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Teleost fish living in freshwater are challenged by passive water influx; however the molecular mechanisms regulating water influx in fish are not well understood. The potential involvement of aquaporins (AQP) and epithelial tight junction proteins in the regulation of transcellular and paracellular water movement was investigated in larval zebrafish (Danio rerio). We observed that the half-time for saturation of water influx (Ku) was 4.3±0.9 min, and reached equilibrium at approximately 30 min. These findings suggest a high turnover rate of water between the fish and the environment. Water influx was reduced by the putative AQP inhibitor phloretin (100 or 500 μM). Immunohistochemistry and confocal microscopy revealed that AQP1a1 protein was expressed in cells on the yolk sac epithelium. A substantial number of these AQP1a1-positive cells were identified as ionocytes, either H+-ATPase-rich cells or Na+/K+-ATPase-rich cells. AQP1a1 appeared to be expressed predominantly on the basolateral membranes of ionocytes, suggesting its potential involvement in regulating ionocyte volume and/or water flux into the circulation. Additionally, translational gene knockdown of AQP1a1 protein reduced water influx by approximately 30%, further indicating a role for AQP1a1 in facilitating transcellular water uptake. On the other hand, incubation with the Ca2+-chelator EDTA or knockdown of the epithelial tight junction protein claudin-b significantly increased water influx. These findings indicate that the epithelial tight junctions normally act to restrict paracellular water influx. Together, the results of the present study provide direct in vivo evidence that water movement can occur through transcellular routes (via AQP); the paracellular routes may become significant when the paracellular permeability is increased. [ABSTRACT FROM AUTHOR]

The functional role of the tight junction protein claudin-b in larval zebrafish (Danio rerio) was investigated. We showed that claudin-b protein is expressed at epithelial cell-cell contacts on the skin. Translational gene knockdown of claudin-b protein expression caused developmental defects, including edema in the pericardial cavity and yolk sac. Claudin-b morphants exhibited an increase in epithelial permeability to the paracellular marker polyethylene glycol (PEG-4000) and fluorescein isothiocyanate- dextran (FD-4). Accumulation of FD-4 was confined mainly to the yolk sac and pericardial cavity in the claudin-b morphants, suggesting these regions became particularly leaky in the absence of claudin-b expression. Additionally, Na+ efflux was substantially increased in the claudin-b morphants, which contributed to a significant reduction in whole-body Na+ levels. These results indicate that claudin-b normally acts as a paracellular barrier to Na+. Nevertheless, the elevated loss of Na+ in the morphants was compensated by an increase in Na+ uptake. Notably, we observed that the increased Na+ uptake in the morphants was attenuated in the presence of the selective Na+/Cl--cotransporter (NCC) inhibitor metolazone, or during exposure to Cl--free water. These results suggested that the increased Na+ uptake in the morphants was, at least in part, mediated by NCC. Furthermore, treatment with an H+-ATPase inhibitor bafilomycin A1 was found to reduce Na+ uptake in the morphants, suggesting that H+-ATPase activity was essential to provide a driving force for Na+ uptake. Overall, the results suggest that claudin-b plays an important role in regulating epithelial permeability and Na+ handling in zebrafish. [ABSTRACT FROM AUTHOR]

Abstract: Mechanisms of ion uptake by freshwater (FW) fish have received considerable attention over the past 80 years. Through an assortment of techniques incorporating whole animal physiology, electrophysiology and molecular biological approaches, three models have been proposed to account for Na+ uptake. (1) Direct exchange of Na+ and H+ via one or more types of Na+/H+ exchanger (slc9), (2) uptake of Na+ through epithelial Na+ channels energized by an electrical gradient created by H+-ATPase and (3) Na+/Cl− co-transport (slc12). While each mechanism is supported at least in part by theoretical or experimental data, there are several outstanding questions that have not yet been fully resolved. Furthermore, there are few details concerning how these Na+ uptake mechanisms are fine tuned in response to the fluctuating FW environments. In this review, we summarize the current understanding of these three Na+ uptake mechanisms and discuss their regulation by endocrine (cortisol and prolactin) and neurohumoral (catecholamines) factors. [Copyright &y& Elsevier]

The potential role of adrenergic systems in regulating Na+ uptake in zebrafish (Danio rerio) larvae was investigated. Treatment with isoproterenol (a generic β-adrenergic receptor agonist) stimulated Na+ uptake, whereas treatment with phenylephrine (an α1-adrenergic receptor agonist) as well as clonidine (an α2-adrenergic receptor agonist) significantly reduced Na+ uptake, suggesting opposing roles of α- and β-adrenergic receptors in Na+ uptake regulation. The increase in Na+ uptake associated with exposure to acidic water (pH = 4.0) was attenuated in the presence of the nonselective β-receptor antagonist propranolol or the β1-receptor blocker atenolol; the β2-receptor antagonist ICI-118551 was without effect. The stimulation of Na+ uptake associated with ion-poor water (32-fold dilution of Ottawa tapwater) was unaffected by β-receptor blockade. Translational gene knockdown of β-receptors using antisense oligonucleotide morpholinos was used as a second method to assess the role of adrenergic systems in the regulation of Na+ uptake. Whereas β1- or β2B-receptor knockdown led to significant decreases in Na+ uptake during exposure to acidic water, only β2A-receptor morphants failed to increase Na+ uptake in response to ion-poor water. In support of the pharmacology and knockdown experiments that demonstrated an involvement of β-adrenergic systems in the control of Na+ uptake, we showed that the H+-ATPase-rich (HR) cell, a subtype of ionocyte known to be a site of Na+ uptake, is innervated and appears to express β-adrenergic receptors (propranolol binding sites) at 4 days postfertilization. These data indicate an important role of adrenergic systems in regulating Na+ uptake in developing zebrafish. [ABSTRACT FROM AUTHOR]

The involvement of a Na+/H+ exchanger (NHE) in mediating Na+ uptake by freshwater fish is currently debated. Although supported indirectly by empirical molecular and pharmacological data, theoretically its operation should be constrained thermodynamically, owing to unfavorable chemical gradients. Recently, there has been an increasing focus on ammonia channels (Rh proteins) as potentially contributing to Na+ uptake across the freshwater fish gill. In this study, we tested the hypothesis that Rhcg1, a specific apical isoform of Rh protein, is critically important in facilitating Na+ uptake in zebrafish larvae via its interaction with NHE. Treating larvae (4 days postfertilization) with 5-(N-ethyl-N-isopropyl) amiloride (EIPA), an inhibitor of NHE, caused a significant reduction in Na+ uptake in fish reared in acidic water (pH ~ 4.0). A role for NHE in Na+ uptake was further confirmed by translational knockdown of NHE3b, an isoform of NHE thought to be responsible for Na+/H+ exchange in zebrafish larvae. Exposing the larvae reared in acidic water to 5 mM external ammonium sulfate or increasing the buffering capacity of the water with 10 mM HEPES caused concurrent reductions in ammonia excretion and Na+ uptake. Furthermore, translational knockdown of Rhcg1 significantly reduced ammonia excretion and Na+ uptake in larvae chronically (4 days) or acutely (24 h) exposed to acidic water. Unlike in sham-injected larvae, EIPA did not affect Na+ uptake in fish experiencing Rhcg1 knockdown. Additionally, exposure of larvae to bafilomycin A1 (an inhibitor of H+-ATPase) significantly reduced Na+ uptake in fish reared in acidic water. These observations suggest the existence of multiple mechanisms of Na+ uptake in larval zebrafish in acidic water: one in which Na+ uptake via NHE3b is linked to ammonia excretion via Rhcg1, and another facilitated by H+-ATPase. [ABSTRACT FROM AUTHOR]

The article presents a study which examines the effects of direct ammonia (NH3)-carbon dioxide (CO2) competition experiments in adult zebrafish and the impact of translational knockdowns of rhesus (Rh) proteins in larvae in Ottawa, Ontario. Adult zebrafish, Danio rerio, that were raised at the core aquatic facility of the University of Ottawa were the subject of the study. Findings of the study provide in vivo evidence for a dual function of Rh proteins as ammonia and CO2 channels, also highlighting that Rh proteins in zebrafish may be common pathways for transport of NH3 and CO2.

Fish exposed to hypoxia develop decreased heart rate, or bradycardia, the physiological significance of which remains unknown. The general muscarinic receptor antagonist atropine abolishes the development of this hypoxic bradycardia, suggesting the involvement of muscarinic receptors. In this study, we tested the hypothesis that the hypoxic bradycardia is mediated specifically by stimulation of the M2 muscarinic receptor, the most abundant subtype in the vertebrate heart. Zebrafish (Danio rerio) were reared at two levels of hypoxia (30 and 40 Torr Po2) from the point of fertilization. in hypoxic fish, the heart rate was significantly lower than in normoxic controls from 2 to 10 days post-fertilization (dpf). At the more severe level of hypoxia (30 Ton Po2), there were significant increases in the relative mRNA expression of M2 and the cardiac type β-adrenergic receptors (β1AR, β2aAR, and β2bAR) at 4 dpf. The hypoxic bradycardia was abolished (at 40 Ton Po2) or significantly attenuated (at 30 Torr Po2) in larvae experiencing M2 receptor knockdown (using morpholino antisense oligonucleotides). Sham-injected larvae exhibited typical hypoxic bradycardia in both hypoxic regimens. The expression of β1AR, β2aAR, β2bAR, and M2 mRNA was altered at various stages between 1 and 4 dpf in larvae experiencing M2 receptor knockdown. Interestingly, M2 receptor knockdown revealed a cardioinhibitory role for the β2-adrenergic receptor. This is the first study to demonstrate a specific role of the M2 muscarinic receptor in the initiation of hypoxic bradycardia in fish. [ABSTRACT FROM AUTHOR]

The goal of the present study was to investigate the role of circulating cortisol and urea in the transcriptional regulation of branchial glutamine synthetase (GS), which incorporates NH3 into glutamate to form glutamine, and the toadfish urea transporter, tUT, which is involved in urea excretion across the gill of the gulf toadfish. GS (of which there are two isoforms, LGS and GGS) and tUT mRNA expression and activity were measured in toadfish exposed to treatments that would induce variable stress responses. In addition, the role of circulating urea in tUT regulation was investigated by infusing toadfish with urea alone or in combination with intraperitoneal injection of RU486, a corticosteroid type II receptor antagonist. There was a 4.8-fold upregulation in the mRNA expression of the gill-specific GS isoform (GGS) in response to cortisol infusion and a similar upregulation in the more ubiquitous isoform (LGS). Furthermore, there was a significant 1.9-fold and 3.3-fold upregulation in the mRNA expression of the toadfish urea transporter, tUT, in response to stress through crowding or exogenous cortisol loading through infusion, respectively. In addition, tUT was found to have a urea-sensitive component to transcriptional regulation that was independent of circulating cortisol concentrations. However, the changes measured in mRNA expression of GGS, LGS and tUT did not correspond with changes in protein activity. To determine the cell type(s) involved in glutamine production and urea excretion, we attempted to localize GGS, LGS and tUT using in situ hybridization. This study is the first to show that GGS and tUT expression appear to occur in gill mitochondria-rich cells of toadfish, suggesting that these cells play a combined glutamine production and urea excretion role, which may have implications for predator avoidance. [ABSTRACT FROM AUTHOR]

Presently, three α1-adrenoceptor (AR) types are recognized in vertebrates: α1A-, α1B-, and α1D-ARs. These α1-subtypes have distinct pharmacology and molecular profiles, play crucial roles in metabolic and vascular control, and are the targets for numerous pharmaceuticals, especially those affecting blood pressure and vascular resistance. To better understand the functional divergence within the α1-AR gene family, we sequenced these α1-AR paralogs in the rainbow trout and performed an extensive phylogenetic analysis. We show that these AR genes evolved by duplication events just before the origin of the jawed vertebrates. Our computational analyses suggest that the differences between the three α1-AR subtypes may affect their tissue specificity, ligand specificity, and possibly signal transduction processes and desensitization. We also show that, within each subtype, differences exist between fish and mammalian receptors, both at the transcriptional and at the physiological level. These differences, however, suggest that the role of α1-ARs in fish is more complex than previously thought. Our integrated analysis of the α1-AR gene family suggests that these receptors evolved these distinct features very early within vertebrates. [ABSTRACT FROM AUTHOR]

Experiments were conducted on rainbow trout to determine the impact of dietary salt on arterial blood pressure. After 4-6 wk, fish fed a salt-enriched diet exhibited a 37% elevation of dorsal aortic pressure (from 23.8 ± 1.2 to 32.6 ± 1.4 mmHg) and an 18% increase in ventral aortic pressure (from 33.0 ± 1.5 to 38.9 ± 1.3 mmHg). The hypertension presumably reflected the increase in cardiac output (from 31.0 ± 0.8 to 36.4 ± 2.2 ml·min-1·kg-1) because systemic and branchial resistances were statistically unaltered by salt feeding. The chronic hypertension was associated with a decrease in the pressor responses of the systemic vasculature to catecholamines and hypercapnia in the salt-fed fish. The reduction in α-adrenergic responsiveness of the systemic vasculature is consistent with desensitization or loss of functional α-adrenoceptors (α-ARs). In support of this idea, the salt-fed fish exhibited significantly decreased levels of α1D-AR mRNA in the dorsal aorta and the afferent (ABA) and efferent branchial arteries (EBA). In contrast, however, the results obtained from norepinephrine dose-response curves for EBA and ABA vascular rings in vitro did not provide evidence for loss of function of branchial artery α1-ARs in the salt-fed fish. Indeed, the EC50 for the EBA norepinephrine dose-response curve was significantly reduced (from 3.75 × 10-7 to 2.12 × 10-7 M) in the salt-fed fish, indicating an increase in the binding affinity of the α1-ARs. [ABSTRACT FROM AUTHOR]

We indirectly tested the idea that the epithelial Ca2+ channel (ECaC) of the trout gill is regulated in an appropriate manner to adjust rates of Ca2+ uptake. This was accomplished by assessing the levels of gill ECaC rnRNA and protein in fish exposed to treatments known to increase or decrease Ca2+ uptake capacity. Exposure of trout to soft water ([Ca2+] = 20-30 nmol/l) for 5 days (a treatment known to increase Ca2+ uptake capacity) caused a significant increase in ECaC mRNA levels and an increase in ECaC protein expression. The inducement of hypercalcemia by infusing fish with CaCl2 (a treatment known to reduce Ca2+ uptake) was associated with a significant decrease in ECaC mRNA levels, yet protein levels were unaltered. ECaC mRNA and protein expression were increased in fish treated with the hypercalcemic hormone cortisol. Finally, exposure of trout to 48 h of hypercapnia (~7.5 mmHg, a treatment known to increase Ca2+ uptake capacity) elicited an ~100-fold increase in the levels of ECaC mRNA and a significant increase in protein expression. immunocytochemical analysis of the gills from hypercapnic fish suggested a marked increase in the apical expression of ECaC on pavement cells and a subpopulation of mitochondria-rich cells. The results of this study provide evidence that Ca2+ uptake rates are, in part, regulated by the numbers of apical membrane Ca2+ channels that, in turn, modulate the inward flux of Ca2+ into gill epithelial cells. [ABSTRACT FROM AUTHOR]

Abstract: This study examined the effect of acute hypoxic and hypercapnic cardiorespiratory stimuli, superimposed on existing cardiorespiratory disturbances in tambaqui. In their natural habitat, these fish often encounter periods of hypoxic hypercapnia that can be acutely exacerbated by water turnover. Tambaqui were exposed to periods of normoxia, hypoxia, hyperoxia and hypercapnia during which, externally oriented O2 and CO2 chemoreceptors were further stimulated, by administration into the inspired water of sodium cyanide and CO2-equilibrated water, respectively. Hyperoxic water increased the sensitivity of the NaCN-evoked increase in breathing frequency (fR) and decrease in heart rate. Hypoxia and hypercapnia attenuated the increase in fR but, aside from blood pressure, did not influence the magnitude of NaCN-evoked cardiovascular changes. Water PO2 influenced the magnitude of the CO2-evoked cardiorespiratory changes and the sensitivity of CO2-evoked changes in heart rate and blood flow. The results indicate that existing respiratory disturbances modulate cardiorespiratory responses to further respiratory challenges reflecting both changes in chemosensitivity and the capacity for further change. [Copyright &y& Elsevier]

This study addressed the hypothesis that the secretion of catecholamines from trout (Oncorhynchus mykiss) chromaffin cells, during hypoxia, is triggered by stimulation of O[sub 2] chemoreceptors located within the gills. Sodium cyanide was administered into the inspired water (external cyanide) or injected into the gill circulation (internal cyanide) to pharmacologically stimulate external (water sensing) or internal (blood sensing) O[sub 2] chemoreceptors, respectively. Both of these treatments caused an elevation of circulating catecholamine levels. The response to external, but not internal, cyanide was abolished by removal of the first gill arch. Hypoxia produced an increase in circulating catecholamine levels that was unaffected by removal of the first gill arch or by denervation of the pseudobranch. Cyanide and hypoxia both caused the well-documented cardiorespiratory reflexes normally observed in this species. This study demonstrates, for the first time, that gill O[sub 2] chemoreceptors can initiate the reflex that leads to catecholamine release from the chromaffin cells and that stimulation of internally oriented O[sub 2] receptors on all gill arches appears to be the physiologically important mechanism for initiating release. [ABSTRACT FROM AUTHOR]

Experiments were performed to test the hypothesis that the marked ventilatory and cardiovascular responses to hypercarbia in rainbow trout Oncorhynchus mykiss arise from specific stimulation of chemoreceptors localised to the first gill arch. This was accomplished by measuring cardiorespiratory variables during acute hypercarbia (20 min at P[sub CO[sub 2]]=8mmHg; 1mmHg=0.133kPa) in fish subjected to selective bilateral extirpation of the first gill arch. The cardiovascular responses to hypercarbia in the intact fish included a significant bradycardia (from 75.0±1.6 to 69.0±2.0 beats min[sup -1]; means ± S.E.M.; N=16), an increase in dorsal aortic blood pressure (from 30.8±1.5 to 41.9±2.5 mmHg; N=16) and a rise in systemic vascular resistance (from 1.1±0.1 to 1.4±0.1 mmHg ml[sup -1] kg[sup -1] min[sup -1]; N=16). Removal of the first gill arch or pre-treatment with the muscarinic receptor antagonist atropine prevented the hypercarbic bradycardia without affecting the pressure or resistance responses. Correlation analysis, however, revealed shallow but significant inverse relationships between water P[sub CO[sub 2]] and cardiac frequency in both atropinised (r²=0.75) and gill-extirpated (r²=0.90) fish, suggesting a direct mild effect of CO[sub 2] on cardiac function. The ventilatory response to hypercarbia in the intact fish consisted of an increase in ventilation amplitude (from 0.62±0.06 to 1.0±0.13cm; N=16) with no change in breathing frequency. Removal of the first gill arch lowered resting breathing frequency and prevented the statistically significant elevation of breathing amplitude. Gill extirpation, however, did not totally abolish the positive correlation between water P[sub CO[sub 2]] and ventilation amplitude (r²=0.84), suggesting the presence of additional (although less important) chemoreceptive sites that are not confined to the first gill arch. Plasma catecholamine... [ABSTRACT FROM AUTHOR]

Tests the hypothesis that efficiency of carbon dioxide (CO[sub2]) excretion is sensitive to changes in blood flow owing to chemical equilibrium limitations in trout. Discussion on CO[sub2] excretion; Relationship of arterial partial pressure of CO[sub2] to cardiac output; Influence of carbonic anhydrase on the relationship of CO[sub2] pressure and cardiac output.

The buffering capacity (β) of rainbow trout (Oncorhynchus mykiss) plasma was manipulated prior to intravascular injection of bovine carbonic anhydrase to test the idea that proton (H+) availability limits the catalysed dehydration of HCO3– within the extracellular compartment. An extracorporeal blood shunt was employed to continuously monitor blood gases in vivo in fish exhibiting normal plasma β (–3.9±0.3 mmol l–1 pH unit–1), and in fish with experimentally (using N-[2-hydroxyethyl]piperazine-N′-[2-ethanesulfonic acid]) elevated plasma β (–12.1±1.1 mmol l–1 pH unit–1). An injection of 5 mg kg–1 carbonic anhydrase equally reduced (after 90 min) the arterial partial pressure of CO2 in trout with regular (–0.23±0.05 Torr) or high (–0.20±0.05 Torr) plasma β; saline injection was without effect. Because ventilation and venous blood gases were unaffected by carbonic anhydrase, the effect of extracellular carbonic anhydrase in lowering arterial partial pressure of CO2 was likely caused solely by a specific enhancement of CO2 excretion owing to acceleration of HCO3– dehydration within the plasma. The lowering of arterial partial pressure of CO2 in trout after injection of exogenous carbonic anhydrase provides the first in vivo evidence that the accessibility of plasma HCO3– to red blood cell carbonic anhydrase constrains CO2 excretion under resting conditions. Because the velocity of red blood cell Cl–/HCO3– exchange governs HCO3– accessibility to red blood cell carbonic anhydrase, the present study also provides evidence that CO2 excretion at rest is limited by the relatively slow rate of Cl–/HCO3– exchange. The effect of carbonic anhydrase in lowering arterial partial pressure of CO2 was unrelated to plasma buffering capacity. While these data could suggest that H+ availability does not limit extracellular HCO3– dehydration in vivo at resting rates of CO2 excretion, it is more likely that the degree to which plasma β was elevated in the present study was insufficient to drive a substantially increased component of HCO3– dehydration through the plasma. [ABSTRACT FROM AUTHOR]

Focuses on a study which assessed the potential direct and modulating effects of acute hypoxia on catecholamine secretion in rainbow trout, Oncorhynchus mykiss using a perfused cardinal vein preparation and chronically cannulated fish. Materials and methods; Effects of hypoxic perfusate on in situ basal catecholamine secretion rates; Influence of acute moderate hypoxia on nicotine-evoked catecholamine release in vivo.

Deals with a study which cloned and characterized the B subunit of the trout H...V-ATPase to examine by northern analysis the expression and tissue distribution of the B subunit mRNA during external hypercapnia. Materials and methods; Results and discussion.

The tambaqui (Colossoma macropomum), migrates annually between whitewater and blackwater rivers of the Amazon. Unlike the whitewater, blackwater is characterized by higher levels of dissolved organic carbon (DOC), including humic acids (HA). Because humic substances impair sensory processes, the current study tested the hypothesis that O 2 and/or CO 2 chemoreception is impeded in blackwater owing to the presence of HA. Thus, the ventilatory responses of tambaqui to hypoxia or hypercapnia were assessed in well water transported from Manaus, local blackwater, and in well water containing HA either extracted from Rio Negro water or obtained commercially (Sigma Aldrich; SA). In well water, tambaqui exhibited typical hyperventilatory responses to hypoxia or hypercapnia. These responses were prevented by simultaneously exposing fish to SA HA (20 mg l−1). The negative effects of SA HA on ventilation were prevented when natural DOC (30 mg l−1; extracted from Rio Negro water after first removing the endogenous HA fraction) was added concurrently, indicating a protective effect of this non-humic acid DOC fraction. The hyperventilatory responses were unaffected during acute exposure or after acclimation of fish to Rio Negro water. HA extracted from Rio Negro water did not impair the hyperventilatory responses to hypoxia or hypercapnia. This study, while demonstrating a negative effect of SA HA derived from peat (coal) on the control of breathing in tambaqui, failed to reveal any detrimental consequences of HA (derived from the decomposition of a variety of lignin-rich plants) naturally occurring in the blackwaters of the Rio Negro. • This study tested the hypothesis that reflex ventilatory responses to would be impaired in Tambaqui in natural blackwater. • Commercial humic acid impaired the ventilatory response to hypoxia or hypercapnia. • Natural blackwater from the Rio Negro or humic acid derived from blackwater was without effect. • The negative effects of commercial humic acid were absent in the presence of DOC (minus the humic acid fraction) [ABSTRACT FROM AUTHOR]

Discusses a study which assessed the relative involvement of nicotinic and muscarinic cholinergic receptors in the neuronal control of catecholamine secretion from the chromaffin tissue of rainbow trout. Background information on the mechanism of catecholamine secretion in teleosts; Materials and methods; Results; Discussion.

Determines the contribution of angiotensin II (Ang-II)-elicited increases in humoral catecholamines levels to rainbow trout cardiovascular control. Effect of homologous rainbow trout Ang-II in plasma catecholamine levels; Cardiovascular effects of Ang-II with and without alpha-adrenoreceptor blockade; Relationship between plasma concentrations and their cardiovascular effects.

Focuses on the structure and function of the branchial chloride cell in freshwater fishes. Role of the chloride cell in ionic regulation and in acid-base regulation; Effects of chloride cell proliferation on blood-to-water diffusion distance; Effects of chloride cell proliferation on respiratory gas transfer.

Investigates the relationships between angiotensins and catecholamine release from the chromaffin tissue of rainbow trout. Evidence that angiotensins can elicit catecholamine release; Method in which angiotensins effects this release.

Assesses the control of catecholamine and serotonin release from the chromaffin tissue of the Atlantic hagfish. Saline-perfused systemic heart/posterior cardinal vein preparation; Potential modulatory effects of NECA, an adenosine receptor antagonist, on catecholamine release; Response to adrenocorticotropic hormone.

Evaluates the involvement of catecholamines in the ventilatory control and blood oxygen transport during hypoxia and hypercapnia in dogfish and rainbow trout. Plasma catecholamine levels; Hyperventilatory responses during hypoxia and hypercapnia; Effect of catecholamine administration on blood oxygen transport.

Examines the response of cannulated rainbow trout to acute hypoxia in fish acclimated to two temperatures (5 and 15 degrees Celsius). Effects of acclimation on catecholamine release; Effects of acclimation temperature on hemoglobin oxygen-affinity; Other potential causes/correlates of catecholamine release.

Presents results of in vivo and in situ experiments on the Atlantic hagfish Myxine glutinosa. Characterization of the levels of circulating catecholamines during acute stresses; Potential mechanisms of catecholamine release from the systemic heart and posterior cardinal vein; Possible involvement of pituitary hormones.