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PubMed1980

Role of catecholamines in the genesis of arrhythmias.

Catecholamines play a major role in the induction of cardiac rhythm disorders. The effects of catecholamines are caused by activation of beta-receptors in the heart and appear to be mediated by the cyclic AMP/protein kinase system. Increased rate of spontaneous diastolic depolarization of cardiac fibers on exposure to endogenous or exogenous catecholamine activity leads to tachyarrhythmias. Because of non-uniform distribution of sympathetic nerve endings, activation of the sympathetic nerve system may result in non-uniform reduction in the refractory period leading to re-entrant excitation. Under abnormal conditions myocardium may become more sensitive to catecholamines. In ischemia, sympathetic stimulation causes more local differences in refractory period and a greater tendency to fibrillate. Following acute coronary ligation there is a direct relationship between rhythm disturbance and levels of myocardial catecholamines. Catecholamines not only cause arrhythmia but also contribute to the development of digitalis-induced arrhythmias. The role of catecholamines in the genesis of certain cardiac arrhythmias is further supported by the fact that beta-blocking drugs which antagonize sympathetic activity are effective for treating various types of acute arrhythmias and for prevention of recurrent arrhythmias.

Arrhythmias, Cardiac↗
PubMed1984

Problems in the development of radioimmunoassay of catecholamines.

This review describes experiments to produce antibodies towards the catecholamines and some catecholamine metabolites with the intention of developing radioimmunological methods. First, attempts to produce antibodies to the catecholamines themselves are described. In the course of synthesis of immunogens of catecholamines, it was necessary to exercise special care - e.g. the introduction of protecting groups - owing to the great susceptibility of the catechol structure to oxidation. Despite many efforts, only one working group (Miwa et al.) has reported in a series of papers the successful production of antibodies to catecholamines, but they did not develop a radioimmunoassay. In contrast, antibodies to some metabolites of the catecholamines - such as 3,4-dimethoxyphenylethylamine, the 3-O-methylated catecholamines (normetanephrine, metaneprine, and 3-methoxytyramine) as well as 3-methoxy-4-hydroxyphenylethyleneglycol - have been produced, whose avidity and specificity were high enough to permit the development of sensitive radioimmunoassays.

Antibody Specificity↗
PubMed1983

Ascorbic acid and catecholamine secretion from cultured chromaffin cells.

Ascorbic acid was found to be secreted from cultured bovine adrenal chromaffin cells coincidentally with catecholamines using a variety of secretagogues, including veratridine, nicotine, acetylcholine, and potassium chloride. Secretion of ascorbic acid was measured by preloading the cells for 3 h with (R)-[14C]ascorbic acid and then quantitating release of the label. The newly transported ascorbic acid constituted nearly 90% of total cellular ascorbic acid. Although chromaffin granules are known to contain endogenous ascorbic acid, only 16% of the total labeled ascorbic acid taken up by cultured cells was localized to the chromaffin granule fraction. Under the same isolation conditions, 95% of the endogenous catecholamines was found in the granule fraction. The secretion of both (R)-[14C] ascorbic acid and catecholamines was calcium dependent. However, only catecholamine secretion was effectively inhibited by the presence in the medium of isethionate, an impermeant ion that inhibits catecholamine secretion from isolated chromaffin granules. Analysis of the ratios of cellular and granular (R)-[14C] ascorbate as well as secreted (R)-[14C]ascorbate and catecholamines revealed that the secreted (R)-[14C]ascorbic acid did not come exclusively from the chromaffin granule fraction but also from a nonsedimenting cytoplasmic compartment. Indeed, for all four agonists, the amounts of (R)-[14C]ascorbic acid secreted were more than 1.5 times greater than could be accounted for by chromaffin granule ascorbate alone. We took these data to indicate that, while ascorbic acid and catecholamines were secreted concomitantly, the sources of the secreted substances were not necessarily identical.

Acetylcholine↗
PubMed1981

[Reduction of catecholamine liberation by drugs. Therapeutic alternative to beta sympathicolysis in coronary disease?].

Plasma catecholamines have been determined in 10 persons with healthy coronary circulation (group A) and in 10 patients with coronary cardiac illness (group B) before and immediately after ergometer loading. The loading dosis amounted on average to 177.5 watts for group A and 80 watts for group B. Under load, the catecholamines rose significantly for group A (p less than 0.01) and highly significantly for group B (p less than 0.001). After 10 days of therapy with a combination preparation (12 mg of diphenhydramine hydrochloride, 100 mg of meprobamate, 5 mg of nicotinic acid = Visano-mini), the catecholamines were again determined for groups A and B before and after loading. The catecholamines were not significantly changed by therapy, neither for group A nor B. Under the therapy, the rise in catecholamines caused by load was distinctly lower than before without therapy, namely significantly lowered for group A (p less than 0.01) and slightly significantly for group B (p less than 0.02). Also significantly lowered under therapy in terms of percentage was the catecholamine rise caused by the load, namely by 27% against 75% for group A, by 35% against 89% for group B. As the first results show, Visano-mini seems to constitute an interesting catecholamine inhibiting combination of substances. Whether this might possibly lead to a therapeutic alternative to the betasympathicolysis will have to be determined on the basis of further investigations.

Adult↗
PubMed1995

Effect of haemorrhagic shock and intraosseous resuscitation on plasma and urine catecholamine concentrations and urinary clearance in pigs.

OBJECTIVE: To evaluate the plasma and urinary catecholamine concentrations after episodes of haemorrhagic shock treated by intraosseous infusion of a small volume of hyperosmotic fluid, followed by whole blood, in a standard porcine model. DESIGN: Randomised open study. SETTING: University hospital, Norway. MATERIAL: 18 piglets. INTERVENTIONS: All animals were bled to an arterial systolic pressure of 60 mm Hg. After 30 minutes 100 ml hyperosmotic (2.4 mol/l) fluid (glucose/sodium chloride) was given either intraosseously (n = 6) or intravenously (n = 6). Ninety minutes later the animals were again bled to a systolic pressure of 60 mm Hg, and after 30 minutes an autologous whole blood transfusion was given by either intraosseous or intravenous infusion. Six animals acted as untreated controls. MAIN OUTCOME MEASURES: Changes in haemodynamic variables and plasma and urinary catecholamine concentrations. RESULTS: Two pigs in the control group died. The hyperosmotic infusion improved the circulatory performance significantly (p < 0.05). Thirty minutes after both bleeds the plasma catecholamine concentrations were increased by 10-15 times, but returned to the reference range in all groups 90 minutes after the hyperosmotic infusion. Two hours after the whole blood infusion the catecholamine concentrations of the treated animals were at baseline values, significantly lower than those of the controls. The corresponding urinary catecholamine concentrations of the controls were significantly increased. There were no differences between the two treatment groups. CONCLUSION: The catecholamine measurements indicate that there may possibly be protective renal excretion of excess shock-induced plasma catecholamines after acute haemorrhage.

Animals↗
PubMedDate not supplied

[Catecholamines, myofibrillary degeneration of the heart muscle and cardiac troponin T in various types of agony].

The stress of agony (the death struggle) induces a rise in serum catecholamines. High doses of catecholamines cause myofibrillar degeneration (MFD), a form of cardiac injury. Severely damaged cardiac myocytes release troponin T (TnT), a myofibrillar cardiac protein, into the circulation. We studied serum catecholamine levels, MFD and TnT in 119 medico-legal autopsy cases. Catecholamine levels increased with the duration of agony: In the instantaneous death cases, the levels were similar to levels in humans at rest, whereas the levels in prolonged agony were comparable to concentrations found in humans in acute maximal stress. Still, it was not possible to infer the duration of agony from the catecholamine level in an individual case. The exceptionally high dopamine levels found in the group 'resuscitation and/or intensive care before death 'were most likely caused by antemortal treatment with dopamine. Slight MFD was diagnosed in nearly all hearts; its severity was neither related to catecholamine levels nor to duration of agony. TnT, not found in blood of healthy people, was present in nearly all postmortem samples, indicating autolytic effects. Heart blood contained more TnT than femoral blood. We could not detect a relationship between the serum cardiac troponin T level and MFD; but cardiac deaths had significantly higher levels of TnT in heart blood than deaths from other causes. The postulated interrelation between catecholamines, MFD and TnT was not evident from the results.

Biomarkers↗
PubMed1977

[Effect of glucocorticolids on catecholamine synthesis in the heart and adrenals of rats in the presence of physical fatigue].

The influence of the adrenal cortex hormones on the catecholamine synthesis in the adrenal glands and the heart of rats following prolonged swimming (8 hours) was studied. Catecholamine synthesis after the incubation of the adrenal glands and heart in the presence of L-tyrosine was sharply inhibited after swimming. Addition of hydrocortisone or prednisolone in vitro (50 microgram per sample) and also administration of these hormones in vivo (50 mg/kg intramuscularly, 3 hours before decapitation) increased catecholamine synthesis in the adrenal glands of swimming, but not of intact rats. After the incubation of the adrenal glands of swimming rats in the presence of L-DOPA and L-noradrenaline, catecholamine synthesis was depressed in comparison with intact animals, and it failed to be restored on addition of glucocorticoids. No stimulating effect of aldosterone on catecholamine synthesis in the adrenal glands in the presence of L-tyrosine was revealed. Catecholamine synthesis was inhibited and not restored under the effect of glucocorticoids in vitro and in vivo after the incubation of the heart tissue of swimming rats in the presence of L-tyrosine and L-DOPA. A conclusion was drawn that glucocorticoid promoted restoration of catecholamine synthesis inhibiteds in case of strong physical fatique at the stage of tyrosin-hydroxylase.

Adrenal Glands↗
PubMed1976

[Catecholamine metabolism. Physiopathology and pathobiochemistry].

UNLABELLED: Metabolic studies on isolated rat organs showed that vanillyl mandelic acid (VMA) is dehydrogenated by liver homogenate and suspension of pseudomonas fluorescens. In the 100000 g supernatant fraction of homogenated rat kidneys enzymatic activity was sufficient for kinetic studies and the examination of substrate specificity, pH dependence and changes with age and sex of rats. Norepinephrine secretion and resorption may be influenced by antiarrhythmic drugs in vivo: after lidocaine, there was no change of the tyramine dependend norepinephrine depletion of rat hearts, Verapamil inhibited the uptake of norepinephrine by rat hearts. Immobilisation of the animals led to a significant decrease in the myocardial levels for norepinephrine and epinephrine, which was antagonised by recreation of 24 hours. Adumbran prevented the catecholamine depletion, so that the influence of the limbic system may be important for the mediation of sympathetic stimuli. CLINICAL STUDIES: Emotional stress was shown to lead to an elevated plasma level of norepinephrine, cortisole and free fatty acids. In patients undergoing surgery, the application of Valium and Fortral inhibited these stress reactions. After physical stress, which did not lead to significant changes of the catecholamine level in plasma of healthy volunteers, there was an elevated norepinephrine plasma level in patients with cardiac failure, which could be prevented by different antiarrhythmic drugs. The excretion of norepinephrine and VMA of these patients was also increased. It was shown, that sinus rate rose according to norepinephrine levels in plasma in this group, which was contrary to the behaviour of healthy volunteers, showing neither a norepinephrine overflow nor increased heart rate. In patients with atrial fibrillation, AV-conduction also increased with elevated norepinephrine levels in plasma. There was, however, no direct correlation. Determination of the cardiac AV-difference of plasma-norepinephrine levels showed a cardiac catecholamine overflow, which could be inhibited by specific and nonspecific antiarrhythmic drugs (Verapamil, Practolol). In studies of catecholamine and glucocorticoid metabolism, no significant difference of catecholamine and VMA could be determined in patients with normal blood pressure and arterial hypertension. There was, however, a tendency to increased values in patients of the last group. In postural hypotension, plasma levels and urinary excretion of catecholamines were decreased and showed no variation after physical stress in orthostasis and after nicotine. In patients with tumors of the adrenal cortex and medulla, a close relation of the disturbance in catecholamine and corticoid metabolism was revealed.

Animals↗
PubMed1991

Distribution of catecholamine uptake sites in human brain as determined by quantitative [3H] mazindol autoradiography.

Because of the importance of the catecholamine system in Parkinson's disease and its relevance to a variety of clinical movement disorders, catecholamine uptake sites were mapped in the human brain using [3H] mazindol autoradiography. Displacement studies with known dopamine (DA) and noradrenaline (NA) uptake blockers showed that binding in the striatum was to dopamine uptake sites; binding in the locus coeruleus was to noradrenergic uptake sites. By using the selective noradrenergic uptake blocker desmethylimipramine (DMI), a comprehensive map of both DA and NA uptake sites was generated. In general, catecholamine uptake sites were better seen in terminals than in cells of origin or axonal projections. In some areas, such as the locus coeruleus, punctate binding could be seen over individual pigmented cells. A variegated pattern of binding was seen in caudate nucleus and putamen and some correspondence of patches of low binding with striosomes was observed in the caudate. The highest levels of binding to DA uptake sites was observed in the striatum, where regional differences in binding occurred. The most dense binding was seen in the ventral striatum, and a rostral-to-caudal decrement in binding levels in caudate nucleus and putamen was evident. Binding was more intense in the putamen compared to the caudate and within the caudate lower values were seen laterally. The highest levels of binding to noradrenergic uptake sites were in the locus coeruleus and dorsal raphé, although these sites may be on terminals from other projections. Whereas uptake sites were more often evident in known catecholamine pathways, [3H] mazindol binding was seen in some areas where catecholamine neurons or terminals had not been identified previously. These maps of the catecholamine uptake system add further information concerning the nature of the distribution of catecholamines in human brain and provide an important baseline for the study of disease and ageing processes.

Aged↗
PubMed1987

Effects of catecholamines on early development of the chick embryo: relationship to effects of calcium and cAMP.

Catecholamines (dopamine or norepinephrine) injected under the blastoderm of the unincubated chick embryo produced a thickened primitive streak and prevented the migration of axial mesoblast after 24 h. The mesoblastic cells that accumulated in the primitive streak contained many intracytoplasmic yolk granules. After 48 h, neural tube, notochord, and somites were severely affected, and their cells appeared loaded with yolk inclusions. Heart, lateral plates, blood cells, and blood vessels differentiated normally. At the onset of gastrulation, the level of glycogen was fivefold lower in catecholamine-treated embryos than in control embryos. Injection of glucose plus dopamine, at equimolar concentrations resulted in normal development both at 24 h and at 48 h. Because adrenergic stimulation of glycogenolysis in differentiated cells is usually mediated by cAMP and/or by calcium, we attempted to determine whether these substances could reproduce the effects of catecholamines. Only calcium was able to produce, to a limited extent, the same morphogenetic disturbances as those produced by catecholamines, whereas the chelating agent, ethylenediamine tetraacetic acid, when administered with dopamine, partially inhibited the effects of catecholamines. An increase in the number of yolk granules was the only common finding among embryos treated with cAMP and catecholamines. Blood and a well differentiated, gastrular endoderm always developed, independently of the nature of the substance with which the embryos had been treated. Morphogenetic disturbances caused by exogenous catecholamines could be due to depletion of glucose. Alternatively, a different metabolic commitment might exist within the diverse populations of cells that constitute the mesoblastic layer.

Abnormalities, Drug-Induced↗
PubMed1996

Modulation of catecholamine storage and release by the pituitary-interrenal axis in the rainbow trout, Oncorhynchus mykiss.

This study examined the effects of pituitary-interrenal hormones on catecholamine storage and release in the rainbow trout Oncorhynchus mykiss. An extract of trout pituitary elicited the release of adrenaline, but not noradrenaline, using an in situ perfusion preparation. A variety of doses of adrenocorticotropic hormone (2-2000 mU) caused the release of both catecholamines in situ which was unaffected by pre-treatment with the ganglion blocker, hexamethonium, or the serotonergic receptor antagonist, methysergide, but was abolished in calcium-free media. Intra-arterial injections of adrenocorticotrophic hormone in vivo caused an elevation of plasma adrenaline but not noradrenaline levels. Injections of cortisol in situ did not elicit catecholamine release. Trout given an intraperitoneal implant of cortisol (50 mg.kg-1 body weight) had significantly higher plasma cortisol concentrations when compared to controls after 7 days of implantation. Increases in the levels of stored catecholamines were observed in various regions of the kidney and posterior cardinal vein following 3 and 7 days of cortisol treatment. The ability of the chromaffin cells to release catecholamines in response to cholinergic stimulation was assessed in situ after 7 days of treatment. Basal (non-stimulated) adrenaline outflowing perfusate levels were greater in the cortisol-treated fish. Cortisol treatment increased the responsiveness of the catecholamine release process to low doses of the cholinoceptor agonist carbachol. Three or 7 days of cortisol treatment did not alter the in vitro activity of the enzyme phenylethanolamine-N-methyl transferase. The results of this study demonstrate that interactions within the pituitary-adrenal axis can influence both catecholamine storage and release in the rainbow trout.

Adrenocorticotropic Hormone↗
PubMed1988

Effects of the sulfhydryl reagent N-ethylmaleimide on reserpine binding to the catecholamine transporter in chromaffin granule membranes.

1. Catecholamines are transported into chromaffin granules via a carrier-mediated, active-transport process which is inhibited by micromolar concentrations of the sulfhydryl reagent, N-ethylmaleimide (NEM). Reserpine is a very potent, competitive inhibitor of the catecholamine transporter and can be used to investigate the characteristics of the catecholamine transporter. 2. The purpose of this study was to determine whether [3H]reserpine binding to the catecholamine transporter present in chromaffin granule membranes isolated from bovine adrenal glands was also inhibited by NEM and, if so, whether this was a direct or an indirect effect of NEM on the catecholamine transporter. 3. Both [3H]norepinephrine transport into and [3H]reserpine binding to the chromaffin granule ghosts isolated from bovine adrenal glands are inhibited by NEM, with IC50 values of 0.63 +/- 0.02 and 2.8 +/- 0.66 microM, respectively. 4. Mg and ATP protected both the [3H]norepinephrine transport into the ghosts and the [3H]reserpine binding to the transporter from inhibition by NEM, shifting the IC50 values to 260 +/- 43 and 120 +/- 29 microM, respectively. 5. NEM inhibition of the catecholamine transport and reserpine binding appears to be due to an action on the proton translocator associated with the Mg ATPase enzyme rather than a direct action on the catecholamine transporter since (a) the concentration of NEM required to inhibit formation of a membrane potential is similar to that required to inhibit [3H]norepinephrine transport into and [3H]reserpine binding to the ghosts and (b) Mg and ATP protected the proton translocation and [3H]norepinephrine transport into the ghosts, and [3H]reserpine binding to the ghosts, from inhibition by NEM.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1985

[Conjugated plasma catecholamines are lower in power athletes at rest and in physical work than in untrained probands].

Lower levels of free plasma catecholamines, noradrenaline and adrenaline were recently described in statically trained athletes under identical work loads during incremental cycling as compared with untrained control subjects. These differences point to a control of sympathetic activity by static training. Theme of the presented investigation is the question of additional training-dependent alterations of the conjugated plasma catecholamines in statically trained athletes. Eight competition weight lifters (21 +/- 2 years of age; 73 +/- 10 kg body weight) and seven untrained healthy control subjects (26 +/- 6 years; 75 +/- 4 kg) were investigated. The conjugated catecholamines were radioenzymatically determined as the difference between total and free catecholamines. The investigated subjects performed an incremental, exhaustive bicycle ergometric test in an upright body position. Before exercise, the levels of conjugated plasma dopamine (P less than 0.10), of conjugated noradrenaline (P less than 0.001) and conjugated adrenaline (P less than 0.10) are 2-3 times lower in statically trained athletes than those of the control subjects. The conjugated catecholamines did not show any significant changes during exercise, the significant differences between both groups (P less than 0.05-P less than 0.01) were therefore also observed during exercise. In contrast to the free plasma catecholamine responses, the conjugated catecholamine fractions are seen as indicators of long term alterations of the sympathetic activity.

Adult↗
PubMed1995

Effect of prolonged catecholamine infusion on immunoregulatory function: implications in congestive heart failure.

OBJECTIVES: This study sought to characterize the effects of prolonged catecholamine infusion on immunoregulatory cell traffic and activation. BACKGROUND: Immunoregulation has been shown to be partially controlled by the sympathetic nervous system. Although short-term elevation of catecholamine levels is known to alter immunoregulatory cell traffic and activation, the effects of prolonged heightened sympathetic nervous system activity have not adequately been studied. We believe that the alterations in immune function seen in patients with congestive heart failure are linked to a prolonged elevation of circulating catecholamine levels. METHODS: To characterize the effects of prolonged elevation of catecholamine levels, rats received 4 weeks of constant infusion of epinephrine or norepinephrine through implanted osmotic minipumps. Peripheral and splenic leukocyte subsets, T cell proliferation and interleukin-2 receptor expression were quantified. Antibody production to the novel antigen keyhole limpet hemocyanin was assessed over the 4-week treatment period. RESULTS: Both epinephrine and norepinephrine caused significant splenic atrophy and cardiac hypertrophy; both were blocked by propranolol. Epinephrine induced lymphocytosis; both catecholamines caused an increase in natural killer cells. In the spleen, both epinephrine and norepinephrine led to a dose-dependent decrease in total T cells, suppressor/cytotoxic T cells and natural killer cells and a significant increase in B cells. Epinephrine at the low dose enhanced mitogen-induced proliferation and interleukin-2 receptor expression. Norepinephrine at the low dose appeared to diminish proliferation. Epinephrine tended to inhibit IgG antibody production, whereas norepinephrine had no effect. CONCLUSIONS: The results of our study indicate that prolonged elevation of catecholamine levels alters immune cell proliferation and differentiation. These alterations differ greatly from those induced by short-term stimulation but, for the most part, parallel those found in patients with congestive heart failure. We postulate that the shifts in immunoregulatory cell type and function seen in patients with congestive heart failure are due, in part, to longstanding increases in circulating catecholamine levels and may play an important role in the pathogenesis and progression of disease.

Animals↗
PubMed1999

Catecholamine metabolism inhibitors and receptor blockades only partially suppress cardiac hypertrophy of juvenile visceral steatosis mice with systemic carnitine deficiency.

To clarify the mechanism of cardiac hypertrophy in carnitine-deficient JVS mice, we studied the possible role of catecholamine metabolism. Cardiac hypertrophy occurs 2 weeks after birth. The turnover of norepinephrine in the ventricles of JVS mice at 2 weeks was 3 times that of control, but it was not different from control at 5 days when the heart weight was not changed. To evaluate the accelerated norepinephrine turnover, we examined the effects of catecholamine metabolism inhibitors (alpha-methyltyrosine and 6-hydroxydopamine) and catecholamine receptor blockades (propranolol, prazosin and yohimbine) on the ratio of heart weight to body weight (HW/BW) and on the augmented expression of atrial natriuretic peptide (ANP) and the down-regulated carnitine deficiency-associated gene expressed in ventricle (CDV-1). The HW/BW ratio in JVS mice treated with catecholamine metabolism inhibitors and receptor blockades was significantly lower than in JVS mice without treatment, but still higher than in controls treated with each drug and in JVS mice treated with carnitine. The HW/BW ratio of JVS mice with propranolol was not significantly different from that of JVS mice treated with catecholamine metabolism inhibitors and was significantly lower than that of JVS mice treated with prazosin and yohimbine. Northern blot analysis showed that the altered expression of ANP and CDV-1 was not corrected in the ventricles of JVS mice treated with any of the drugs except carnitine. These results suggest that the catecholamine metabolism accelerated in JVS mice ventricles at 2 weeks is not the major cause of cardiac hypertrophy, but probably promotes cardiac hypertrophy mainly through the beta-adrenergic signaling pathway. The aberrant gene expression of ANP and CDV-1 found in JVS mice seems to be independent of catecholamine metabolism, and mediated primarily by the systemic carnitine deficiency.

Adrenergic Antagonists↗
PubMed1998

The adrenergic stress response in fish: control of catecholamine storage and release.

In fish, the catecholamine hormones adrenaline and noradrenaline are released into the circulation, from chromaffin cells, during numerous 'stressful' situations. The physiological and biochemical actions of these hormones (the efferent adrenergic response) have been the focus of numerous investigations over the past several decades. However, until recently, few studies have examined aspects involved in controlling/modulating catecholamine storage and release in fish. This review provides a detailed account of the afferent limb of the adrenergic response in fish, from the biosynthesis of catecholamines to the exocytotic release of these hormones from the chromaffin cells. The emphasis is on three particular topics: (1) catecholamine biosynthesis and storage within the chromaffin cells including the different types of chromaffin cells and their varying arrangement amongst species; (2) situations eliciting the secretion of catecholamines (e.g. hypoxia, hypercapnia, chasing); (3) cholinergic and non-cholinergic (i.e. serotonin, adrenocorticotropic hormone, angiotensin, adenosine) control of catecholamine secretion. As such, this review will demonstrate that the control of catecholamine storage and release in fish chromaffin cells is a complex processes involving regulation via numerous hormones, neurotransmitters and second messenger systems.

Animals↗
PubMed2000

High urinary catecholamine excretion predicts mortality and functional decline in high-functioning, community-dwelling older persons: MacArthur Studies of Successful Aging.

PURPOSE: Catecholamine release is a marker of stress, and high plasma norepinephrine levels have been associated with increased mortality. The predictive value of high urinary catecholamine excretion for functional decline and mortality in healthier older persons has not been determined. SUBJECTS AND METHODS: We used data from the MacArthur Studies of Successful Aging to determine the effects of high urinary catecholamine excretion on 3- and 7-year mortality and functional decline. In 1988, 765 high-functioning older subjects provided complete overnight urine samples for norepinephrine and epinephrine, and 199 of these provided repeat samples in 1991. Subjects who were in the top tertile of urinary norepinephrine or epinephrine excretion in 1988 were considered high excreters; those in the top tertile in both 1988 and 1991 were considered sustained high excreters. We used bivariate and multivariate analysis to examine the relations between high catecholamine excretion and mortality and Rosow-Breslau functional decline in 1991 and 1995. RESULTS: In multivariate analyses, subjects with high baseline urinary excretion of epinephrine, norepinephrine, or either catecholamine were at higher risk for mortality and functional decline at 3 and 7 years, although the magnitude of risk (adjusted odds-ratios ranged from 1.1 to 3.1) varied depending upon specific catecholamine and outcome measure. Subjects who had sustained high urinary norepinephrine excretion were also at increased risk for 4-year mortality or functional decline. CONCLUSIONS: High urinary catecholamine excretion in high-functioning, community-dwelling older persons likely reflects subclinical sympathetic stimulation and is a marker of increased risk for functional decline and mortality.

Aged↗
PubMedDate not supplied

An increase in urinary catecholamines of renal origin in patients with "borderline" hypertension.

Plasma and urinary catecholamines (norepinephrine and epinephrine) and urinary dopamine excretion were studied in 45 essential hypertensive patients subdivided into borderline (labile) and stable hypertension. Borderline hypertensive patients had a higher mean fractional renal clearance of catecholamines (the clearance of catecholamines relative to creatinine clearance) than both control subjects and stable hypertensive patients. A significantly positive correlation between the renal clearance of catecholamines and urinary dopamine excretion was also found in those with borderline hypertension, but not in control subjects or those with stable hypertension. These data indicate that patients with borderline hypertension have a relatively exaggerated renal catecholamine release. They probably reflect an increased sympathetic discharge to the kidney in "borderline" hypertension, occuring to a lesser degree in stable hypertension and control subjects. Thus, urinary catecholamine measurements do not specifically reflect the level of circulating catecholamines, particularly in borderline hypertension.

Adult↗