-5) M) at 15-min intervals evoked progressively smaller catecholamine secretory responses over the course of 1 hr. At higher doses, atropine, azaprophen and aprophen also inhibited the nicotine-induced catecholamine secretion. In contrast, pirenzepine had no effect on the nicotinic response. The IC50 values for atropine, azaprophen and aprophen were 2.7 x 10(-6), 1.5 x 10(-6), and 3.2 x 10(-6) M, respectively. Because the antinicotinic effect of atropine and azaprophen was achieved at concentrations 2 to 3 orders of magnitude higher than those needed for the antimuscarinic effect, it was most likely not pharmacologically significant, but rather due to nonspecific inhibition of the nicotinic receptor.

Adrenal Glands↗
PubMed1987

Effect of antidepressant on behavior and central catecholamine of depression-model rats.

Effect of antidepressant on behavior and central catecholamine were investigated in depression-model rats produced by long-term forced running stress. Changes in the spontaneous running activity and the concentration and turnover of catecholamine were examined in non-stressed rats injected with saline and depression-model rats injected with saline, imipramine and MOD-20 (a candidate for a tetracyclic antidepressant). Running activity was significantly restored by injection of imipramine and MOD-20. In depression-model rats, the concentrations of central catecholamine increased in the cell bodies and nerve terminals of the ascending noradrenaline system, and turnover rates of the catecholamine decreased in the terminal region. The increased concentrations were returned to the non-stressed level after injection of the drugs. However, decreased turnover rates were not recovered after the injection. These results suggested that MOD-20 was a potent antidepressant and the therapeutic efficacy of antidepressants might be due to the restoration of catecholamine concentrations.

Animals↗
PubMed1987

[Participation of catecholamines in the mechanism of heart damage during the alcohol withdrawal syndrome in rats].

Withdrawal syndrome in rats was induced after ethanol administration in a dose of 4-5 g/kg b. w. twice daily for 5 consecutive days. Creatine phosphokinase and lactate dehydrogenase release from the isolated heart and catecholamine distribution in the heart have been investigated in rats suffering from alcohol withdrawal syndrome. Maximum rate of enzyme release was observed on the third day of withdrawal. The density of catecholamine neurons in intact hearts and the hearts of rats sacrificed 2-6 hours, 1, 3, and 7 days after the last ethanol administration was 86, 64, 28, 7 and 38%, respectively. The area of extraneuronal catecholamine distribution accounted for 2, 19, 46, 82 and 4%. Synchronous changes observed in catecholamine distribution and the rate of enzyme release suggest that catecholamines act as a trigger of heart damage in rats with alcohol withdrawal syndrome.

Animals↗
PubMed1979

Use of catecholamines in acute myocardial infarction.

We review the hemodynamic effects and clinical usefulness of five natural and synthetic catecholamines. Their actions are best understood by an appreciation of the relative ability of each catecholamine to activate alpha, beta 1 and beta 2 adrenergic receptors in the myocardium and peripheral vasculature. Epinephrine, the first catecholamine isolated, is shown to have little useful role in the therapy of acute myocardial infarction. L-norepinephrine has powerful alpha and moderate beta 1 effects. It is the catecholamine of choice in the initial treatment of cardiogenic shock associated with acute myocardial infarction. Isproterenol markedly increases myocardial contractility and heart rate by beta 1 stimulation, while simultaneously decreasing peripheral vascular resistance and, therefore, arterial pressure through its action on beta 2 receptors. It increases cardiac output, but its metabolic costs are high in the presence of ischemia. Its role in the therapy of acute myocardial infarction has largely been supplanted by more selective agents. Dopamine causes slightly less vasoconstriction than l-norepinephrine and slightly less myocardial stimulation than isoproterenol. In low doses, it increases renal and mesenteric blood flow by activation of a non-adrenergic receptor. Tachycardia and associated metabolic deterioration render it a second-line drug in the treatment of severe cardiogenic shock. Dobutamine, a new synthetic catecholamine, has primarily beta 1 activity. It increases myocardial contractility with little effect on heart rate or peripheral vascular resistance. It is ineffective in cardiogenic shock, but may eventually be shown to have a role in the treatment of left ventricular failure uncomplicated by severe hypotension.

Animals↗
PubMed1979

Protonmotive force and catecholamine transport in isolated chromaffin granules.

The effect of the transmembrane potential (delta psi) and the proton concentration gradient (delta pH) across the chromaffin granule membrane upon the rate and extent of catecholamine accumulation was studied in isolated bovine chromaffin granules. Freshly isolated chromaffin granules had an intragranular pH of 5.5 as measured by [14C]methylamine distribution. The addition of ATP to a suspension of granules resulted in the generation of a membrane potential, positive inside, as measured by [14C]thiocyanate (SCN-) distribution. The addition of carboxyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP), a proton translocator, resulted in a reversal of the potential to negative values (measured by [3H]tetramethylphenylphosphonium (TPMP+)) approaching -90 mV. Changing the external pH of a granular suspension incubated with FCCP produced a linear perturbation in the measured potential from positive to negative values, which can be explained by the distribution of protons according to their electrochemical gradient. When ammonia (1 to 50 mM) was added to highly buffered suspensions of chromaffin granules there was a dose-dependent decrease in the transmembrane proton gradient (delta pH) and an increase in the membrane potential (delta psi). On the other hand, thiocyanate or FCCP, at varying concentration, produced a dose-related collapse of the membrane potential and had no effect upon the transmembrane proton gradient. The addition of larger concentrations of catecholamines caused a decrease in the transmembrane proton gradient and an increase in the membrane potential. Time-resolved influx of catecholamines into the granules was studied radiochemically using low external catecholamine concentrations. The accumulation of epinephrine or norepinephrine was over one order of magnitude greater in the presence of ATP than in its absence. The rate and extent of amine accumulation was found to be related to the magnitude of the membrane potential at fixed transmembrane proton concentration (delta pH) values. Likewise, the accumulation was related to the magnitude of the delta pH at fixed membrane potential values. These results suggest that the existence of both a transmembrane proton gradient and a membrane potential are required for optimal catecholamine accumulation to occur.

Adrenal Glands↗
PubMed1979

Effects of muscle relaxants on catecholamine release from adrenal medulla.

Bovine adrenals were perfused with secretagogues in the presence or absence of muscle relaxants. On a molar basis, Dially-nor-toxiferine was as potent as tubocurarine in inhibiting the catecholamine release induced by carbachol; pancuronium was about 100 times less potent than tubocurarine, whereas gallamine and succinylcholine produced no inhibition whatsoever. KCl-induced catechoamine release was not affected by any of these compounds. Nicotine-induced catecholamine release was inhibitedby diallyl-nor-toxiferine, tubocurarine and pancuronium, but not by gallamine or succinylcholine. Muscarine failed to stimulate the adrenal medulla to release catecholamines. The results show that the inhibition of catecholamine release is based on the specific block of the nicotinic receptor, whereas gallamine and succinylcholine possess no blocking action, and that diallyl-nor-toxiferine and tubocurarine might affect clinical symptoms under conditions in which catecholamine release from the adrenal is increased by a compensatory mechanism.

Adrenal Medulla↗
PubMed1984

Effect of erythrosin B on hyperpolarizing responses to catecholamines in amphibian sympathetic ganglia.

The food dye erythrosin B has been reported to inhibit the neuronal uptake of catecholamines. To test this hypothesis we examined the effect of the dye on the responses of neurons in amphibian sympathetic ganglia to both dopamine and epinephrine. Although the hyperpolarizations induced by both catecholamines were potentiated by the conventional uptake blocker, desipramine (0.5 microM), low doses of erythrosin B (1-10 microM) produced an irreversible blockade. It was therefore not possible to evaluate the hypothesis that the dye might block catecholamine uptake. Xanthine dyes such as erythrosin B have also been reported to inhibit Na-K-adenosine triphosphatase. In agreement with this possibility we found that erythrosin B promoted irreversible inhibition of the (nicotinic) acetylcholine after-hyperpolarization. This response is generated by the electrogenic activity of the Na+ pump. Neither this Na+ pump inhibition nor erythrosin-induced membrane hyperpolarization appeared to account for the effect of the dye on catecholamine responses. The irreversible antagonism of epinephrine and dopamine by erythrosin was specific in that hyperpolarizing responses to muscarinic antagonists such as methacholine were relatively insensitive to the dye. It is therefore concluded that erythrosin B selectively antagonizes responses to catecholamines in amphibian sympathetic ganglia. No information as to the exact molecular mechanism of this antagonism is available from the present experiments.

Animals↗
PubMed1981

Comparison of the receptors mediating the catecholamine hyperpolarization and slow inhibitory postsynaptic potential in sympathetic ganglia.

We investigated the proposed catecholamine receptor in the superior cervical ganglion of the rabbit with the sucrose-gap technique to characterize the receptor pharmacologically. It has been suggested that this receptor is involved in the slow inhibitory postsynaptic potential in sympathetic ganglia. Epinephrine, norepinephrine and dopamine consistently hyperpolarized the ganglion membrane (N = 60). The order of potency was epinephrine greater than or equal to norepinephrine much greater than dopamine. Clonidine (10(-5) M), phenylephrine (10(-4) M) and isoproterenol (10(-3) M) also hyperpolarized the ganglion. However, apomorphine, even at millimolar concentration, did not hyperpolarize the membrane. The alpha antagonists phentolamine (10(-6) M) and yohimbine (10(-6) M) depressed the response to all catecholamines and shifted the catecholamine concentration-response curve to the right; dopamine and beta antagonists and the alpha-1 antagonist prazosin had no effect on the catecholamine hyperpolarizations. In contrast, the nerve-evoked slow inhibitory postsynaptic potential was selectively depressed only by atropine (10(-7) M). In conclusion, we characterized an alpha-2 adrenergic receptor in the rabbit superior cervical ganglion responsible for the catecholamine hyperpolarization and found that the slow inhibitory postsynaptic potential does not appear to be mediated by the same receptor.

Adrenergic alpha-Antagonists↗
PubMed1983

Modulatory interactions between enkephalin and catecholamines: anatomical and physiological substrates.

The anatomical and electrophysiological basis of enkephalin-catecholamine interactions was studied in the central nervous system of the Sprague-Dawley rat. Sections of fetal rat brain were treated alternatively with antibodies raised against enkephalin or tyrosine hydroxylase (EC 1.14.16.2). Enkephalinergic fibers were found to innervate almost all brain areas known to contain catecholamine cell bodies or terminal fields. The possible electrophysiological correlates of such an overlap in enkephalin and catecholamine terminal fields was investigated in frontal neocortex. Parenteral administration of antipsychotic agents known to block catecholamine receptors, such as spiroperidol, alpha-flupenthixol, and (+)-butaclamol, reversibly antagonized enkephalin-induced depressions of neuronal activity. The biochemically inactive isomers of these antipsychotics, beta-flupenthixol and (-)-butaclamol, manifested no such activity. Unilateral lesions of the catecholaminergic projections to frontal cortex produced by interstitial injection of 6-hydroxydopamine resulted in an ipsilateral decrease in enkephalin efficacy and in an elimination of the antagonisms of enkephalin depressions by antipsychotic agents. It is hypothesized that catecholamines may act as modulators to augment responsiveness to peptides such as enkephalins.

Animals↗
PubMed1983

[Experimental studies on the effects of administration of catecholamines on fat metabolism].

Metabolism of fat was studied in Sprague-Dowley rats receiving catecholamines as an experimental model of "stressed condition". These rats were fed with intravenous hyperalimentation with glucose only (G-group) or glucose and fat (F-group). Changes in body weight, cumulative nitrogen balance, blood sugar, serum IRI, free fatty acid, and triglyceride content of the liver were determined before and after five days intravenous hyperalimentation. Animals receiving intravenous hyperalimentation but no catecholamines were also subjected to the studies as control group. The following results were obtained from the present studies: In control group, G-group gained much more body weight and spared much more nitrogen than F-group. In catecholamine receiving groups, there was no significant difference of changes in body weight and cumulative nitrogen balance between G-group and F-group. In catecholamine receiving group, triglyceride content of the liver tissue was higher in G-group than in F-group, whereas triglyceride content of the liver tissue in control group was lower in G-group than in F-group. There was a positive correlation between the accumulation of triglyceride in the liver tissue and blood sugar level, or serum IRI level. A negative correlation was found between the accumulation of triglyceride in the liver tissue and plasma free fatty acid level. These results suggest that "stressed condition" induced by the administration of catecholamines enhanced the utilization of fat as an energy source without producing fatty liver.

Animals↗
PubMed1984

Effect of oestradiol on catecholamine-stimulated lipolysis.

The authors studied the effect of a single in vivo dose of oestradiol (OE) on adrenergic lipolysis in the epididymal adipose tissue of adult and juvenile male rats, and the effect of OE on plasma free fatty acids (FFA), cholesterol and beta-lipoprotein levels at various intervals after its administration. It was found that OE injected 24 h beforehand in vivo (s.c.), in doses of 100 and 200 micrograms X kg-1 body weight, significantly potentiated the lipid-mobilizing action of the catecholamines noradrenaline (NOR) and isoprenaline (ISO) in adult rats (the action of ISO was potentiated more intensively); in addition, the adipose tissue became more sensitive to the action of NOR, but not of ISO. Raising the dose of OE to 400 micrograms X kg-1 did not enhance the potentiation of the lipolytic action of the catecholamines any further; on the contrary, the lipid mobilizing effect of the catecholamines was potentiated less than after half this dose. Following the s.c. injection of an oily OE solution, the lipolytic effect was potentiated after more than 7 h; the potentiation was strongest after 12 h, but only as far as the maximum attainable degree of lipolysis was concerned. Potentiation of adrenergic lipolysis was found only in adult male rats. In male rats weighing 130-150 g the lipolytic effect of catecholamines (in mumol/g adipose tissue) was significantly greater than in adult animals and the pre-administration of OE did not potentiate adrenergic lipolysis any further. Determination of plasma FFA, cholesterol and beta-lipoprotein levels 1, 2, 4 and 6 hours after the s.c. injection of OE showed only nonsignificant changes (an increase in FFA and a decrease in cholesterol). The authors consider it important to distinguish between the effect of OE on catecholamine-stimulated lipolysis in depot adipose tissue and its effect on lipid metabolism. In their opinion, the dose-dependent effect of OE on muscular and metabolic adrenergic reactions could be one of the factors co-reversible for certain side reactions to steroid contraceptives.

Adipose Tissue↗
PubMed1983

Mechanism of plasma catecholamine increases during coronary artery bypass and valve procedures.

Nineteen patients undergoing coronary revascularization (14 patients) or valve replacement (five patients) were studied to monitor the catecholamine levels following operation and for each of three consecutive postoperative days. A significant (p less than 0.01) elevation was observed in both the serum norepinephrine and epinephrine levels immediately following operation, with both responding in a similar fashion (r = 0.804, p = 0.016). While epinephrine returned to control levels within 3 days of operation, the norepinephrine levels remained above control. The elevation in catecholamines associated with cardiac operation is presumed to be secondary to (1) the stress of surgical trauma and (2) the influence of cardiopulmonary bypass, with its attendant hypothermia and hemodynamic alterations. A comparative analysis was performed of (1) the type of operation, (2) the sex of the patient, (3) the presence of postoperative arrhythmia, (4) the history of receiving propranolol, (5) the duration of cardiopulmonary bypass, (6) the duration of operation, and (7) the volume of fluid gradient absorbed during operation. None of these parameters except the sex of the patient was significantly related to the change in either norepinephrine or epinephrine associated with the operation. There was a significantly (p less than 0.05) higher epinephrine level at day 2 and 3 following operation in women than in men. None of the 19 patients had postoperative complications except for arrhythmias, which developed in nine patients and were not associated with the catecholamine responses. It is concluded that peak catecholamine stimulation does not reflect the ease of postoperative recovery. The duration of bypass and operation were also not directly related to the level of stimulation. It is apparent that there are multiple factors which combine to influence catecholamine secretion during cardiopulmonary bypass.

Adult↗
PubMed1984

Free and conjugated plasma catecholamines in patients with congestive heart failure.

Conjugation is an important mechanism in the deactivation process of circulating catecholamines, because most of the circulating catecholamines are found in the conjugated rather than the free form. To determine whether a defect in conjugation might account for some of the elevated free plasma norepinephrine in patients with CHF, we measured free and conjugated circulating catecholamines in 12 patients with chronic CHF. These measurements were also obtained in eight age-matched control subjects without clinical heart disease. The data demonstrate that the free plasma norepinephrine in patients with heart failure (566 +/- 227 (SD) pg/ml) is significantly greater than the free plasma norepinephrine in normal age-matched control subjects (337 +/- 148 pg/ml, p less than 0.05). The amount of free circulating epinephrine in the patients with heart failure (51 +/- 25 pg/ml) is similar to that in the control population (46 +/- 50 pg/ml), whereas the free circulating dopamine content is greater in the heart failure population (36 +/- 21 pg/ml) compared with normal (17 +/- 15 pg/ml, p less than 0.05). Although the absolute conjugated catecholamines are also increased in patients with heart failure, the percent conjugation of norepinephrine in heart failure (73%) did not vary from control values (71%). The percent conjugation of epinephrine in the group with heart failure (81%) was similar to that in the control group (76%), as was the percent conjugation of dopamine in the two groups (99%). Therefore, it is unlikely that a defect in conjugation of catecholamines is contributing to the excessive free plasma norepinephrine found in patients with congestive heart failure.

Adult↗
PubMed1984

Increased catecholamine levels in cord venous plasma of distressed fetuses.

The concentrations of catecholamines in cord venous plasma were measured by trihydroxyindole fluorimetric assay in four fetuses with normal fetal heart rate (FHR) and three distressed fetuses with late deceleration of pathologic FHR. The concentrations (nmol/l) of norepinephrine and epinephrine in normal fetuses were 40.3 +/- 7.9 (mean +/- SD) and 5.4 +/- 1.5, respectively, whereas those in distressed fetuses were 156.8 +/- 48.0 and 12.1 +/- 4.5, respectively. In normal fetuses about 88% of total catecholamines consisted of norepinephrine, the remaining 12%, epinephrine. The ratio of norepinephrine to epinephrine in distressed fetuses (12.9) was thus higher than the ratio in normal fetuses (7.5). Higher levels of total catecholamine concentrations were associated with the presence of late deceleration of pathologic FHR pattern, low one-minute Apgar score, low umbilical arterial pH value (pH less than 7.20), and fetal hypertriglyceridemia (greater than 48 mg/100 ml). The relationship between fetal hypertriglyceridemia and elevated concentration of cord plasma total catecholamines is elucidated and the physiologic significance of increased secretion of catecholamines in distressed fetuses is discussed.

Apgar Score↗
PubMed1978

Inhibition by trichlormethiazide of catecholamine release from perfused bovine adrenals.

Effect of thiazides on catecholamine release was examined using perfused bovine adrenal glands in vitro. Thiazides, such as trichlormethiazide and methyclothiazide inhibited catecholamine release evoked by carbamylcholine although they did not inhibit catecholamine release evoked by excess potassium. Thus it seems that these drugs inhibit catecholamine release release by an anticholinergic mechanism. Such inhibitory effect of thiazide on catecholamine release may be involved in the antihypertensive effect of these drugs.

Adrenal Glands↗
PubMed1982

Distribution of catecholamine and indoleamine neurons in the brain of the common marmoset (Callithrix jacchus).

The distribution of monoamine neurons in the brains of ten common marmosets (Callithrix jacchus) was examined by means of the Falck-Hillarp formaldehyde histofluorescence technique. Large populations of catecholamine and indoleamine neurons were found throughout the brain stem. Catecholamine cell bodies corresponded essentially to th noradrenaline and dopamine groups defined as A1-A7 and A8-A14, respectively. In contrast to Old World primate species, however, the noradrenaline cell populations (particularly the pontine coeruleal A6 group) were less numerous. Ascending catecholamine fibre pathways were not observed within the medulla or pons, although numerous axons were found near the mesodiencephalic border. These were fine and smooth in appearance in contrast to those of other species and this finding may represent a significant morphological difference. The catecholamine terminal innervation of the diencephalon was modest in the marmoset and was less dense than in other primates. In contrast, limbic areas and the striatum contained very large numbers of terminals. Indoleamine cell bodies, equivalent to the serotonin groups defined as B1-B9, were also observed. The most rostral cell populations (B7-9) were large. In addition, pontine and medullary indoleamine neurons extended laterally through the tegmentum as noted in other primates, such that they often adjacent to catecholamine neurons. A prominent bundle of indoleamine axons was observed in the mesencephalon and corresponded to a fibre pathway seen in rodents and other primates. No terminal varicosities were noted.

Amines↗