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PubMed1994

Catecholamines stimulate the synthesis and release of insulin-like growth factor binding protein-1 (IGFBP-1) by fetal sheep liver in vivo.

In fetal sheep, prolonged hypoxia (for 24 h) induced by a reduction in maternal uterine artery blood flow, increases insulin-like growth factor binding protein-1 (IGFBP-1) levels and decreases IGFBP-2 levels in the plasma, with corresponding changes in messenger RNA (mRNA) levels in the liver. Since IGFBP-1 synthesis in liver cells in vitro is stimulated by compounds that increase intracellular cAMP concentrations, we hypothesized that the increased IGFBP-1 synthesis during prolonged hypoxemia may be induced by circulating catecholamines, that are released during hypoxia, and that elevate fetal liver cAMP levels. Our aim was to determine the effect of 24-h catecholamine infusions on the synthesis and release of IGFBP-1 and IGFBP-2 in fetal sheep. Vascular catheters were implanted into fetuses at 110-115 days gestation in 14 pregnant ewes. After a 5-day recovery period, fetuses received a 24-h infusion of either norepinephrine (1 micrograms/kg.min, n = 5), epinephrine (0.25 micrograms/kg.min, n = 5), or vehicle (normal saline, n = 4). Fetal carotid arterial samples were collected at specified intervals throughout the infusion for the determination of blood glucose concentrations, plasma catecholamine concentrations by HPLC, insulin, and glucagon concentrations by RIA, and IGFBP levels by Western ligand blotting. After 24 h, the ewe and fetus were killed and selected fetal tissues (liver and kidney) were collected, and analyzed for IGFBP mRNA levels by northern blotting followed by laser densitometric quantification. Plasma catecholamine concentrations were increased in treated fetuses to levels that may be expected in fetuses subjected to prolonged hypoxia. In epinephrine and norepinephrine infused fetuses, blood glucose and plasma glucagon concentrations were increased significantly, whereas plasma insulin concentrations were decreased significantly. Norepinephrine and epinephrine infusions increased IGFBP-1 levels significantly (2- to 5-fold) in fetal plasma within 8-12 h, and the time course pattern of elevation of plasma IGFBP-1 levels was similar to that observed in prolonged hypoxia. After 24 h of either norepinephrine or epinephrine infusion, IGFBP-1 mRNA levels in the liver of fetuses were increased significantly (5- to 7-fold) compared to those of vehicle infused fetuses. IGFBP-2, -3, and -4 levels in fetal plasma were not affected by either infusion, nor were IGFBP-2 mRNA levels in fetal liver and kidney.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1999

Interleukin-1beta and catecholamines synergistically stimulate interleukin-6 release from rat C6 glioma cells in vitro: a potential role for lysophosphatidylcholine.

Interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) are proinflammatory cytokines that affect the secretion of several neuroendocrine hormones. In addition, glial cells synthesize and release IL-6, suggesting a paracrine role for this cytokine in the brain. We have examined the regulation of IL-6 release from glial cells by cytokines and catecholamines. Forty ng/ml IL-1beta induced a maximal 30-fold stimulation of IL-6 release (P < 0.01); higher and lower concentrations of IL-1beta were less effective. In the presence of (Bu)2cAMP, IL-1beta induced a strongly synergistic response with respect to IL-6 release; thus, the combination of these two agents resulted in a release of IL-6 that was much larger that the release attributed to either agent alone (i.e. 30-fold higher). Similarly, the combination of IL-1beta and the diterpene forskolin (but not the inactive analog 1,9-dideoxyforskolin) or cholera toxin also resulted in a synergistic stimulation of C6 glioma IL-6 release. Thus, increases in intracellular cAMP concentrations act in a synergistic fashion with the IL-1beta signaling pathway for IL-6 release. Because catecholamines increase intracellular cAMP levels, we investigated the effects of dopamine, epinephrine, and norepinephrine on IL-6 release. The combination of 1.0 to 100 microM of each catecholamine with IL-1beta resulted in the synergistic stimulation of IL-6 release. The coincubation of the beta-agonist isoproterenol and IL-1beta resulted in a striking 25-fold synergistic induction of IL-6 release. The synergistic increases in IL-6 release caused by IL-1beta and isoproterenol as well as IL-1beta and norepinephrine were blocked by the pretreatment of C6 cells with the beta-receptor antagonist propranolol. Because lysophosphatidylcholine (LPC) may function as a second messenger for IL-1beta, we also investigated the effects of LPC. Exogenous LPC (5 to 40 microM) stimulated IL-6 release from C6 glioma cells in a concentration-related manner (P < 0.01). The coincubation of LPC with norepinephrine provoked a synergistic release in IL-6 comparable with that obtained with IL-1beta and norepinephrine. Exposure of [3H]choline-labeled C6 cells to IL-1beta resulted in an increase in the [3H]LPC species as well as a decrease in [3H]phosphatidylcholine. Finally, while TNF alpha was less efficacious than IL-1beta for the stimulation of IL-6 release from C6 cells, the combination of IL-1beta and TNF alpha resulted in a significant synergistic induction of IL-6 release. We have demonstrated that IL-1beta stimulates IL-6 release from rat C6 glioma cells via a noncAMP-mediated mechanism that may involve LPC. The synergistic induction by cytokines and catecholamines of glial cell-derived IL-6 may subsequently affect inflammatory, neurodegenerative or neurotropic processes in the CNS.

Adrenergic beta-Agonists↗
PubMed2003

A comparison of biochemical tests for pheochromocytoma: measurement of fractionated plasma metanephrines compared with the combination of 24-hour urinary metanephrines and catecholamines.

We compared the diagnostic efficacy of fractionated plasma metanephrine measurements to measurements of 24-h urinary total metanephrines and catecholamines in outpatients tested for pheochromocytoma at Mayo Clinic Rochester from January 1, 1999, until November 27, 2000. Catecholaminesecreting tumors were histologically proven. The sensitivity of fractionated plasma metanephrines was 97% (30 of 31 patients), compared with a sensitivity of 90% (28 of 31) for urinary total metanephrines and catecholamines (P = 0.63). The specificity of fractionated plasma metanephrines was 85% (221 of 261), compared with 98% (257 of 261; P < 0.001) for urinary measurements. The likelihood ratios for positive tests were 6.3 (95% confidence interval, 4.7 to 8.5) for fractionated plasma metanephrines and 58.9 (95% confidence interval, 22.1 to 156.9) for urinary total metanephrines and catecholamines. An adrenal pheochromocytoma was missed by urinary testing in two patients with familial syndromes and one asymptomatic patient with an incidentally discovered adrenal mass. An extra-adrenal paraganglioma was missed by plasma testing in one patient. In conclusion, measurements of 24-h urinary total metanephrines and catecholamines yield fewer false-positive results, an attribute preferred for testing low-risk patients, but fractionated plasma metanephrine measurements may be preferred in high-risk patients with familial endocrine syndromes.

Adolescent↗
PubMed1977

Glucagon and catecholamine secretion during hypoglycemia in normal and diabetic man.

To examine the role of catecholamines in glucopenia-induced glucagon secretion, urinary epinephrine and norepinephrine and plasma immunoreactive glucagon (IRG) were measured during insulin-induced hypoglycemia in normal and insulin-dependent diabetic-man. Despite equivalent levels of hypoglycemia the mean plasma IRG increment in diabetes was only 15% of normals. The increases in epinephrine and norepinephrine were comparable in diabetics and normals; thus, the blunted response in plasma IRG to the stimulus of low blood sugar in diabetics cannot be explained by a generalized defect in catecholamine secretion. It is suggested that an alpha-cell glucoreceptor defect may account for the abnormal response to glucopenia in diabetics. To evaluate the possibility that impaired sensitivity to circulating catecholamines could explain the alpha cell dysfunction in diabetics, exogenous epinephrine was infused in normals and insulin-dependent diabetics. Elevated plasma IRG during epinephrine infusion was observed in only 50% of normals. The diabetics were hyperresponsive; mean increment in plasma IRG 3 times that of normals. The data demonstrate enhanced rather than impaired sensitivity to catecholamines in diabetes mellitus.

Adolescent↗
PubMed1986

Distribution of catecholamines between fetal and maternal compartments during human pregnancy with emphasis on L-dopa and dopamine.

This study was undertaken to determine the differential distribution of catecholamines, in particular L-dihydroxyphenylalanine (L-dopa) and dopamine, between the fetal and maternal compartments during human pregnancy. Amniotic fluid and fetal and maternal blood were obtained from two groups of pregnant women with uncomplicated pregnancies. One group was at 15-20 weeks of gestation and the second group was in labor after 36-41 weeks of gestation. Samples were analyzed for L-dopa, dopamine, norepinephrine, and epinephrine by radioenzymatic assays. L-Dopa constituted about 80% of the total circulating fetal catecholamines, and levels were 2- to 3-fold higher in fetal than maternal plasma. Marked increases in norepinephrine, small rises in epinephrine, but no changes in L-dopa or dopamine concentrations occurred in fetal plasma from mid- to late gestation. Maternal plasma catecholamines did not change. Towards the end of gestation, dopamine in the amniotic fluid increased 15-fold, and norepinephrine increased 5- to 6-fold; L-dopa remained high and unchanged. We conclude that L-dopa is the predominant catecholamine in fetal plasma and amniotic fluid during human pregnancy. No significant changes in its concentrations occur in either compartment between mid- and late gestation. In contrast, dopamine levels, which are 30- to 50-fold lower than those of L-dopa in amniotic fluid during midgestation, show a striking elevation toward the time of labor. Neither the sources nor the possible physiological functions of either L-dopa or dopamine during fetal life are known.

Amniotic Fluid↗
PubMed1986

Ontogeny of enkephalin and catecholamine-synthesizing enzymes in the primate fetal adrenal medulla.

Adrenal medullary cells in adult primates contain catecholamines and several neuropeptides. Among these peptides are several products of the three opiate precursor proteins: proenkephalin, prodynorphin, and proopiomelanocortin. We used immunocytochemistry to study the ontogeny of leu-enkephalin and the catecholamine-synthesizing enzymes dopamine beta-hydroxylase and phenylethanolamine N-methyltransferase in adjacent sections of 14 fetal rhesus and 31 fetal human adrenal glands. The adrenal medulla of a 24-week-old human fetus as well as medullas of 11 134- to 172-day-old rhesus fetuses were immunopositive with all 3 antisera employed. Furthermore, in thin serial sections of these glands, dopamine beta-hydroxylase, phenylethanolamine N-methyltransferase, and leu-enkephalin appeared to be colocalized in the same cells of the adrenal medulla. Twenty-six adrenals from fetuses 15-26 weeks stained lightly with one or more of the antisera. Dopamine beta-hydroxylase could be detected at 15 weeks, followed by leu-enkephalin and phenylethanolamine N-methyltransferase at 18-19 weeks. The role of the enkephalins during fetal life or in the adaptation to extrauterine life is not yet clear. In adults, enkephalins are cosecreted with catecholamines in response to stress. Our results suggest that the fetal adrenal may be capable of cosecretion of catecholamines and enkephalins, at least by the end of the second trimester of gestation.

Adrenal Medulla↗
PubMed1991

Inhibition of endogenous catecholamine synthesis augments early follicular phase luteinizing hormone secretion.

The physiological role of catecholamines, particularly dopamine and norepinephrine, in the regulation of gonadotropin secretion in humans is unclear. We administered the tyrosine hydroxylase inhibitor alpha-methyl-p-tyrosine (AMPT, 500 mg at 800 and 1000 h) to five women in the early follicular phase of the menstrual cycle and compared LH secretion patterns to those in five untreated controls. Commencing at 800 h, blood was drawn every 15 min for LH and PRL measurements until 1600 h. AMPT elevated PRL concentrations (mean +/- SEM) from a baseline of 14.72 +/- 2.51 micrograms/L to a peak of 102.2 +/- 24 micrograms/L. LH concentrations [21.97 +/- 0.56 (AMPT) vs. 13.51 +/- 0.16 IU/L (control), P less than 0.0001], LH area under the curve [11014 +/- 1815 (AMPT) vs. 7009 +/- 404 IU.min/L (control), P = 0.05] and LH pulse amplitude [9.99 +/- 2.38 (AMPT) vs. 4.03 +/- 0.61 IU/L (control), P = 0.04] were all greater in the group in which catecholamine synthesis was inhibited. There was no difference in pulse frequency between the groups (7.4 +/- 0.51 vs. 6.6 +/- 0.24 pulses/8 h, P greater than 0.05). We conclude 1) inhibition of endogenous catecholamine synthesis augments LH levels in the early follicular phase, and 2) increased LH secretion during catecholamine synthesis inhibition is due, at least in part, to increased LH pulse amplitude but not increased LH pulse frequency.

Catecholamines↗
PubMed1999

Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: clinical implications.

The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on catecholamine and interleukin-2 (IL-2) levels in humans. Circulating levels of catecholamines and IL-2 were sampled every 30 min during 2 nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600 h) in 17 healthy male volunteers. Sleep was monitored somnopolygraphically. Sleep onset was associated with a significant (P < 0.05) decline of circulating concentrations of norepinephrine and epinephrine, with a nocturnal nadir that occurred 1 h after nocturnal sleep. On the PSD-L night, levels of norepinephrine and epinephrine significantly (P < 0.05) increased in association with nocturnal awakening. During stage 3-4 sleep, levels of norepinephrine, but not epinephrine, were significantly lower (P < 0.05) compared to average levels during the awake period, stages 1-2 sleep, and rapid eye movement sleep. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or the various sleep stages. We conclude that sleep onset is associated with changes in levels of circulating catecholamines. Loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.

Adult↗
PubMed1993

Cardioprotection by superoxide dismutase: a catecholamine-dependent process?

Oxygen-derived free radicals may contribute to tissue injury in myocardial ischemia although the mechanism is unclear. Catecholamines possibly could be involved in the genesis of free radicals because it has been demonstrated that oxygen free radicals may be generated by autooxidation of noradrenaline. Superoxide dismutase (SOD) protects the myocardium against injury by superoxide anion radicals. We, therefore, examined whether the cardioprotective effect of superoxide dismutase still could be demonstrated after depletion of catecholamine stores by reserpine (7 mg/kg intraperitoneally 24 h premortem). We used electrically paced isolated hearts perfused according to Langendorff (Tyrode's solution, Ca2+ 1.8 mmol/L, constant perfusion pressure: 70 cm H2O, 3 Hz). Myocardial ischemia was induced by occlusion of a left coronary artery branch. Epicardial NADH-fluorescence was used for quantitation of the myocardial ischemia. SOD (48 U/mL) did not influence global coronary flow or left ventricular pressure significantly (P > 0.05). In control hearts, SOD significantly diminished both size and intensity of epicardial NADH-fluorescence after repetitive coronary ligatures (-45%) (P < 0.05). In hearts with depleted catecholamine stores, this cardioprotection by SOD was no longer observed (P > 0.05). Stimulation of noradrenaline overflow by increasing the pacing rate of control hearts from 180/min up to 300/min after coronary occlusion also significantly enlarged myocardial ischemia (P < 0.05). This pacing rate-dependent growth of myocardial ischemia could be prevented completely by either prior depletion of catecholamine stores with reserpine or SOD. Therefore, noradrenaline seems to be the most important source for the generation of oxygen free radicals during myocardial ischemia in isolated saline-perfused rabbit hearts.

Animals↗
PubMed1993

Interaction of catecholamines and nitrous oxide ventilation during incomplete brain ischemia in rats.

The interaction of plasma catecholamines and nitrous oxide (N2O) ventilation was examined during brain ischemia in rats. Group 1 (n = 19) was anesthetized with 50 micrograms.kg-1 x h-1 of fentanyl and ventilated with 70% nitrogen in oxygen. Group 2 (n = 19) was anesthetized with intravenous fentanyl (25 micrograms.kg-1 x h-1) and 70% N2O ventilation in oxygen. Group 3 (n = 10) received 25 micrograms.kg-1 x h-1 of fentanyl and 70% N2O ventilation and 100 micrograms/kg of dexmedetomidine, an alpha 2-adrenergic receptor agonist that decreases sympathetic activity. Incomplete brain ischemia was produced by right carotid ligation combined with hemorrhagic hypotension to 30 mm Hg for 30 min. Plasma catecholamines were measured during ischemia. Cerebral blood flow (CBF) was evaluated by using laser Doppler. Neurologic outcome was evaluated for 3 days after ischemia. Plasma epinephrine and norepinephrine and were decreased 20% and neurologic outcome was significantly worse in Group 2 ventilated with N2O compared with fentanyl-anesthetized controls (P < 0.05). Dexmedetomidine-treated rats had lower plasma catecholamines (20% of control) and larger decreases in CBF during ischemia compared with controls. Dexmedetomidine (Group 3) improved outcome from ischemia in comparison to both Groups 1 and 2 (P < 0.05). These results suggest that catecholamines play a major role in worsening ischemic outcome. N2O ventilation may increase neuronal injury by enhancing the sympathetic response to ischemia.

Adrenergic alpha-Agonists↗
PubMed1986

Intrinsic mechanical properties of the perfused rainbow trout heart and the effects of catecholamines and extracellular calcium under control and acidotic conditions.

A perfused rainbow trout heart was developed which generated its own intrinsic heart rate and a physiological power output. This preparation was used to examine the intrinsic mechanical properties of the trout heart, the dose-response effects of catecholamines and extracellular calcium on these properties, and the effects of catecholamines and extracellular calcium during exposure to acidotic conditions. The trout heart was relatively pressure-insensitive to a physiological range of ventral aortic pressures. Preload exerted an important control over cardiac output through the Starling response. Heart rate was independent of both these intrinsic mechanisms. The intrinsic mechanical capabilities of the trout heart were greater than those observed previously in less active, benthic teleosts. Physiological concentrations of catecholamines significantly improved cardiac contractility through positive inotropy and chronotropy. Adrenaline was more potent than noradrenaline, indicating that these effects were mediated by beta 2-adrenoceptors. Elevated extracellular calcium produced only a modest improvement of cardiac contractility compared to that produced by adrenaline. Positive inotropy and negative chronotropy were observed with elevated extracellular calcium. Extracellular acidosis always reduced cardiac contractility through negative chronotropy and inotropy. Extracellular calcium improved the inotropic state of the acidotic heart and restored contractility, but the overall improvement of cardiac performance was compromised by an accompanying negative chronotropy. Physiological levels of adrenaline improved cardiac performance during extracellular acidosis. The roles of catecholamines and extracellular calcium are discussed with respect to post-exercise cardiac performance in trout.

Acidosis↗
PubMed1999

Antarctic fishes have a limited capacity for catecholamine synthesis.

To determine whether an attenuated stress response is a general feature of Antarctic fish or is dependent on ecotype, the capacity for catecholamine synthesis within the head kidney and plasma levels of the primary stress hormones (catecholamines and cortisol) were determined in species with a range of activity patterns. Tyrosine hydroxylase (TH) activities were similar in both sluggish (Gobionotothen gibberifons, 153+/-22 nmol g(-)(1 )h(-)(1), mean +/- s.e.m.) and active (Notothenia rossii, 185+/-39 nmol g(-)(1 )h(-)(1), Dissostichus mawsoni, 128+/-31 nmol g(-)(1 )h(-)(1)) pelagic nototheniids, but only 30 % of those in Atlantic cod (Gadus morhua, 393+/-88 nmol g(-)(1 )h(-)(1)) at the same temperature. TH activities were even lower in white-blooded channichthyids (Chaenocephalus aceratus, 74+/-16 nmol g(-)(1 )h(-)(1) and Champsocephalus gunnari, 53+/-17 nmol g(-)(1 )h(-)(1)), although values in Chionodraco rastrospinosus were similar to red-blooded species (178+/-45 nmol g(-)(1 )h(-)(1)). Circulating catecholamine levels were extremely high in all species after fishing stress, with adrenaline levels 3-4 times higher than noradrenaline levels. Cortisol levels remained low, ranging from 1.33+/-0.58 ng ml(-)(1) in Champsocephalus gunnari to 44.9+/-25.0 ng ml(-)(1 )in Dissostichus mawsoni. These data suggest that depressed catecholamine synthesis is typical of Antarctic fish regardless of life style, although they are able to release extensive stores from the chromaffin tissue under conditions of extreme trauma. Cortisol does not appear to be an important primary stress hormone in these species.

Animals↗
PubMed1998

Effect of preischemic catecholamine treatment on ischemia-reperfusion injury of the myocardium: subtype, dose, and temperature dependency.

Preischemic adrenergic stimulation may affect postischemic cardiac function. Using an isolated working heart model, we investigated the effects of preischemic catecholamine treatment on postischemic recovery. Hearts from Wistar rats were perfused in working mode for 20 min, in Langendorff mode for 15 min, and again in working mode for 20 min (W2). Hearts were treated with isoproterenol (8.0 and 40.0 nmol/L), phenylephrine (0.06, 0.30, and 1.50 micromol/L), or epinephrine (16 and 80 nmol/L) during the W2 period and then arrested with St Thomas' Hospital cardioplegic solution (STH) and subjected to global ischemia (37 degrees C or 20 degrees C), followed by reperfusion. At 37 degrees C, isoproterenol had a beneficial effect at the lower dose but a harmful effect at the higher dose; phenylephrine and epinephrine had a harmful effect at all doses. At 20 degrees C, isoproterenol and epinephrine had a harmful effect at a high dose; phenylephrine had no harmful effect at any dose. In a separate study, the influence of calcium modulators (diltiazem and ryanodine, added in the STH) on the catecholamine effect was investigated. The harmful effect of preischemic treatment with isoproterenol (24.0 nmol/L) or phenylephrine (0.9 micromol/L) was abolished by the calcium modulators. Thus, preischemic beta-adrenergic or alpha + beta-adrenergic stimulation has a deleterious effect on postischemic recovery of the myocardium. The effect could be altered depending on the subtype and dose of catecholamine and the ischemic temperature. Intracellular calcium movement could be involved in the mechanism responsible for the harmful effect of preischemic catecholamine treatment.

Adrenergic beta-Agonists↗
PubMed1994

Stimulatory effect of pituitary adenylate cyclase-activating polypeptide on catecholamine synthesis in cultured bovine adrenal chromaffin cells: involvements of tyrosine hydroxylase phosphorylation caused by Ca2+ influx and cAMP.

In cultured bovine adrenal chromaffin cells, pituitary adenylate cylase-activating polypeptide (PACAP) stimulated [14C]catecholamine synthesis from [14C]tyrosine (but not from [14C]DOPA) in a concentration-dependent manner, causing maximal stimulation at 10(-7) M. The stimulatory action of PACAP was not affected by staurosporine (an inhibitor of protein kinase C) or in the cells in which protein kinase C was down-regulated by prolonged exposure to TPA (an activator of protein kinase C), whereas it was partially attenuated in Ca(2+)-free medium. PACAP (10(-7) M) increased the formation of [3H]inositol phosphates, [Ca2+]i and 45Ca2+ uptake as well as cAMP. The peptide also stimulated the phosphorylation of tyrosine hydroxylase, the enzyme catalyzing the rate-limiting step in catecholamine synthesis. Catecholamine synthesis and tyrosine hydroxylase phosphorylation stimulated by the maximal effective concentration of dibutyryl cAMP or high K+, which activates Ca2+ uptake, were further enhanced by PACAP, suggesting that both cAMP- and Ca(2+)-dependent protein kinases may be involved in the stimulation of tyrosine hydroxylase phosphorylation and catecholamine synthesis caused by PACAP.

Adrenal Medulla↗
PubMed1995

Cardiotoxicity of catecholamines after application of L-DOPA in Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR).

In order to estimate the role of the sympatho-adrenal system as a trigger in cardiovascular mortality risk after L-DOPA administration in patients with Parkinsons disease we performed the following experiments in normotensive Wistar-Kyoto-rats (WKY) and spontaneously hypertensive rats (SHR). L-DOPA was given orally in increasing doses (30, 100, 300 mg/kg b.w.). Haemodynamic parameters (BP, HR) were measured by tail cuff plethysmography and catecholamine concentrations in tissues assayed by high pressure liquid chromatography. Stressful situations were induced by experimental myocardial infarction. After administration of L-DOPA a dose-dependent increase in blood pressure in both WKY and SHR was observed with a prolongation in SHR. Significantly increased concentrations of dopamine in the hearts were measured in both strains. Noradrenaline stores in the heart of WKY were more filled than in the heart of SHR. Only in SHR high adrenaline concentration in the adrenal medulla were measured after L-DOPA administration. Circulating adrenaline concentrations were significantly enhanced after myocardial infarction in WKY and could be further elevated by pretreatment with L-DOPA. From the results obtained it is concluded that L-DOPA administration in WKY and SHR leads to exaggerate synthesis and massive release of catecholamines and in consequence to an enhanced cardiovascular mortality risk due to cardiotoxicity of catecholamines. It can be extrapolated that increased cardiovascular mortality risk seen in Parkinson patients treated with L-DOPA and benzerazide is probably associated with increased synthesis and release of catecholamines during stressful situations.

Animals↗
PubMed1980

[The correlation between climacteric symptoms and plasma levels of catecholamines (author's transl)].

Although climacteric symptoms, particularly, vasomotor symptoms such as hot flushes, have been suggested to correlate with depletion of ovarian estrogen secretion, its precise mechanism to producing these symptoms has still remained unknown. On the other hand, catecholamines have been presumed to be related to an onset of the climacteric symptoms. This study was carried out to elucidate the correlation between the climacteric symptoms and plasma levels of catecholamines. Thirty-eight women complaining of climacteric symptoms were studied. These subjects were evaluated for their symptoms and the severity of the symptoms was expressed in numerical figure, 0 to 3, according to its degrees: none, slight, moderate, and marked, respectively. At the same time venous blood samples were drawn to determine the plasma levels of catecholamines, using an Renzini's fluorimetric assay method improved by Miura. Eventually, a correlation between severities of the symptoms and plasma catecholamines was made. Plasma epinephrine levels were found to be elevated as the severity of the hot flush progressed from none to marked. No symptoms other than hot flush showed such significant correlation with plasma epinephrine or norepinephrine levels. This result suggests that the onset of hot flush is closely related with an increased activity of the adrenomedullary sympathetic nervous system.

Adult↗
PubMed1989

[Effect of TRH and histidyl-proline diketopiperazine (cyclo(His-Pro] on catecholamine secretion].

The effects of TRH and its metabolite, histidyl-proline diketopiperazine (cyclo(His-Pro] on catecholamine metabolism in the central nervous system, peripheral tissues and plasma were examined in adult and young Wistar rats aged 3 weeks. The intravenous administration of 50 micrograms of TRH produced an increase in plasma epinephrine, cerebral dopamine and a reciprocal decrease in norepinephrine and dopamine in diencephalon and midbrain. In contrast, 50 micrograms of cyclo(His-Pro) induced a rise in plasma dopamine and a decrease of dopamine in cerebellum, pons and medulla oblongata. After intraperitoneal injection of 3 mg of alpha-methyl-p-tyrosine, which blocked re-uptake of catecholamines in synapses, intrathecal administration of 30 ng TRH accelerated 2 times metabolic turnover of norepinephrine and dopamine in cerebral hemisphere, diencephalon and midbrain as well as norepinephrine turnover in cerebellum, pons, medulla oblongata, heart and brown adipose tissue. Consecutive intrathecal administration of TRH for 6 days enhanced cerebral catecholamine content. These results indicate that (1) TRH accelerates metabolic rate of catecholamine in the central nervous system as well as peripheral tissues, and (2) TRH acts on both noradrenergic and dopaminergic neurons in cerebral hemisphere, diencephalon and midbrain, whereas cyclo(His-Pro) acts mainly on dopaminergic neurons in cerebellum, pons and medulla oblongata.

Animals↗
PubMed1980

Single-isotope enzymatic derivative method for measuring catecholamines in human plasma.

The radioenzymatic determination of plasma catecholamines with a modification of the method of da Prada & Zürcher ((1976), Life Sci 19, 1161-1174) is described. The several reaction steps were optimized with respect to the quantities of substrate and enzyme, and reaction time. There were particular methodological difficulties concerning the blanks, which were determined by using sodium metaperiodate-oxidized plasma. The reliability criteria of the method were determined. Coefficients of variation between 3.4 and 8.6% were found for the intra-assay variability of 10 pg of norepinephrine and 3 pg of epinephrine or dopamine, resp. The recoveries o the three catecholamines ranged from 88-93%. The detection limits were calculated from the standard deviation of the blanks and amounted to 12 ng/l (norepinephrine), 6 ng/l (dopamine) and 3 ng/l (epinephrine). The method was used for the analysis of plasma samples from patients. In a further investigation we examined the stability of plasma catecholamines stored at different temperatures. It was found that samples can be stored for 1-2 hours at room temperature and for several weeks at -27 degrees C without losses in catecholamine content.

Animals↗