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PubMed1985

Photoaffinity labelling of MSH receptors on Anolis melanophores: effects of catecholamines, calcium and forskolin.

Photoaffinity labelling of MSH receptors on Anolis melanophores was used as a tool for studying the effects of catecholamines, calcium and forskolin on hormone-receptor interaction and receptor-adenylate cyclase coupling. Covalent attachment of photoreactive alpha-MSH to its receptor was suppressed in calcium-free buffer but was hardly influenced by catecholamines or forskolin. The longlasting signal generated by the covalent MSH-receptor complex was readily and reversibly abolished by adrenaline, noradrenaline, dopamine or clonidine or by the absence of calcium. The suppression of pigment dispersion by catecholamines was blocked by the simultaneous presence of yohimbine but not prazosin, indicating that the catecholamines antagonize the alpha-MSH signal by inhibitory action on the adenylate cyclase system through an alpha-2 receptor. Forskolin, which stimulates melanophores by direct action on the catalytic unit of the adenylate cyclase and at about the same speed as alpha-MSH, produced a slower and weaker response in the presence of noradrenaline. If MSH receptors were covalently labelled and then exposed to noradrenaline, the characteristics of the forskolin-induced response were identical to those of unlabelled cells that had not been exposed to noradrenaline. This may point to a partial restoration of receptor-adenylate cyclase coupling by forskolin. The results show that the longlasting stimulation of Anolis melanophores by photoaffinity labelling proceeds via a permanently stimulated adenylate-cyclase system whose coupling to the receptor depends on calcium and is abolished by alpha-2 receptor agonists. Calcium is also essential for hormone-receptor binding.

Adrenergic alpha-Agonists↗
PubMed1981

Urinary excretion of catecholamines in the night monkey (Aotus trivirgatus) (Primates, Cebidae).

A seasonal variation in the urinary catecholamines output has been demonstrated in two simians kept under constant ambient conditions : the nocturnal Aotus and the diurnal Saïmiri sciureus. In Aotus, catecholamines output (NA + A), in spring, is higher than in other Primates including man and even more so in winter. Cold exposure increases the NA + A excretion in Aotus as it does in squirrel monkey and rat but the A output is particularly prominent in Saïmiri. Fasting does not alter significantly the catecholamines excretion. Associated fasting and cold exposure do not modify the adrenosympathetic response observed in Aotus in cold conditions alone, but depresses the sympathetic activity and greatly enhance the adrenomedullary excretion in squirrel monkey, as it is the case in rat. Associated fasting and cold represents a highly stressful situation for squirrel monkey but not for night monkey. Catecholamines metabolites (MN, NMN, DOPAC, HVA, VMA and MHPG) are found in urine of both species, DOPAC and VMA being predominant in Aotus but DOPAC and MHPG in Saïmiri. The proportions of conjugated forms vary according to the metabolite : DOPAC and VMA are mainly under free form but NMN, MN and MHPG are mostly conjugated in both species. The daily output of pooled adrenergic metabolites (expressed as ng/mg creatinine) is higher in Aotus than in Saïmiri and man. Both monkey species display a high adrenosympathetic activity which does not correlate with their resting metabolic rate.

Animals↗
PubMed1990

Interactions of nimodipine and cocaine on endogenous catecholamines in the squirrel monkey.

The effects of nimodipine on the cocaine-induced alterations in blood pressure, heart rate, and plasma catecholamines were studied in the squirrel monkey. Cocaine in intravenously administered doses of 0.5, 1, and 2 mg/kg produced significant increases in blood pressure and significant decreases in heart rate. These cardiovascular changes were associated with transient episodes of arrhythmias and with significant increases in plasma concentrations of dopamine, epinephrine, and norepinephrine. Nimodipine, 1 micrograms/kg/min for 5 min administered intravenously 5 min after cocaine, corrects the cardiovascular and plasma catecholamine concentration changes induced by this alkaloid. The same dose of nimodipine administered 5 min before cocaine prevents elevations of blood pressure. Plasma catecholamine increments are also prevented except for the highest dose of cocaine. Cardiovascular changes induced by cocaine administration in the squirrel monkey are temporally associated with significant increments in plasma catecholamines. Administration of nimodipine prevents or minimizes these endocrine and physiologic changes.

Animals↗
PubMed1990

Stereostructure activity relationships of catecholamines on human platelet function.

The concentration-dependent effects of clonidine, isomers of epinephrine, norepinephrine (NE), isoproterenol, cobefrin and alpha-methyldopamine, and related desoxy analogs (epinine, dopamine, N-isopropyldopamine) were examined on human platelets. The rank order of aggregatory potency (pD2 values) was R(-)-epinephrine (6.3) greater than R(-)-NE (5.9) greater than (+/-)-erythro-cobefrin (5.3) greater than S(+)-epinephrine (4.7) = S(+)-NE (4.7) = clonidine (4.7) = dopamine (4.6) greater than epinine (4.4) greater than S(+)-alpha-methyldopamine (4.3) = R(-)-alpha-methyldopamine (4.3) greater than (+/-)-threo-cobefrin (3.7). The isoproterenol isomers and N-isopropyl-dopamine were inactive as agonists. In 9 of 16 platelet-rich plasma preparations, R(-)-epinephrine, R(-)-NE, and (+/-)erythro-cobefrin were agonists and the remaining analogs blocked R(-)-NE-induced aggregation with a rank order of inhibitory potencies (pKB values) of clonidine (6.2) greater than S(+)-alpha-methyldopamine (5.0) greater than dopamine (4.6) = R(-)-alpha-methyldopamine (4.4) greater than or equal to S(+)-NE (4.3) greater than N-isopropyldopamine (4.1) greater than S(+)-isoproterenol (3.7) = R(-)-isoproterenol (3.5). Each compound was also able to reverse prostaglandin E1 (PGE1) (0.1 microM)-induced blockade of the maximal aggregation response to ADP. At high concentrations, R(-)-isoproterenol was more potent than either the S(+)-isomer or desoxy analog, N-isopropyldopamine, in the reversal of PGE1 inhibition of ADP aggregation. Phentolamine blocked these alpha 2-adrenoceptor-mediated actions against PGE1 on ADP aggregation. The rank order of potency for the reversal of PGE1-mediated inhibition of ADP aggregation by these catecholamines was similar to that observed for platelet aggregation. Our results indicate that (i) the stereochemical requirements for the interaction of catecholamines with platelet alpha 2-adrenoceptors are in agreement with the Easson-Stedman hypothesis and other alpha-adrenoceptor tissues; (ii) catecholamines lacking a benzylic hydroxyl group in the R-configuration and/or possessing an N-isopropyl group were alpha 2-adrenoceptor antagonists; (iii) clonidine gave quantitatively different responses compared with catecholamines for interaction with alpha 2-adrenoceptors; and (iv) inhibition of platelet adenylate cyclase is correlated to the inhibition of epinephrine-induced aggregation response for this series of compounds.

Adenosine Diphosphate↗
PubMed2001

Calcitonin gene-related peptide (CGRP), acting via CGRP type 1 receptors, inhibits potassium-stimulated aldosterone secretion and enhances basal catecholamine secretion from rat adrenal gland.

Calcitonin gene-related peptide (CGRP) is a potent hypotensive peptide, that acts via two main subtypes of receptors, named CGRP1 and CGRP2. CGRP belongs to a regulatory-peptide family, that includes adrenomedullin (ADM) whose aldosterone antisecretagogue and catecholamine secretagogue actions are well demonstrated. Quantitative autoradiography showed the presence of [125I]CGRP binding sites in both rat adrenal zona glomerulosa (ZG) and medulla. Binding was displaced by the CGRP1-receptor antagonist CGRP(8-37), but not by the CGRP2-receptor agonist [cys(Et)2,7]-alphaCGRP (CGRP2-A). CGRP concentration-dependently inhibited 10 mM-stimulated (but not basal) aldosterone secretion from dispersed rat ZG cells, and enhanced basal catecholamine secretion from rat adrenomedullary fragments. The responses to the maximal effective concentration of CGRP (10-8 M) were blocked by 10-7 M CGRP(8-37). CGRP2-A (10-7 M) neither altered aldosterone response to 10 mM K+ nor enhanced basal catecholamine secretion. The conclusion is drawn that CGRP, like ADM, inhibits agonist-stimulated aldosterone secretion and stimulates basal catecholamine release in the rat, exclusively acting via CGRP1 receptors.

Adrenal Glands↗
PubMed2000

A forward-facilitating influence of cortisol on catecholamines assessed during the work of garbage collectors.

OBJECTIVES: In this study, the hypothesis was tested of whether part of the hypothalamic-pituitary-adrenal system can have a facilitating influence on mean adrenomedullary reactivity during a workday. METHODS: Data of a field study on 115 male garbage collectors were used for this purpose. Catecholamines and cortisol were assessed by urinary sampling during a workday and during a day off. The within-subjects baseline levels of the catecholamines, personal factors, physical work load, and work characteristics were controlled for in the analyses. RESULTS: The results showed that there is reason to assume a "forward-facilitating influence" between the aforementioned systems. The morning cortisol excretion rate explained a reasonable amount of the mean catecholamine excretion rates during a workday. The morning cortisol level explained more variance in the adrenaline than in the noradrenaline values, and for both catecholamines the influence of cortisol was more pronounced than the influence of psychosocial stress factors like autonomy and job demands. CONCLUSIONS: The morning level of cortisol proved to be a more powerful predictor of the reactivity of adrenaline than that of noradrenaline during work. The association between the pituitary adrenocortical system and the adrenomedullary system could therefore be a "forward-facilitating influence". It is recommended that future research should focus on cortisol as the predictor of neuroendocrine reactivity and on determining whether this predictive power is expandable to work-induced health complaints.

Adrenal Medulla↗
PubMed1999

[Catecholamine plasma levels during the tilt-table test in patients with vasovagal syncope].

BACKGROUND: The head-up tilt test (HUT) makes it possible to diagnose vasovagal syncope. The objective of the trial was to follow up changes of catecholamine plasma levels during HUT and test their importance in the pathogenesis of vasovagal syncope. METHODS AND RESULTS: In 25 patients with syncope of obscure etiology during HUT the noradrenalin, adrenalin and dopamine levels were followed up. In 125 patients (8 men and 7 women, mean age 34.3 years) HUT was positive. The control group was formed by 10 patients with negative HUT (4 men, 6 women, mean age 41.1 years). The catecholamine levels were assessed by the method of high resolution liquid chromatography during minutes 0, 5 and after completion of the test (i.e. during development of the syncope or the 45th minute). On comparison by the t-test no statistically significant difference between the group with vasovagal syncope and the control group was found. Noradrenalin 0 min: 186.4 +/- 61.6 pg/ml vs. 190.5 +/- 67.4 pg/ml (n.s.), 5th min. 506.3 +/- 178.9 pg/ml vs. 566.8 +/- 195.6 pg/ml (n.s.), end of test 457.3 +/- 154.1 pg/ml vs. 352.3 +/- 169.9 pg/ml (n.s.). Adrenalin 0 min. 54.0 +/- 12.6 pg/ml vs. 54.9 +/- 13.6 pg/ml (n.s.), 5th min. 114.3 +/- 35.6 pg/ml vs. 128.1 +/- 41.0 pg/ml n.s., end of test 98.2 +/- 40.6 vs. 783 +/- 31.2 pg/ml (n.s.). Dopamine 0 min. 113.9 +/- 36.5 pg/ml vs. 158.4 +/- 67.2 pg/ml (n.s.), 5th min. 318.1 +/- 72.7 vs. 328.5 +/- 119.7 pg/ml (n.s.), end of test 279.4 +/- 93.8 pg/ml vs. 231.7 +/- 98.5 pg/ml (n.s.). CONCLUSIONS: Catecholamine plasma levels in patients with vasovagal syncope did not differ from the control group. The importance of catecholamines in the pathogenesis of vasovagal syncope thus cannot be confirmed.

Adult↗
PubMed2000

Attenuation of histamine-induced endothelial permeability responses after pacing-induced heart failure: role for endogenous catecholamines.

OBJECTIVE: After congestive heart failure (CHF), lung endothelial permeability responses to a number of perturbations, including acute barotrauma, angiotensin II, and thapsigargin are blunted. Our hypothesis was that similar attenuation of permeability responses occurs in peripheral vascular beds after CHF. We compared peripheral microvascular permeability responses to the autacoid histamine in control dogs and in dogs paced to heart failure (245 bpm for approximately 36 days). Since catecholamines attenuate autacoid-induced increases in microvascular permeability in skin and muscle in normal animals, we also tested whether the known elevation in catecholamines in CHF was involved in any downregulation of permeability responses in this group. METHODS: Control and paced dogs were anesthetized, intubated, and ventilated, and a hindpaw lymphatic cannulated. The reflection coefficient for total proteins (sigma) was measured at baseline and during one-hour, local intra-arterial histamine infusion. RESULTS: In controls, sigma fell from 0.83 +/- 0.02 to 0.73 +/- 0.04 after histamine (p < 0.05), while in the paced group sigma was no different from that at baseline (0.77 +/- 0.02). To test whether this difference was due to endogenous catecholamines, dogs were pretreated with propranolol (controls only) or the specific beta 2-antagonist ICI 118,551 prior to histamine infusion. After beta-blockade, histamine significantly reduced sigma in both control (0.83 +/- 0.01 to 0.55 +/- 0.05) and paced (0.83 +/- 0.01 to 0.57 +/- 0.07) groups (p < 0.05). CONCLUSION: We conclude that endogenous catecholamines, acting via beta 2-adrenergic receptors, attenuate the permeability response to histamine in pacing-induced heart failure.

Adrenergic beta-Antagonists↗
PubMed1975

Plasma catecholamines and postoperative gastric emptying and small intestinal propulsion in the rat.

The role of adrenal medullary discharge of catecholamines on inhibition of gastric emptying and small intestinal propulsion after laparotomy was examined in rats. The rate of movement of a 51Cr-labeled liquid test meal, which had been introduced by gastric intubation, out of the stomach and through the small intestine, was retarded 12 hr after laparotomy. Adrenal demedullation produced a striking decrease in plasma catecholamines and abolished surgically induced elevation of the catecholamines, but had no significant effect on gastric emptying or intestinal propulsion in rats subjected to laparotomy or in the unoperated control animals. Thus circulating catecholamines play little if any role in controlling normal gastroinestinal motility or in the postoperative decrease in rate of gastric emptying and small intestinal motility.

Abdomen↗
PubMed1975

Inhibition of brain catecholamine synthesis and release of prolactin and luteinizing hormone in the ovariectomized rat.

The effects of alpha-methyl-p-tyrosine (alpha-MT) on brain catecholamine synthesis and plasma prolactin and luteinizing hormone levels were determined in ovariectomized rats to ascertain whether the release of either hormone from the anterior pituitary is dependent on the release of newly synthesized dopamine and norepinephrine. Doses of alpha-MT ranging from 3.15 to 25 mg/kg were administered via a carotid cannula to unrestrained ovariectomized rats. Within 10 minutes, alpha-MT caused a significant dose-related increase in plasma concentrations of prolactin which became maximal 20 to 25 minutes after the injection. Plasma levels of luteinizing hormone were not affected. Alpha-MT caused a dose-related decrease in the accumulation of 3-H-norepinephrine and 3-H-dopamine in the brain after the administration of 3-H-tyrosine. The time course of the inhibition of catecholamine synthesis closely paralleled the increase in plasma prolactin concentration. Alpha-MT had no effect on endogenous catecholamines. The results suggest that catecholamine-containing neurons exert a tonic inhibitory influence on the release of prolactin in ovariectomized rats.

Analysis of Variance↗
PubMedDate not supplied

Urinary catecholamines as a measure of emotional stress in children with a digit-sucking habit: a preliminary study.

This cross-sectional study investigated the relationship between digit-sucking habit and emotional stress measured by the urinary catecholamines in 314 children, boys and girls, ages six to eight years. The digit-sucking habit was recorded by an interview. A twenty-four hour urine sample was collected for each subject and a representative sample was analyzed by the HPLC technique to assay the catecholamine content. Socioeconomic factors were recorded by a questionnaire distributed to the parents. The logistic multiple-regression analysis was used to test the impact of catecholamines and other related factors on the presence of a digit-sucking habit. The results showed that emotional stress measured by the urinary catecholamines did not have a significant effect on the presence of a digit-sucking habit. Of the socioeconomic factors, father's education had a significant negative effect on the presence of the habit. The evidence provided by this investigation cannot support the view of psychoanalytic theory that continuation of the habit beyond the early childhood is due to emotional stress.

Catecholamines↗
PubMed1976

Effect of adrenergic blockade on gastric secretion altered by catecholamines in rats.

The effect of adrenergic blockade on gastric secretion altered by catecholamines was studied for 4 hr after injection in rats with chronic gastric fistulas. The alpha-adrenergic blockers phenoxybenzamine and phentolamine significantly inhibited the basal secretion of HCl and pepsin. Blockade of the beta-adrenergic receptors with propranolol did not change this secretion. Practolol in small doses slightly increased and in larger doses inhibited HCl out-put. Of the catecholamines, adrenaline and dopamine most markedly reduced HCl and pepsin secretion, while noradrenaline and isoprenaline had a weaker effect. Neither alpha- nor beta-adrenergic blockers prevented the inhibitory action of the catecholamines employed, but intensified the depression of the gastric secretion provoked by them. Adrenergic blockers inhibited secretion after catecholamines as well as basal secretion. This indicates that these two antagonistic groups of compounds act independently on the mechanism controlling gastric secretion. It is unlikely that this takes place indirectly through changes in the blood supply of the gastric mucosa.

Adrenergic alpha-Antagonists↗
PubMed2000

[Determination of catecholamine secreted from rat adrenal medulla by in vivo voltammetry].

In vivo voltammetry using carbon fiber electrodes was employed to determine the catecholamine secreted from the adrenal medulla. The basal level of catecholamine in the medulla was between 0.1 and 0.5 micromol/L, but it increased markedly up to 5 30 micromol/L when the gland was made ischemic. The spontaneous release of catecholamine from the medulla was observed in both normal and ischemia conditions, but the frequency and amplitude of spontaneous release were increased significantly by ischemia. This implied that the animal was under serious stress condition. The above results also show that acetylcholine can induce the secretion of catecholamine in a dose-dependent manner.

Acetylcholine↗
PubMed1975

[Secretion of catecholamines during pregnancy].

The excretion of total catecholamines in the urine of 18 females being in various stages of gestation was examined. These women did not take during their pregnancy any drug affecting the synthesis, storage, release, reuptake or metabolism of catecholamines. From the assessment of total catecholamines of 24 hours no statistically significant difference was observed as to the excretion of catecholamines as compared to the amount excreted by non-pregnant normal females.

Catecholamines↗
PubMed1975

[The role of disorders in the functions of the cerebral catecholamine system in the pathogenesis of chronic alcoholism].

The authors studied the functions of central and peripheral catecholamine systems in patients with chronic alcoholism. The influence of acute and chronic administration of alcohol was studied in experiments in animals as well as its discontinuation on the catecholamine structures in different areas of the CNS. The obtained data demonstrated that alcohol exerts a specific influence on the catecholamine brain systems which has typical regularities. An analysis of the acheived results permits to assume that the influence of alcohol on the catecholamine brain structures is one of the main links in the pathogenesis of chronic alcoholism.

Alcoholic Intoxication↗
PubMedDate not supplied

[DNA fusion in the presence of catecholamines and substances close to them in structure].

Using an Cphi-4A spectrophotometer (USSR), denaturation of DNA containing approximately 2% residual protein has been studied in the presence of catecholamines and their precursors: epinephrine, beta-3,4-dioxyphenylalanine, norepinephrine, 3,4-dimethoxyphenylethylamine, tyrosine, and phenylalanine. All these substances, excluding phenylalanine, induce positive excessive hyperchromicity (as compared to initial DNA). The correlation between this effect and molecular structures of the substances studied has been shown to exist. An increase of DNA hyperchromicity in the presence of catecholamines has been found to result from the oxygen presence in the aromatic rings of the catecholamines molecules. It is assumed that the interaction between the negative O-atoms in catecholamines and bivalent metal cations in the nucleoprotein complex weakens the DNA-protein binding. This leads to an additional disorientation due to the heat of nucleic acid bases, which were previously bound by the residual protein.

Catecholamines↗
PubMed2003

Inhibitory action of cilostazol, a phosphodiesterase III inhibitor, on catecholamine secretion from cultured bovine adrenal chromaffin cells.

The effect of cilostazol, a phosphodiesterase III inhibitor, on catecholamine secretion was examined using bovine adrenal chromaffin cells in culture. Catecholamine secretion evoked by acetylcholine was markedly inhibited by cilostazol. In contrast, 56 mM K+-evoked secretion was slightly inhibited by cilostazol. Cilostazol elevated the level of cyclic AMP in the cells. However, a cyclic AMP analog (dibutyryl cAMP) or an adenylate cyclase activator (forskolin) failed to inhibit secretion of catecholamine induced by acetylcholine. Cilostazol decreased the level of intracellular free Ca2+ stimulated by acetylcholine. Cilostazol thus inhibits secretion of catecholamine through its blocking action on Ca2+ movement in the adrenal chromaffin cells.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2002

[Perioperative anesthetic management for the excision of phaeochromocytoma complicated with catecholamine cardiomyopathy].

OBJECTIVE: To summarize experience of perioperative anesthetic management for patients undergone excision of pheochromocytoma and complicated with catecholamine cardiomyopathy. METHODS: Perioperative anesthetic management for surgical treatment of three cases of pheochromocytoma complicated with catecholamine cardiomyopathy was described and discussed according to literature reports. RESULTS: The catecholamine cardiomyopathy of the three cases presented with left ventricular hypertrophy, congestive cardiac failure and acute myocardial infarction. After removal of the pheochromocytoma under general anesthesia, a prolonged hypotension occurred in all of the three cases. In order to maintain stable hemodynamics, large dose of catecholamine was required after surgery. All of the three patients were survived and discharged. CONCLUSIONS: It is suggested that myocardial dysfunction may be another important factor for the prolonged hypotension after removal of the tumor. Meticulous preoperative assessment of heart function is of primary importance for the management of anaesthesia during surgical procedures.

Adrenal Gland Neoplasms↗