Academic literature on the topic 'Catecholamines Physiological effect'
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Journal articles on the topic "Catecholamines Physiological effect"
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Barnea, Eytan R., Rina Perlman, Hassan Fakih, Tova Bick, Shahar Kol, and Zeev Hochberg. "The role of catecholamines in estradiol and progesterone secretion by cultured explants and cells of human term placentae." Acta Endocrinologica 121, no. 6 (December 1989): 767–72. http://dx.doi.org/10.1530/acta.0.1210767.
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Abstract. The effects of physiological concentrations of the native catecholamines norepinephrine and epinephrine upon term placental hormonal function were examined by measuring estradiol and progesterone secretion by organ and cell culture systems. Results show that, in explants, both catecholamines caused a significant increase in the secretion of both sex steroids, p < 0.05. Estradiol secretion was blocked by the alpha and beta adrenergic receptors antagonists, phenoxybenzamine and propranolol, respectively, p < 0.05. Norepinephrine but not epinephrine dependent progesterone secretion was blocked by propranolol. In cells, epinephrine stimulated cyclic AMP generation and caused a 30% increase in estradiol secretion, p < 0.05. Both were abrogated by propranolol. Norepinephrine increased secretion by 25%, p < 0.05. This was inhibited by yohimbin and prazosin, alpha-1 and -2 receptors antagonists, respectively. In conclusion, the placenta in vitro is a target organ for catecholamines. The marked response of the explant system as compared with the marginal response of the cell culture system indicates that cell to cell contact/communication is required for full expression of catecholamine effect.
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Haas, M., and T. J. McManus. "Effect of norepinephrine on swelling-induced potassium transport in duck red cells. Evidence against a volume-regulatory decrease under physiological conditions." Journal of General Physiology 85, no. 5 (May 1, 1985): 649–67. http://dx.doi.org/10.1085/jgp.85.5.649.
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Duck red cells exhibit specific volume-sensitive ion transport processes that are inhibited by furosemide, but not by ouabain. Swelling cells in a hypotonic synthetic medium activates a chloride-dependent, but sodium-independent, potassium transport. Shrinking cells in a hypertonic synthetic medium stimulates an electrically neutral co-transport of [Na + K + 2 Cl] with an associated 1:1 K/K (or K/Rb) exchange. These shrinkage-induced modes can also be activated in both hypo- and hypertonic solutions by beta-adrenergic catecholamines (e.g., norepinephrine). Freshly drawn cells spontaneously shrink approximately 4-5% when removed from the influence of endogenous plasma catecholamines, either by incubation in a catecholamine-free, plasma-like synthetic medium, or in plasma to which a beta-receptor blocking dose of propranolol has been added. This spontaneous shrinkage resembles the response of hypotonically swollen cells in that it is due to a net loss of KCl with no change in cell sodium. Norepinephrine abolishes the net potassium transport seen in both fresh and hypotonically swollen cells. Moreover, cells swollen in diluted plasma, at physiological pH and extracellular potassium, show no net loss of KCl and water ("volume-regulatory decrease") unless propranolol is added. Examination of the individual cation fluxes in the presence of catecholamines demonstrates that activation of [Na + K + 2Cl] co-transport with its associated K/Rb exchange prevents, or overrides, swelling-induced [K + Cl] co-transport. These results, therefore, cast doubt on whether the swelling-induced [K + Cl] system can serve a volume-regulatory function under in vivo conditions.
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Keating, Damien J., and Chen Chen. "Activin A stimulates catecholamine secretion from rat adrenal chromaffin cells: a new physiological mechanism." Journal of Endocrinology 186, no. 2 (August 2005): R1—R5. http://dx.doi.org/10.1677/joe.1.06301.
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Activin A is a member of the transforming growth factor-β family and has known roles in the adrenal cortex, from which activin A is secreted. We aimed to find whether activin A induces secretion of catecholamines from chromaffin cells of the adrenal medulla, which neighbours the adrenal cortex in vivo. Using carbon fibre amperometry, we were able to measure catecholamine secretion in real-time from single chromaffin cells dissociated from the rat adrenal medulla. Activin A stimulated catecholamine secretion in a rapid and dose-dependent manner from chromaffin cells. This effect was fully reversible upon washout of activin A. The minimum dose at which activin A had a maximal effect was 2 nM, with an EC50 of 1.1 nM. The degree of secretion induced by activin A (2 nM) was smaller than that due to membrane depolarization caused by an increase in the external K+ concentration from 5 to 70 mM. No response to activin A was seen when Ca2+ channels were blocked by Cd2+ (200 μM). We conclude from these findings that activin A is capable of stimulating a robust level of catecholamine secretion from adrenal chromaffin cells in a concentration-dependent manner. This occurs via the opening of voltage-gated Ca2+ channels, causing Ca2+ entry, thereby triggering exocytosis. These findings illustrate a new physiological role of activin A and a new mechanism in the control of catecholamine secretion from the adrenal medulla.
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Mayerhofer, A., RW Steger, G. Gow, and A. Bartke. "Catecholamines stimulate testicular testosterone release of the immature golden hamster via interaction with alpha- and beta-adrenergic receptors." Acta Endocrinologica 127, no. 6 (December 1992): 526–30. http://dx.doi.org/10.1530/acta.0.1270526.
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Several lines of evidence suggest that catecholamines are involved in the regulation of the development of the testis. We have therefore investigated the ability of testicular parenchyma (decapsulated pieces of testes) from 18 to 20-day-old golden hamsters to respond to catecholaminergic stimuli in vitro. Norepinephrine and epinephrine, as well as the beta-receptor agonist isoproterenol and the alpha-adrenoreceptor agonist phenylephrine were able to significantly stimulate testicular testosterone production. Dopamine and serotonin were not effective. The stimulatory action of norepinephrine on testosterone production was dependent on the concentration. In incubations of testes with human chorionic gonadotropin (hCG) and norepinephrine, no synergistic effects on testosterone release were observed. The stimulatory effect of norepinephrine could be partially blocked by incubation with beta-receptor antagonist propranolol, or with alpha-receptor antagonist prazosin, while a combination of propranolol and prazosin completely inhibited the norepinephrine-induced testosterone production. Moreover, isoproterenol and phenylephrine in combination stimulated testosterone more than either drug did alone. Measurements of concentrations of norepinephrine and epinephrine in testicular homogenates revealed higher values for these catecholamines than in the plasma, implying that catecholamine levels in the interstitial spaces of the testis might be in the range of concentrations effectively stimulating testosterone production in vitro. This suggests that in the immature testis of the golden hamster, catecholamines acting through both alpha- and beta-adrenergic receptors may be potent physiological stimulators of testosterone production.
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Fulop, Tiberiu, and Corey Smith. "Physiological stimulation regulates the exocytic mode through calcium activation of protein kinase C in mouse chromaffin cells." Biochemical Journal 399, no. 1 (September 13, 2006): 111–19. http://dx.doi.org/10.1042/bj20060654.
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Adrenal medullary chromaffin cells release catecholamines and neuropeptides in an activity-dependent manner controlled by the sympathetic nervous system. Under basal sympathetic tone, catecholamines are preferentially secreted. During acute stress, increased sympathetic firing evokes release of both catecholamines as well as neuropeptides. Both signalling molecules are co-packaged in the same large dense core granules, thus release of neuropeptide transmitters must be regulated after granule fusion with the cell surface. Previous work has indicated this may be achieved through a size-exclusion mechanism whereby, under basal sympathetic firing, the catecholamines are selectively released through a restricted fusion pore, while less-soluble neuropeptides are left behind in the dense core. Only under the elevated firing experienced during the sympathetic stress response do the granules fully collapse to expel catecholamines and neuropeptides. However, mechanistic description and physiological regulation of this process remain to be determined. We employ electrochemical amperometry, fluid-phase dye uptake and electrophysiological capacitance noise analysis to probe the fusion intermediate in mouse chromaffin cells under physiological electrical stimulation. We show that basal firing rates result in the selective release of catecholamines through an Ω-form ‘kiss and run’ fusion event characterized by a narrow fusion pore. Increased firing raises calcium levels and activates protein kinase C, which then promotes fusion pore dilation until full granule collapse occurs. Our results demonstrate that the transition between ‘kiss and run’ and ‘full collapse’ exocytosis serves a vital physiological regulation in neuroendocrine chromaffin cells and help effect a proper acute stress response.
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Perry, S. F., R. Fritsche, and S. Thomas. "STORAGE AND RELEASE OF CATECHOLAMINES FROM THE CHROMAFFIN TISSUE OF THE ATLANTIC HAGFISH MYXINE GLUTINOSA." Journal of Experimental Biology 183, no. 1 (October 1, 1993): 165–84. http://dx.doi.org/10.1242/jeb.183.1.165.
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A variety of in vivo and in situ experiments were performed on the Atlantic hagfish (Myxine glutinosa) (i) to characterize the levels of circulating catecholamines during acute stresses, including hypoxia, anoxia or physical disturbance (air-exposure), and (ii) to evaluate the potential mechanisms of catecholamine release from the major sites of storage, the systemic heart and posterior cardinal vein (PCV). Adrenaline and noradrenaline were stored at roughly equivalent concentrations (approximately 20 microgram g-1) in cardiac tissue, whereas noradrenaline was the predominant catecholamine stored in the PCV (approximately 50 microgram g-1). The heart stored larger quantities of total catecholamines than did the PCV (approximately three times greater) owing to its larger mass and higher concentration of adrenaline. Exposure of chronically cannulated hagfish to acute hypoxia [mean water PO2 (PwO2)=1.4 kPa; 10.5 mmHg) for 30 min caused a significant decrease in arterial PO2 (from 11.5+/−1.3 kPa to 1.2+/−0.3 kPa) and arterial O2 content (from 3.9+/−0.3 ml 100 ml-1 to 0.9+/−0.2 ml 100 ml-1). The hypoxaemia was associated with a significant increase in plasma noradrenaline levels, whereas plasma adrenaline levels were unaffected. Exposure of uncannulated fish to anoxia (PwO2 approximately 0 kPa) or physical disturbance (15 min of air-exposure) also elicited pronounced increases in plasma noradrenaline levels (6–10 times) and, to a lesser extent, adrenaline levels (2–3 times). An in situ saline-perfused heart preparation was utilized in an attempt to elucidate the mechanism(s) underlying the stress-induced release of catecholamines from the chromaffin tissue of the heart and PCV. Non-specific cell membrane depolarization using 40 or 60 mmol l-1 K+ in the saline elicited a marked release of catecholamines, confirming the suitability of the preparation to assess specific physiological mechanisms of catecholamine release. Lower concentrations of K+ (15–20 mmol l-1) did not evoke catecholamine release, indicating that relatively minor elevation in plasma [K+], as might occur during hypoxia, is not a contributing factor. The cholinergic receptor agonist carbachol (10–5-10-4 mol kg-1) caused a significant release of catecholamines, yet the likelihood of a similar mechanism operating in vivo is doubtful because the hagfish heart is not thought to be innervated. Simulation of (i) internal hypoxaemia by perfusing with anoxic saline or (ii) physical disturbance by perfusing with relatively acidic saline (pH approximately 7.0) failed to elicit catecholamine release. Further, the elevation of perfusion (input) pressure to simulate a rise in venous blood pressure, as might occur during hypoxia or physical disturbance, was also without effect on release. The addition of pituitary extract (from Atlantic cod, Gadus morhua) to the inflowing saline caused a marked release of catecholamines from the chromaffin tissue.
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Fritsche, R., S. G. Reid, S. Thomas, and S. F. Perry. "SEROTONIN-MEDIATED RELEASE OF CATECHOLAMINES IN THE RAINBOW TROUT ONCORHYNCHUS MYKISS." Journal of Experimental Biology 178, no. 1 (May 1, 1993): 191–204. http://dx.doi.org/10.1242/jeb.178.1.191.
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The effects of serotonin (5-hydroxytryptamine; 5-HT) on catecholamine release from chromaffin tissue were investigated in the rainbow trout (Oncorhynchus mykiss) in vivo and in situ. Intra-arterial injections of serotonin in vivo caused dose-dependent (50–250 nmol kg-1) increases in both plasma noradrenaline and adrenaline levels. Pre-treatment of fish with the serotonergic receptor antagonist methysergide did not abolish these increases. An in situ saline-perfused head kidney preparation was developed and validated to study the potential direct effect of serotonin on catecholamine release. The chromaffin cells in the preparation showed a dose-dependent release of catecholamines in response to bolus injections of the cholinergic receptor agonist carbachol (10–7-10-4 mol kg-1). The carbachol-induced release of noradrenaline, but not of adrenaline, was reduced significantly when the nicotinic receptor antagonist hexamethonium (10–4 mol l-1) was present in the perfusion fluid. The removal of calcium from the perfusion fluid prevented the usual release of catecholamines evoked by carbachol. Bolus injections of serotonin (250 nmol kg-1) into the inflowing perfusion fluid resulted in significantly increased levels of adrenaline and noradrenaline in the outflowing perfusate. Addition of hexamethonium to the perfusion fluid did not abolish this serotonin-induced release of catecholamines. The serotonin-induced release of adrenaline, however, was abolished totally by the addition of methysergide. Serotonin is present in high concentrations (44.61+/−5.96 microgram g-1 tissue) in the anterior region of the posterior cardinal vein within the head kidney. Carbachol (10–5 mol kg-1) did not elicit release of the stored serotonin from the perfused head kidney preparation. We conclude that the chromaffin cells in the perfused trout head kidney preparation display characteristics similar to those of other vertebrates and that this preparation is a useful tool for studying the control of catecholamine release in fish. The results demonstrate that serotonin has a direct impact on the chromaffin cells by interacting with methysergide-sensitive receptors to initiate the release of adrenaline. The potential physiological role of serotonin on catecholamine release in trout is discussed.
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Maggs, D. G., and I. A. Macdonald. "Physiological and Symptomatic Responses to Postural Change in Non-Diabetic Subjects during Hypoglycaemia." Clinical Science 87, no. 2 (August 1, 1994): 193–99. http://dx.doi.org/10.1042/cs0870193.
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1. Insulin-induced hypoglycaemia is characterized by an autonomic disturbance which produces some of the symptoms of hypoglycaemia. How an additional autonomic stress like postural change may alter physiological responses and symptoms of hypoglycaemia is not known. In 10 healthy male subjects (mean age 24 years) we observed physiological and symptomatic responses to postural change during acute (20 min) and prolonged (60 min) hyperinsulinaemic (60 m-units min−1 m−2) hypoglycaemia (2.5 mmol/l) and euglycaemia (4.5 mmol/l), and placebo control (saline). 2. In all studies standing increased plasma catecholamines (adrenaline, P < 0.001; noradrenaline, P < 0.0001), blood pressure (P < 0.0001) and heart rate (P < 0.0001). Catecholamine responses to standing were augmented by acute hypoglycaemia (adrenaline, P < 0.005; noradrenaline, P < 0.01), but less so by prolonged hypoglycaemia (adrenaline, P < 0.05; noradrenaline, P < 0.05). Supine heart rate was higher before standing during prolonged hypoglycaemia (P < 0.05), but did not increase as much on standing when compared with acute hypoglycaemia and prolonged euglycaemia. 3. During acute hypoglycaemia, autonomic symptoms increased on standing, but during prolonged hypoglycaemia, in the presence of generally higher symptom scores, standing had no effect. Autonomic symptoms, with the exception of hunger, tended to decrease with time (P < 0.05) during prolonged hypoglycaemia. 4. To conclude, posture does modify the catecholamine and symptomatic responses to hypoglycaemia, but this effect is dependent on the duration of hypoglycaemia. Hypoglycaemia and hyperinsulinaemia had little or no effect on the cardiovascular responses to changing posture.
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Mader, S. L., C. L. Downing, and E. Van Lunteren. "Effect of age and hypoxia on beta-adrenergic receptors in rat heart." Journal of Applied Physiology 71, no. 6 (December 1, 1991): 2094–98. http://dx.doi.org/10.1152/jappl.1991.71.6.2094.
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Previous reports suggest that hypoxia downregulates cardiac beta-adrenergic receptors from young rats. Because aging alters response to stress, we hypothesized an age-related alteration in the response to hypoxia. Male Fischer-344 rats, aged 3 and 20 mo, were divided into control and hypoxic groups. The hypoxic rats were exposed to hypobaric hypoxia (0.5 atm) for 3 wk. After hypoxic exposure, body weight decreased, hematocrit increased, right ventricular weight increased, and left ventricular weight decreased in all animals. beta-Adrenergic receptor density declined after hypoxic exposure in the young but not in the older animals, a change that was confined to the left ventricle. beta-Adrenergic receptor density in the right ventricle was significantly lower in the older animals than in the young animals. Plasma catecholamines (norepinephrine, epinephrine) drawn after the animals were killed (stress levels) decreased in young rats and increased in old rats after the exposure to hypoxia. Hypoxia is a useful physiological stress that elucidates age-related changes in cardiac beta-adrenergic receptor and catecholamine regulation that have not previously been described.
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Pinz, Ilka, and Hans-O. Pörtner. "Metabolic costs induced by lactate in the toad Bufo marinus: new mechanism behind oxygen debt?" Journal of Applied Physiology 94, no. 3 (March 1, 2003): 1177–85. http://dx.doi.org/10.1152/japplphysiol.00131.2002.
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The mechanism of an increase in metabolic rate induced by lactate was investigated in the toad Bufo marinus. Oxygen consumption (V˙o 2) was analyzed in fully aerobic animals under hypoxic conditions (7% O2 in air), accompanied by measurements of catecholamines in the plasma, and was measured in isolated hepatocytes in vitro under normoxia by using specific inhibitors of lactate proton symport [α-cyano-4-hydroxycinnamate (CHC)] and sodium proton exchange (EIPA). The rise in metabolic rate in vivo can be elicited by infusions of hyperosmotic (previous findings) or isosmotic sodium lactate solutions (this study). Despite previous findings of reduced metabolic stimulation under the effect of adrenergic blockers, the increase inV˙o 2 in vivo was not associated with elevated plasma catecholamine levels, suggesting local release and effect. In addition to the possible in vivo effect via catecholamines, lactate induced a rise in V˙o 2 of isolated hepatocytes, depending on the concentration present in a weakly buffered Ringer solution at pH 7.0. No increase was found at higher pH values (7.4 or 7.8) or in HEPES-buffered Ringer solution. Inhibition of the Lac−-H+ transporter with α-CHC or of the Na+/H+ exchanger with EIPA prevented the increase in metabolic rate. We conclude that increasedV˙o 2 at an elevated systemic lactate level may involve catecholamine action, but it is also caused by an increased energy demand of cellular acid-base regulation via stimulation of Na+/H+ exchange and thereby Na+-K+-ATPase. The effect depends on entry of lactic acid into the cells via lactate proton symport, which is likely favored by low cellular surface pH. We suggest that these energetic costs should also be considered in other physiological phenomena, e.g., when lactate is present during excess, postexerciseV˙o 2.
Dissertations / Theses on the topic "Catecholamines Physiological effect"
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Klipp, Robert Carl. "Catecholamine Interactions with the Cardiac Ryanodine Receptor." PDXScholar, 2013. https://pdxscholar.library.pdx.edu/open_access_etds/1439.
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The cardiac ryanodine receptor (RyR2) is a Ca2+ ion channel found in the sarcoplasmic reticulum (SR), an intracellular membranous Ca2+ storage system. It is well known that a destabilization of RyR2 can lead to a Ca2+ flux out of the SR, which results in an overload of intracellular Ca2+; this can also lead to arrhythmias and heart failure. The catecholamines play a large role in the regulation of RyR2; stimulation of the Beta-adrenergic receptor on the cell membrane can lead to a hyperphosphorylation of RyR2, making it more leaky to Ca2+. We have previously shown that strong electron donors will inhibit RyR2. It is hypothesized that the catecholamines, sharing a similar structure with other proven inhibitors of RyR2, will also inhibit RyR2. Here we confirm this hypothesis and show for the first time that the catecholamines, isoproterenol and epinephrine, act as strong electron donors and inhibit RyR2 activity at the single channel level. This data suggests that the catecholamines can influence RyR2 activity at two levels. This offers promising insight into the potential development of a new class of drugs to treat heart failure and arrhythmia; ones that can both prevent the hyperphosphorylation of RyR2 by blocking the Beta;-adrenergic receptor, but can also directly inhibit the release of Ca2+ from RyR2.
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St, John-Allan Katherine Marie. "The effects of repeated daily cocaine administration on rat cardiac norepinephrine content." Scholarly Commons, 1990. https://scholarlycommons.pacific.edu/uop_etds/2199.
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Cocaine, the principal biologically active alkaloid of Erythroxylon coca, acts as both a local anesthetic agent and an indirect-acting sympathomimetic. These two very different activities make research on and subsequent interpretation of cocaine's multiplicity of varied effects difficult. Not surprisingly, investigations into the central effects of cocaine have yielded mixed results. However, there is a certain body of evidence which points to the euphoric and self-administrating properties of cocaine as appearing to involve the acute activation of central dopamine neuronal systems . With chronic cocaine use, central neurotransmitter alterations have been observed to occur. Dopamine depletion has been hypothesized to result from the overstimulation of these central neurons and the excessive synaptic metabolism of the neurotransmitter. This depletion may underlie the dysphoric aspects of cocaine abstinence and cravings. The potential cardiotoxicity of chronic cocaine abuse has been welldocumented. The possible mechanisms for this remain unclear. The present study was designed to evaluate the effects of repeated daily administration of two different doses (15 and 30 mg/kg/day) of cocaine on male Sprague-Dawely rat cardiac norepinephrine levels. Seven time intervals of sustained dosing were acute (1 dose), 1, 2, 4, 8, 12 and 20 weeks. The catecholamine levels of the whole heart were measured using an HPLC with electrochemical detection. Cardiac norepinephrine levels were unaffected by an acute injection of either cocaine dose. The lower dose elicited a slight increase of 5.8% while the higher dose evoked a small decrease at the 1 week administration period. At 2, 4, and 8 weeks cardiac neurotransmitter levels decreased an average of 13% compared to control values for both doses. At 20 weeks, the catecholamine content was similar to that of the controls. It was observed that cocaine in regard to cardiac norepinephrine content failed to elicit a dose-dependent response. The lower dose of 15 mg/kg/day evoked a greater reduction than that of the higher dose, especially at the 12 week time increment ( -23% and -11%, respectively) which was statistically significant. This is one of the first studies to investigate the effects that repeated daily cocaine dosing has on cardiovascular biochemical pharmacology. It is difficult to postulate the possible etiology and functionality of this decrease. Previous studies have indicated that cocaine might cause alterations in tyrosine hydroxylase activity, the rate-limiting enzyme in the biosynthesis of catecholamines which could be responsible for the reduction observed.
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Scobie, David Roger. "Short term effects of stress hormones on cell division rate in wool follicles : a thesis submitted in fulfilment of the requirements for the degree of Doctor of Philosophy." Title page, abstract and contents only, 1992. http://web4.library.adelaide.edu.au/theses/09PH/09phs421.pdf.
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Includes bibliographical references (leaves 183-207) A local intradermal technique using colchicine to estimate cell division rate in wool follicles is refined and used throughout the thesis. Statistical methods used to analyse data obtained with this method are described and discussed. The implications of the findings are of great significance to research into the influence of physiological changes on wool production, and suggest experiments should be conducted under controlled environmental conditions, with a minimum of stress imposed on the animals.
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Anderson, Dawn E. "Effects of caffeine on the metabolic and catecholamine responses to exercise in 5 and 28p0sC environments." Virtual Press, 1992. http://liblink.bsu.edu/uhtbin/catkey/833465.
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The influence of caffeine on the metabolic and catecholamine responses to mild exercise in a cold and a warm environment was studied in eight healthy males. The subjects performed 60 minutes of cycling at 50% VO2max in a cold environment (5°C and 70% relative humidity) and a warm environment (28°C and 50% relative humidity) 30 minutes after ingesting caffeine (5mg/kg body weight) or placebo (dextrose). Caffeine ingestion prior to exercise in the warm environment resulted in increased plasma epinephrine, with no effect on plasma norepinephrine. Neither lipid nor carbohydrate metabolism was altered by caffeine in the warm trial. Exercise in the cold environment (placebo) produced increased oxygen consumption and carbohydrate metabolism, decreased lipid metabolism, and no difference in plasma catecholamines compared with the warm-placebo trial. Responses to the combination of caffeine ingestion and the cold environment did not differ from cold-placebo responses in oxygen consumption or respiratory exchange ratio during the cycling bout. However, in the cold-caffeine trial plasma epinephrine was elevated. In addition, fat oxidation, serum free fatty acids, and serum glycerol were elevated in the cold-caffeine condition. Carbohydrate oxidation was depressed, while serum glucose and blood lactate were elevated in this trial. The results of this study indicate that caffeine increases plasma epinephrine; cold increases oxygen consumption and carbohydrate metabolism, while decreasing lipid metabolism; and the combination of caffeine and cold during exercise increases plasma epinephrine and lipid metabolism, but decreases carbohydrate metabolism.Human Performance Laboratory
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Lacombe, A. M. A. "Effects of circulating catecholamines on diving in ducks (Anas platyrhynchos)." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30724.
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Plasma catecholamines have been measured in chronically adrenalectomised (ADX) ducks, in chronically adrenal denervated ducks (DNX), in their respective sham-operated controls (SH-adx, SH-dnx) as well as in intact ducks after 3 minutes forced submergence. The results showed that 100% of the plasma Epinephrine (EP) and 40 to 80% of plasma Norepinephrine (NE) released during the dive came from the adrenal glands. 20 to 60% of plasma NE came from endings of the autonomic vascular sympathetic nerves which are strongly stimulated during diving.
Adrenal catecholamines were released by nerve activation only; non neural mechanisms did not play any role in their release.
Maximum dive times (MDT) in chronically adrenalectomised ducks (ADX: 5 min. 19 ± 20 sec.) and in chronically adrenal denervated ducks (DNX: 7 min. 10 ± 13 sec.) were significantly
lower than in sham-operated controls (respectively SH-adx: 9 min. 58 ± 45 sec., SH-dnx: 12 min. 10 ± 28 sec). Venous infusion of catecholamines in ADX and DNX during the dive increased MDT: MDT of DNX ducks perfused with catecholamines (9 min. 46 ± 20 sec.) were significantly higher than in DNX perfused with saline (7 min. 21 ± 17 sec.), but did not reach the MDT observed in the SH-dnx: other adrenal products must be involved. Diving heart rates of ADX and DNX (at 4 min. dive respectively: 62 ± 16 and 31 ± 2 beats/min.) were significantly
higher than in their sham-operated controls (23 ± 3 and 17 ± 2 beats/min.) . Blood pressure during the dive was signifi-
cantly lower in ADX and DNX (at 4 min. dive respectively: 93 ± 8 and 98 ± 4 mmHg) compared with their sham-operated controls (131 ± 12 and 118 ± 6 mmHg). Infusion of catecholamines in DNX raised blood pressure towards SH-dnx values, but there was no change in heart rate. PaO₂, CaO₂, pHa and lactate levels in DNX (respectively: 42 ± 2 mmHg, 4.5 ± 0.8 ml 02 /100ml blood, 7.233 ± 0.016, 3.1 + 0.3 mM) were significantly lower than in SH-dnx after 5 minutes submergence (53 ± 1 mmHg, 6.8 ± 0.4 ml 02 /100 ml blood, 7.301 ± 0.007, 4.8 + 0.4 mM). There was also a significant increase of plasma N⁺ (+ 5.4 ± 1.7 mEq/L) in SH-dnx after 5 minutes submergence, but this was not the case in DNX where it was K⁺ (+ 1.1 ± 0.4 mEq/L) which increased. This suggested that adrenal catecholamines increase tolerance to underwater submersion by enhancing peripheral vasoconstriction,
thus preserving the O₂ stores for the heart and brain. Moreover, they may affect the acid-base equilibrium during diving by increasing the activity of the Na⁺K⁺ pump and may also have a direct effect on the rate of glycogenolysis.
Preventing the actions of catecholamines on the heart by injecting beta-blocker during forced submersion did not decrease
MDT; however the cardiovascular response was markedly affected. During beta-blockade, diving heart rate rose steadily
from 24 ± 6 beats/minute after 2 minutes to 52 ± 8 beats/minute after 6 minutes diving. In contrast, heart rates remained close to the levels reached at 2 minutes (17 ± 3 and 19 ± 4 beats/minute) throughout the control dives.
Perfusion pressure and blood flow have been recorded simultaneously in both hind limbs of ducks. One leg was perfused
with different blood mixtures devoid of catecholamines (Test leg) and compared with the other, perfused with the ducks'own blood (autoperfused leg). This showed that hyper-capnia has a depressant effect on the neural component of the peripheral vasoconstriction. Perfusion of test legs with hypoxic-hypercapnic blood to which catecholamines were added, showed that circulating catecholamines are needed to increase peripheral vasoconstriction during diving.
In summary, during forced submergence circulating catecholamines,
released mainly by the adrenal glands, compensate
for the depressant action of hypercapnia on the neural component of peripheral vasoconstriction. Maintenance of this peripheral vasoconstriction during forced diving ensures that O₂ stores are not wasted on peripheral tissues, and this explains how MDT is prolonged.Science, Faculty of
Zoology, Department of
Graduate
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Ye, Xuemin. "The effect of water pH on swimming performance, blood pH, red cell pH, ion concentrations and catecholamine concentrations in plasma, and gill potential in rainbow trout (Salmo gairdneri)." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/26676.
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The effect of transferring fish from water at pH 7.0 to either more acid or more alkaline conditions was to reduce the maximum critical velocity of the fish. In water of pH 4.0, 5.0, and 10.0, the maximum critical velocity was only 54.5%, 66.5%, and 61% respectively of that recorded for fish in the water of pH 7.0. Thus, both acid and alkaline conditions in the water reduce the aerobic swimming capacity of trout.
Exposure to acid conditions increased mucus secretion and this was associated with an increase in coughing and breathing frequency in resting fish. Coughing rate increased from 41/hr to 592/hr; and respiration frequency increased from 81/min to 104/min when fish were transferred from water at pH 7.0 to water at pH 4.0.
In comparing fish exposed to acid and alkaline waters, the results indicates that fish have a greater capacity to regulate blood pH in acid than in alkaline conditions.
The gill potential was strongly dependent on water pH, being negative in neutral water, but positive in acid water and more negative in alkaline solution. Catecholamine levels increased significantly during acid exposure, but were not altered during alkaline exposure. The increasing catecholamine levels appeared at different time periods in different fish during acid exposure and seemed to be associated with the death of the fish.
Na⁺ and C1⁻ ion concentrations in plasma decreased significantly after 24hrs of acid exposure, but did not change significantly in alkaline water. This may indicate that ionoregulatory disturbance in plasma is one of the reasons for the decrease in the maximum critical velocity in acid water, but not in alkaline water.Science, Faculty of
Zoology, Department of
Graduate
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Can, Adem 1977. "Effects of experience and novelty on sexual behavior and associated neuronal activity in male Japanese quail." 2008. http://hdl.handle.net/2152/17780.
Full textAbstract:
In many behavioral paradigms, repeated exposures to a particular stimulus or event results in lower immediate early gene (IEG) expression. First, it was investigated if a similar reduction in IEG expression in the brain areas controlling male sexual behaviors would be observed after repeated copulation experiences in male Japanese quail. The results showed that IEG expression, as assessed by egr-1 immunoreactivity, did not increase in the POM, the BST, or the PAG after a copulation episode in highly sexually experienced subjects. One possibility was that the pattern of initial elevation of neuronal activity during the early trials of sexual interactions and the lack of increase in IEG expression later was associated with the novelty of sexual stimuli. While early exposures to certain stimuli constitute a new learning experience, the significance of such exposures would be lower as the level of experience increases. It was hypothesized that the introduction of a novel stimulus would increase the IEG expression in the POM, the BST and the PAG of experienced subjects. To evaluate this prediction, subjects were tested to see if they learn to respond to females decorated with distinct novel artificial cues after repeated exposures. The results showed that control subjects that did not have sexual experiences with decorated females discriminate against such females and directed their responses to normal females. Trained subjects did not show such preferences and responded to both types of females. In the next experiment, contrary to the prediction, no increase in IEG expression was observed after the introduction of the novel stimulus. This might be due to lower sexual motivation in subjects exposed to novel females. Effects of sexual experience were also tested in the catecholaminergic system. It was hypothesized that TH innervation in the POM and the BST would increase as a result of sexual experience. IEG expression in the catecholaminergic areas was predicted to be lower after repeated sexual experiences. The results showed no effect of experience in either tyrosine hydroxylase (TH) innervation, nor TH-egr-1 colocalization. These findings suggest that experience-related changes in male sexual behavior may be mediated by a different neurotransmitter system.text
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Young, Jennifer Charity. "Supplemental vitamin B-6 and endurance exercise effects on plasma catecholamines of trained male cyclists." Thesis, 1996. http://hdl.handle.net/1957/27440.
Full textAbstract:
This study examined the effect of vitamin B-6 supplementation and exhaustive
submaximal exercise on plasma catecholamine concentrations, and the relationship
between plasma catecholamines and fuel use, heart rate and oxygen consumption. Five
trained men (age= 18-35 years; V0₂max=53 ml 0₂/kg/min.) participated in two controlled
dietary periods that were identical except for the addition of 20 mg/d pyridoxine (PN)
supplementation during the second period. On the seventh morning of each period, fasted
subjects exercised to exhaustion on a cycle ergometer at 74.5% ± 7.8 V0₂max. Blood
was drawn pre-exercise (twice), 60 minutes into exercise, immediately post-exercise and
60 minutes post-exercise. Plasma was analyzed for norepinephrine, epinephrine, glucose,
pyridoxal 5'-phosphate (PLP), lactic acid, glycerol and free fatty acids (FFA). Heart rate
and oxygen consumption were measured pre-exercise and at 10-minute intervals during
exercise. Mean plasma PLP concentration was significantly higher during the
supplemented versus the nonsupplemented trial at all time points. There were no
statistically significant differences in mean plasma catecholamine concentrations or mean
plasma fuel concentrations between the nonsupplemented and supplemented trials at any of
the time points examined. There were significant changes in the mean plasma
concentrations of norepinephrine, lactic acid, glycerol and FFA over time in both trials.
Respiratory exchange ratios (R) were higher during the supplemented trial compared to the
nonsupplemented trial, but the differences did not attain statistical significance. There
were no significant differences in mean exercise times to exhaustion or mean heart rates
between the trials. The overall mean oxygen consumption during exercise was
consistently higher during the supplemented versus the nonsupplemented trial and the
difference attained significance (p=0.016) at one time point (10 min.). The mean oxygen
consumption during rest was lower during supplementation versus nonsupplementation,
but the difference was not statistically significant. The percent plasma volume change
(PVC) was significantly greater at post-exercise, relative to pre-exercise, during the
supplemented versus the nonsupplemented trial. The percent PVC also increased
significantly over time during the supplemented but not the nonsupplemented trial. These
results suggest that 20 mg/d of vitamin B-6 supplementation does not effect plasma
catecholamine concentrations, fuel utilization or heart rate at rest or during submaximal
exercise to exhaustion. The results may suggest a higher oxygen consumption during
exhaustive exercise after PN supplementation.Graduation date: 1996
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Scobie, David Roger. "Short term effects of stress hormones on cell division rate in wool follicles / by David Roger Scobie." Thesis, 1992. http://hdl.handle.net/2440/21634.
Full textAbstract:
Includes bibliographical references (leaves 183-207)ix, 207 leaves : ill. (some col.) ; 30 cm.
A local intradermal technique using colchicine to estimate cell division rate in wool follicles is refined and used throughout the thesis. Statistical methods used to analyse data obtained with this method are described and discussed. The implications of the findings are of great significance to research into the influence of physiological changes on wool production, and suggest experiments should be conducted under controlled environmental conditions, with a minimum of stress imposed on the animals.
Thesis (Ph.D.)--University of Adelaide, Dept. of Animal Sciences, 1992
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Hikoi, Hirotaka. "The effects of opioid receptor antagonism on plasma catecholamines and fat metabolism during prolonged exercise above or below lactate threshold in males." Thesis, 1999. http://hdl.handle.net/1957/33383.
Full textBooks on the topic "Catecholamines Physiological effect"
1
Nira, Ben-Jonathan, Bahr Janice M, and Weiner Richard I, eds. Catecholamines as hormone regulators. New York: Raven Press, 1985.
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2
International Symposium on Catecholamines and Other Neurotransmitters in Stress (7th 1999 Smolenice, Slovakia). Stress: Neural, endocrine, and molecular studies. London: Taylor & Francis, 2002.
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3
Stress, catecholamines, and cardiovascular disease. New York: Oxford University Press, 1995.
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4
Annica, Dahlström, Belmaker Robert H, and Sandler Merton, eds. Progress in catecholamine research: Proceedings of the Sixth International Catecholamine Symposium, held in Jerusalem, Israel, June 14-19, 1987. New York: Liss, 1988.
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5
The catecholaminergic innervation of the rat amygdala. Berlin: Springer, 1998.
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Vaudry, Hubert. Phylogenetic aspects of neuropeptides: From invertebrates to humans. Edited by New York Academy of Sciences. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2010.
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International, Symposium on Catecholamines and Other Neurotransmitters in Stress (6th 1995 Smolenice Slovakia). Stress: Molecular genetic and neurobiological advances : proceedings of the Sixth International Symposium on Catecholamines and Other Neurotransmitters in Stress, Smolenice Castle, Slovakia, June 19-24 1995. Australia: Harwood Academic Publishers, 1996.
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International Symposium on Catecholamines and Other Neurotransmitters in Stress (5th 1991 Smolenice, Slovakia). Stress: Neuroendocrine and molecular approaches : proceedings of the Fifth International Symposium on Catecholamines and Other Neurotransmitters in Stress, Smolenice Castle, Czechoslovakia, 24-29 June, 1991. Philadelphia: Gordon and Breach Science Publishers, 1992.
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International Symposium on Catecholamines and Other Neurotransmitters in Stress (9th 2007 Smolenice Castle, Slovakia). Stress, neurotransmitters, and hormones: Neuroendocrine and genetic mechanisms. Edited by Kvetňanský Richard, Ústav experimentálnej endokrinólogie (Slovenská akadémia vied), and National Institutes of Health (U.S.). Malden: Wiley-Blackwell, 2008.
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P, Nijkamp F., Wied David de 1925-, and Jong W. de, eds. Hypertension, brain catecholamines and peptides. Elsevier, 1989.
Find full textBook chapters on the topic "Catecholamines Physiological effect"
1
Kayabekir, Murat. "Neurophysiology of Basic Molecules Affecting Sleep and Wakefulness Mechanisms, Fundamentals of Sleep Pharmacology." In Sleep Medicine and the Evolution of Contemporary Sleep Pharmacotherapy [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.100166.
Full textAbstract:
As part of the biological rhythm, the human brain has a healthy functioning with the ability to differentiate between day and night hours in any given day (sleep rhythm, life rhythm). From the control of hormone levels to muscle tonus, from the regulation of respiratory rate to the content of our thoughts, sleep has an impact on all bodily and cognitive functions. It is not surprising to see such effects of sleep on the body as it leads to significant changes in the electrical activity of the brain in general. Electrical signal changes in the brain (sleep-wakefulness rhythm) are regulated by neurohormonal molecules and their receptors in the body. Neurotransmitters that control sleep and wakefulness can be listed as “Glutamate, Acetylcholine, Histamine, Norepinephrine and GABA”. Main hormones are: Melatonin, Corticotropin Releasing Hormone (CRH), cortisol, prolactin, Growth Hormone (GH), Insulin like Growth Factor (IGF-1, Somatomedin-C), Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH), progesterone, estrogen, testosterone, catecholamines, leptin and neuropeptide Y″. The effects of pharmacological agents on sleep and wakefulness cycles are materialized through the following molecules and their receptors: Hypnotics (GABA A agonists, benzodiazepines, gabapentin, tiagabine), sedative antidepressants (tricyclic antidepressants, trazadone, mitrazapine), antihistamines, medications used for the treatment of sleeplessness (melatonin and melatonin analogues), amphetamine (most commonly used stimulant), secretion of monoamines (dopamine), non-amphetamine stimulants used in the treatment of hypersomnia and narcolepsy (modafinil, bupropion, selegiline, caffeine) and other substances (alcohol, nicotine, anesthetics). To the extent we can conceptualize the physiological mechanisms of these basic molecules listed above and the regions they affect, we can appreciate the effects of these substances on sleep physiology and sleep disorders.
Conference papers on the topic "Catecholamines Physiological effect"
1
Kirenskaya, A. V., M. A. Gruden, V. Yu Novototsky-Vlasov, A. M. Ryabova, and Z. I. Storozheva. "EFFECT OF VAL158MET CATECHOLAMINE O-METHYLTRANSFERASE GENE POLYMORPHISM ON INTERHEMISPHERIC ASYMMETRY IN ANTISACCADE TASK." In MODERN PROBLEMS IN SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTIONS. NPG Publishing, 2019. http://dx.doi.org/10.24108/5-2019-confnf-38.
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