Catecholamine Mobilization Research Articles

Influence of supraphysiological cortisol manipulation on predator avoidance behaviors and physiological responses to a predation threat in a wild marine teleost fish.

The stress axis in teleost fish attempts to maintain internal homeostasis in the face of allostatic loading. However, stress axis induction has been associated with a higher predation rate in fish. To date, the physiological and behavioral factors associated with this outcome are poorly understood. The purpose of the present study was to investigate the impact of experimental cortisol elevation on anti-predator behavior and physiological responses to predator presence. We hypothesized that semi-chronic cortisol elevation would increase susceptibility to predation by increasing stress-induced risk-taking behaviors. To test this hypothesis, schoolmaster snapper were given cocoa butter implants without cortisol (sham) or with cortisol (50 mg/kg body weight) and tethered to cover. Fish were exposed to either a lemon shark or control conditions for 15-min. Space use and activity were recorded throughout and fish were terminally sampled for blood. Cortisol implantation, relative to shams, resulted in higher blood glucose and plasma cortisol concentrations with a lower plasma lactate concentration. Shark exposure, relative to controls, elicited higher blood glucose and lactate concentrations but had no effect on plasma cortisol concentration. No interactions were detected between shark exposure and cortisol treatment for any physiological trait. Behavioral metrics, including shelter use and activity, were unaffected by either cortisol implantation or shark exposure. Physiological responses to cortisol implantation likely resulted from enhanced gluconeogenic activity, whereas alterations under predator exposure may have been the product of catecholamine mobilization. Further work should address context-specific influences of stress in mediating behavioral responses to predation.

Fish in hot water: Hypoxaemia does not trigger catecholamine mobilization during heat shock in rainbow trout (Oncorhynchus mykiss)

Rainbow trout (Oncorhynchus mykiss) exposed to an acute heat shock (1h at 25°C after raising water temperature from 13°C to 25°C over 4h) mount a significant catecholamine response. The present study investigated the proximate mechanisms underlying catecholamine mobilization. Trout exposed to heat shock in vivo exhibited a significant reduction in arterial O2 tension, but arterial O2 concentration was not affected by heat shock, nor was catecholamine release during heat shock prevented by prior and concomitant exposure to hyperoxia (to prevent the fall in arterial O2 tension). Thus, catecholamine mobilization probably was not triggered by impaired blood O2 transport. Heat-shocked trout also exhibited an elevation of arterial CO2 tension coupled with a fall in arterial pH, but these factors are not expected to trigger catecholamine release. The changes in blood O2 and CO2 tension occurred despite a significant hyperventilatory response to heat shock. Future studies should investigate whether catecholamine mobilization during heat shock in rainbow trout is triggered by a specific effect of high temperature activating the sympathetic nervous system via a thermosensitive transient receptor potential channel.

Low social status impairs hypoxia tolerance in rainbow trout (Oncorhynchus mykiss)

In the present study, chronic behavioural stress resulting from low social status affected the physiological responses of rainbow trout (Oncorhynchus mykiss) to a subsequent acute stressor, exposure to hypoxia. Rainbow trout were confined in fork-length matched pairs for 48-72h, and social rank was assigned based on behaviour. Dominant and subordinate fish were then exposed individually to graded hypoxia (final water PO(2), PwO(2)=40Torr). Catecholamine mobilization profiles differed between dominant and subordinate fish. Whereas dominant fish exhibited generally low circulating catecholamine levels until a distinct threshold for release was reached (PwO(2)=51.5Torr corresponding to arterial PO(2), PaO(2)=24.1Torr), plasma catecholamine concentrations in subordinate fish were more variable and identification of a distinct threshold for release was problematic. Among fish that mobilized catecholamines (i.e. circulating catecholamines rose above the 95% confidence interval around the baseline value), however, the circulating levels achieved in subordinate fish were significantly higher (459.9±142.2nmolL(-1), mean±SEM, N=12) than those in dominant fish (130.9±37.9nmolL(-1), N=12). The differences in catecholamine mobilization occurred despite similar P(50) values in dominant (22.0±1.5Torr, N=6) and subordinate (22.1±2.2Torr, N=8) fish, and higher PaO(2) values in subordinate fish under severely hypoxic conditions (i.e. PwO(2)<60Torr). The higher PaO(2) values of subordinate fish likely reflected the greater ventilatory rates and amplitudes exhibited by these fish during severe hypoxia. At the most severe level of hypoxia, subordinate fish were unable to defend arterial blood O(2) content, which fell to approximately half (0.60±0.13mLO(2)g(-1) haemoglobin, N=9) that of dominant fish (1.08±0.09mLO(2)g(-1) haemoglobin, N=9). Collectively, these data indicate that chronic social stress impacts the ability of trout to respond to the additional, acute stress of hypoxia.

NON-RESPONDING OF THE SYMPATHOADRENAL SYSTEM - A DIAGNOSTIC SIGN FOR THE OVERTRAINING SYNDROME 446

The goal of this study was to investigate the exercise induced response of the sympathoadrenal system during a period of overtraining. A parasympathicotonic overtraining syndrome was generated in 6 experienced long-distance runners by increase of exercise volume and intensity over 7 weeks. Weekly clinical investigations detected normal state (N), overload (OL) and overtraining syndrome (OT). Before, during and after exhaustive exercise tests on a treadmill cortisol and free plasma-catecholamines were determined. The ratio between maximum and basal concentrations (catecholamine mobilization factor - CMF) served as a criterion for the capacity of the sympathoadrenal system to secrete catecholamines. Insulin-like growth factor I (IGF I) was used to detect inadequate caloric or carbohydrate intake. Both factors lower resting levels. Results are presented by medians, differences are detected by non-parametric tests. CMF for norepinephrine (NE) was significantly lowered from 15.1 (N) and 28.0 (OL) to 3.9 (OT; p<0.01), for epinephrine (E) from 23.1 (N) and 31.5 (OL) to 2.3 (OT; p<0.05). IGF I (N 306 ng/ml) was reduced in OL (267 ng/ml) and OT (221 ng/ml), although no weight reduction was detected. The exercised-induced rise of cortisol (N 30.7%) was increased in OL(62.6%) and lowered in OT (18.6%). Conclusions: 1) The lowered exercise induced CMF and inadequate glucocorticoid response in a state of carbohydrate deficiency indicate an exhaustion of the sympathoadrenal and adrenocortical secretion capacity. 2) CMF seems to be an useful parameter in the training-concomitant monitoring of athletes' workload as well as for the diagnosis of OT. 3) The inverse relationship between intensity and CMF points out that parasympathicotonic OT is less generated by the absolute amount of training volume than by training intensity.

Relationship between blood O2 content and catecholamine levels during hypoxia in rainbow trout and American eel.

Plasma catecholamine levels and arterial blood respiratory variables were monitored in rainbow trout (Oncorhynchus mykiss) and American eel (Anguilla rostrata) acutely exposed (30 min) to graded levels of external hypoxia [water PO2 (PWO2) 20-90 Torr]. The experiments were designed to evaluate the factors controlling catecholamine mobilization in hypoxic fish and to elucidate the basis of marked interspecific differences. In trout, plasma catecholamine levels were unchanged when PWO2 remained above 50 Torr but increased markedly when PWO2 was lowered below this value; the predominant catecholamine released into the circulation was epinephrine. In eel, there was no such obvious PWO2 threshold for catecholamine release although plasma levels were consistently elevated above baseline only at PWO2 less than 35 Torr. The magnitude of the catecholamine release in eel was approximately an order of magnitude less than in trout. Unlike in trout, there was no increase in the plasma epinephrine-to-norepinephrine concentration ratio. During hypoxia, the relationship between arterial blood PO2 (PaO2) and PWO2 was similar in both species and thus could not explain the differences in the PWO2 thresholds for catecholamine release. In trout, the calculated PaO2 thresholds for catecholamine release were 25.3 (epinephrine) and 20.5 Torr (norepinephrine) whereas in eel the corresponding values were 12.5 and 11.6 Torr, respectively. These PaO2 thresholds were in good agreement with the in vivo values for PaO2 at half-maximal hemoglobin (Hb)-O2 saturation (P50) for trout and eel blood of 22.9 and 11.1 Torr, respectively. Thus both species displayed essentially equivalent catecholamine release thresholds when expressed in terms of arterial blood O2 content corresponding to approximately 45-60% Hb-O2 saturation.

The effects of endogenous or exogenous catecholamines on blood respiratory status during acute hypoxia in rainbow trout (Oncorhynchus mykiss).

An extracorporeal circulation of rainbow trout (Oncorhynchus mykiss) was utilized to continuously monitor the rapid and progressive effects of endogenous or exogenous catecholamines on blood respiratory/acid-base status, and to provide in vivo evidence for adrenergic retention of carbon dioxide (CO2) in fish blood (cf. Wood and Perry 1985). Exposure of fish to severe aquatic hypoxia (final PwO2 = 40-60 torr; reached within 10-20 min) elicited an initial respiratory alkalosis resulting from hypoxia-induced hyperventilation. However, at a critical arterial oxygen tension (PaO2) between 15 and 25 torr, fish became agitated for approximately 5 s and a marked (0.2-0.4 pH unit) but transient arterial blood acidosis ensued. This response is characteristic of abrupt catecholamine mobilization into the circulation and subsequent adrenergic activation of red blood cell (RBC) Na+/H+ exchange (Fievet et al. 1987). Within approximately 1-2 min after the activation of RBC Na+/H+ exchange by endogenous catecholamines, there was a significant rise in arterial PCO2 (PaCO2) whereas arterial PO2 was unaltered; the elevation of PaCO2 could not be explained by changes in gill ventilation. Pre-treatment of fish with the alpha-adrenoceptor antagonist phentolamine did not prevent the apparent catecholamine-mediated increase of PaCO2. Conversely, pre-treatment with the beta-adrenoceptor antagonist sotalol abolished both the activation of the RBC Na+/H+ antiporter and the associated rise in PaCO2, suggesting a causal relationship between the stimulation of RBC Na+/H+ exchange and the elevation of PaCO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Branchial Ion and Acid-Base Transfer in Freshwater Teleost Fish: Environmental Hyperoxia as a Probe

In freshwater fish, linked ion and acid-base fluxes across the gills are dynamically manipulated to regulate internal acid-base status in the face of environmental challenges. Relevant theory, methodology, and a synthesis of current ideas are presented, based on experiments with hypercapnia, low pH, acid and base infusion, temperature change, enforced exercise, toxicants, and other challenges. Hyperoxia may be the most useful of these treatments, for it is devoid of confounding factors caused by other probes-high water [H⁺], catecholamine mobilization, and metabolic rate changes. In rainbow trout, hyperoxia (inspired \documentclass{aastex} \usepackage{amsbsy} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{bm} \usepackage{mathrsfs} \usepackage{pifont} \usepackage{stmaryrd} \usepackage{textcomp} \usepackage{portland,xspace} \usepackage{amsmath,amsxtra} \usepackage{wasysym} \pagestyle{empty} \DeclareMathSizes{10}{9}{7}{6} \begin{document}${\mathrm{P_{O_{2}}}[{\mathrm{P_{IO_{2}}}}] > 500 {\mathrm{Tor...

Control of Catecholamine ReleaseIn VivoandIn Situin the Atlantic Cod(Gadus Morhua) During Hypoxia

ABSTRACTWe have characterized the elevation of circulating catecholamines in the intact Atlantic cod (Gadus morhua) during graded acute (30 min) hypoxia. The potential mechanisms contributing to the mobilization of catecholamines during hypoxia were then assessed in vivo using nerve sectioning and pharmacological techniques and in situ using a perfused head kidney preparation.Pre-branchial plasma adrenaline concentrations were significantly elevated at all levels of aquatic hypoxia utilised [water PO2 (PwO2) = 10 kPa (75 mmHg), 7.3kPa (55 mmHg) or 5.3 kPa (40mmHg)], whereas noradrenaline levels did not increase significantly in these particular experiments in which PwO2 was lowered gradually over a 30 min period. All subsequent experiments were performed using a more rapid induction of hypoxia to reach a final PwO2 of 5.3 kPa within the first 5-10 min of exposure. Blood withdrawn from pre-branchial (ventral aortic) and post-branchial (dorsal aortic) cannulae after 30 min revealed pronounced reductions in PO2 and O2 content (CO2) as well as elevated pH. These data support the notion that blood acidosis is not a prerequisite for catecholamine mobilization during hypoxia. Bilateral sectioning of spinal nerves 1–4 innervating the head kidney prevented the elevation of noradrenaline during rapidly induced hypoxia, but had no effect on the rise in plasma adrenaline concentration. After each experiment, fish were exposed to air for 3 min to induce severe stress. Plasma catecholamine levels were significantly reduced during stress, suggesting that the sectioning of the spinal nerves to the head kidney was indeed effective. These results indicated that mechanisms other than neural stimulation of head kidney chromaffin tissue were contributing to the rise in plasma adrenaline level during hypoxia. Neuronal overflow into the circulation, however, was an unlikely possibility since the increase of adrenaline could not be prevented by treating denervated fish with bretylium (an inhibitor of catecholamine release from adrenergic nerve terminals). These data suggested a local direct stimulatory effect of blood hypoxaemia on adrenaline release from chromaffin tissue. This hypothesis was confirmed using a blood-perfused head kidney preparation in which hypoxaemia markedly stimulated adrenaline overflow into the effluent blood. Further experiments using a Ringer-perfused head kidney preparation were designed to test the hypothesis that blood catecholamine levels in vivo are, in part, controlled by the concentration of catecholamines in the blood entering the head kidney. The results show conclusively that overflow of a particular catecholamine during cholinergic stimulation of the head kidney is controlled independently by the inflowing concentration of that catecholamine. We suggest that this mechanism of ‘auto-inhibition’ of catecholamine overflow is a functional negative feedback mechanism involved in the control of plasma catecholamine levels in the cod.

Control and coordination of gas transfer in fishes

Recent developments pertaining to the control and coordination of gas transfer in fishes have been reviewed. Gill ventilatory water flow can markedly affect blood respiratory and blood acid–base status. Although arterial oxygen content traditionally has been considered the predominant factor controlling ventilation, we present evidence for additional involvement of both blood acid–base status and circulating catecholamines. An analysis of the independent effects of blood oxygen content, acid–base status, and catecholamines in controlling ventilation is confounded by the interrelationships among these variables. It is likely, however, that each factor is involved to some extent in ventilatory control in fishes. Blood oxygen transport is affected by the carrying capacity of the blood and red blood cell chemical status. Blood oxygen-carrying capacity is increased during periods of stress by adrenergic release of red blood cells from the spleen. Concurrently, adrenergic stimulation of red blood cell Na+–H+ exchange, reduction of intracellular nucleoside triphosphates, swelling of red blood cells, and respiratory alkalosis all tend to increase oxygen affinity and capacity of hemoglobin. Results of recent in vivo studies indicate that adrenergic inhibition of plasma bicarbonate dehydration may contribute to the respiratory acidosis after exhaustive exercise in fishes. Evidence is presented to show that hypoxemia, rather than blood acidosis per se, is the proximate stimulus for catecholamine mobilization during periods of stress in fishes.

Evidence that hypoxemia promotes catecholamine release during hypercapnic acidosis in rainbow trout ( Salmo gairneri)

The concentrations of plasma catecholamines, epinephrine and norepinephrine, were monitored in rainbow trout ( Salmo gairdneri) after acute (30 min) exposure to various levels of external hypercapnia water P CO 2 (Pw CO 2) = 0–11.3 Torr) under normoxic (water P O 2 (Pw O 2) = 153 ± 1.1 Torr) or hyperoxic Pw O 2 = 653 ± 27.0 Torr) conditions. Whole blood pH decreased to a similar extent as a function of external carbon dioxide tensions in both the normoxic and hyperoxic hypercapnic groups. Arterial oxygen content, however, declined only during normoxic hypercapnia. Similarly, plasma catecholamines (primarily epinephrine) increased only during normoxic hypercapnia in proportion to the severity of the whole blood acidosis. Epinephrine levels were elevated 10-fold from 0.70 ± 0.06 nM to 7.06 ± 3.7 nM at the highest concentration of external CO 2 (11.3 Torr) whereas norepinephrine incre ased 3-fold from 0.56 ± 0.07 nM to 1.62 ± 0.40 nM. The absence of catecholamine release into the circulation during hyperoxic hypercapnia was not due to inhibition of the ‘catecholamine-releasing process’ by abnormally elevated arterial oxygen tensions (Pa O2 = ≈400 Torr) because acutely anaemic and thus hypoxemic fish (haematocrit = 4.9 ± 0.7%) displayed identical elevations of plasma catecholamines under both normoxic and hyperoxic conditions. The results of these experiments demonstrate that arterial hypoxemia, rather then blood acidosis per se, is the proximate stimulus causing catecholamine mobilization in rainbow trout during short-term environmental hypercapnia.

Adrenergic Analysis of Extracellular and Intracellular Lactate and H+Dynamics after Strenuous Exercise in the Starry Flounder Platichthys stellatus

Adrenergic blockade with a selective a antagonist (yohimbine) and β antagonist (propranolol) was employed to test whether catecholamine mobilization was involved in lactate and acidic equivalents (H⁺) dynamics following strenuous exercise in chronically cannulated starry flounder. In control fish (not blocked) sampled repetitively for 8 h after exercise, arterial [lactate] remained characteristically low (<2 mmol/liter), and acid-base, hematological, and glucose changes were similar to those seen in other studies. Neither α nor β blockade immediately after exercise nor β blockade before exercise had significant influence on most responses, though hyperglycemia was inhibited by α blockade and prolonged by β blockade. Blood [lactate] was also marginally elevated, and red blood cell (RBC) swelling was reduced by β antagonism. A second series involving single-terminal sampling of cannulated flounder demonstrated that RBC intracellular pH (pHi), [NTP], and arterial PO₂ remained unchanged in the face of severe ...

Brain injury and early catecholamine mobilization

Brain injury and early catecholamine mobilization

Adenine Nucleotides and Catecholamine Mobilization in Adrenal Medulla and in Sympathetic Nerves

Acta Physiologica ScandinavicaVolume 74, Issue s1 p. 40A-41A Adenine Nucleotides and Catecholamine Mobilization in Adrenal Medulla and in Sympathetic Nerves P. Hedqvist, P. Hedqvist Department of Physiology, Karolinska Institutet, Stockholm, SwedenSearch for more papers by this authorH. Lagercrantz, H. Lagercrantz Department of Physiology, Karolinska Institutet, Stockholm, SwedenSearch for more papers by this authorL. Stjärne, L. Stjärne Department of Physiology, Karolinska Institutet, Stockholm, SwedenSearch for more papers by this author P. Hedqvist, P. Hedqvist Department of Physiology, Karolinska Institutet, Stockholm, SwedenSearch for more papers by this authorH. Lagercrantz, H. Lagercrantz Department of Physiology, Karolinska Institutet, Stockholm, SwedenSearch for more papers by this authorL. Stjärne, L. Stjärne Department of Physiology, Karolinska Institutet, Stockholm, SwedenSearch for more papers by this author First published: August 1968 https://doi.org/10.1111/j.1748-1716.1968.tb04313.xCitations: 4AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume74, Issues1August 1968Pages 40A-41A RelatedInformation

THE RELATION OF ENDOGENOUS CATECHOLAMINE TO THE ACTION OF STROPHANTHIN-G ON ATRIAL CONTRACTIONS OF RABBITS AND GUINEA-PIGS

It is generally accepted that the remarkable effect of digitalis on heart falure is caused by its specific action on the contractile mechanism of the heart muscle. The mode of pharmacological action of digitalis glycosides have been studied by many investigators, and it has been claimed that digitalis might have some influence on the energy production mechanism of the heart. The metabolic pathway of heart muscle contraction is not positively influenced by digitalis glycosides, though they do bring about an increase in contractile force [Wollenberger (1), Bing et al. (2, 3)]. Szent-Gyorgyi (4) reported that actomyosin is influenced by ATP and inorganic ions but not by digitalis. However, it has been reported that ATP-ase activity in the muscle cell membrane of rat hearts is promoted by digitalis in therapeutic dosage [Repke (5)]. On the other hand, Hadju and Szent-Gyorgyi (6) reported that the decrease in K-ion concentrations in the heart muscle induces an increase in contraction, and digitalis augments an efflux of the K-ions in the heart muscle. On contrary, Klaus et al. (7) reported that the influx of 42K-ions into the heart muscle cells was increased by digitalis in therapeutic doses. The cardiac action of digitalis has been explained by some investigators as that of an autonomic drug due to the result that digitalis increases adrenaline action [Donielpolu (8), Fujita (9)]. Our experiment were carried out to discover the relation of digitalis action to endogenous catecholamine mobilization in the atria from the standpoint that the catecholamines in heart muscle are mostly in a bound form and the contractile function of heart is controlled by the released catecholamine available.