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ABSTRACT: NMDA receptors mediate hypoxia-induced ventilatory frequency and blood pressure increases in fish. Here we continue to resolve whether non-NMDA receptors participate in chemoreflexes. Shorthorn sculpins, instrumented for cardiorespiratory measurements, were kept unrestrained or positioned in a stereotaxic frame. Chemoreflexes were elicited (hypoxia/NaCN-induced) before/after administration of either the specific AMPA receptor antagonist, GYKI52466 (systemically), or the specific kainate receptor antagonist, UBP293 (microinjections into fourth ventricle). Immunohistochemistry was performed on medullary cross-sections to identify non-NMDA receptor subunits in the chemoreflex-pathway. Kainate receptors mediate the chemoreflex-mediated increase in ventilation amplitude, since the response was abolished by UBP293. GYKI52466 attenuated the ventilatory frequency increase, and induced more regular breathing patterns and higher heart rate in both normoxic and hypoxic conditions, suggesting that AMPA receptors also partake in cardiorespiratory control. This together with immunohistochemical findings of both AMPA and kainate receptor subunits in the chemoreflex-pathway, show that non-NMDA receptors play a role in both chemoreflex-activation and normoxic cardiorespiratory regulation in fish.
Respiratory Physiology & Neurobiology 03/2010; 172(3):83-93. · 2.24 Impact Factor
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ABSTRACT: Increased ventilation frequency (fV) in response to hypoxia in adult fish depends on ionotropic N-methyl-d-aspartate (NMDA) receptors. Nonetheless, the ontogeny of central control mechanisms mediating hypoxic ventilatory chemoreflexes in lower vertebrates has not been studied. Therefore, the aim of this study was to determine when the hypoxic ventilatory response during zebrafish (Danio rerio) development is mediated via NMDA receptors, by performing physiological experiments and western blot analysis of NMDA receptor subunits. Zebrafish larvae at stages 4–16 days post-fertilisation (dpf) were exposed to an hypoxic pulse in control groups and in groups treated with MK801 (NMDA receptor antagonist). The hypoxic increase in fV was present at all larval stages, and it matured during development. The reflex became MK801 sensitive at 8 dpf, but did not completely rely on a glutamatergic transmission until 13 dpf. This, together with changing subunit composition during the different stages (increasing amounts of NMDAR1 subunits and appearance of NMDAR2A subunits in adults), suggests that the amount of functional NMDA receptors needed to achieve a fully developed reflex is not attained until later stages. Furthermore, our results suggest that other non-NMDA receptor mechanisms are responsible for the hypoxia-induced increase in fV during the earlier developmental stages.
Comparative Biochemistry and Physiology - Part A Molecular & Integrative Physiology 04/2006; · 2.23 Impact Factor
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ABSTRACT: To investigate central respiratory control mechanisms in channel catfish, microinjections of kainic acid (causing chemical lesion of neurons) or kynurenic acid (an antagonist of N-methyl-D-aspartate (NMDA), kainate and alpha-amino-3-OH-5-methyl-4-isooxazole-propionic-acid (AMPA) receptors) were made into the general visceral nucleus (nGV) of the medulla in anaesthetised spontaneously breathing animals. Kainic acid abolished the ventilatory movements, indicating that neurons in the nGV are crucial for maintaining normal breathing. Kynurenic acid did not affect normal breathing, but abolished the ventilatory responses to hypoxia, showing that ionotropic glutamate receptors in the nGV are vital for the production of oxygen chemoreceptor activated respiratory reflexes. In addition, immunohistochemistry of brain slices showed that interneurons and nerve fibres in the nGV display NMDA-immunoreactivity, which corroborates the physiological experiments. The results of this study suggest that neurons and glutamatergic pathways in the nGV are essential for ventilatory functions and hypoxic reflexes in channel catfish.
Respiratory Physiology & Neurobiology 11/2003; 138(1):77-86. · 2.24 Impact Factor
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ABSTRACT: Glutamate microinjected into the vagal sensory area in the medulla produces cardiorespiratory responses mimicking oxygen chemoreflexes in fish. Here we directly investigate whether these reflexes are dependent on the ionotropic N-methyl-D-aspartate (NMDA) glutamate receptor. Fish were equipped with opercular, branchial and snout cannulae for measurements of cardiorespiratory parameters and drug injections. Oxygen chemoreceptor reflexes were evoked by rapid hypoxia, NaCN added into the blood (internal, 0.3 ml, 50 microg ml(-1)) and the mouth (external, 0.5 ml, 1 mg ml(-1)), before and after systemic administration of the NMDA receptor antagonist MK801 (3 mg kg(-1)). Hypoxia produced an MK801-sensitive increase in blood pressure and ventilation frequency, whereas the marked bradycardia and the increased ventilation amplitude were NMDA receptor-independent. The fish appeared more responsive to externally applied cyanide, but the injections and MK801 treatment did not distinguish whether external or internal oxygen receptors were differently involved in the hypoxic responses. In addition, using single-labelling immunohistochemistry on sections from the medulla and ganglion nodosum, the presence of glutamate and NMDA receptors in the vagal oxygen chemoreceptor pathway was established. In conclusion, these results suggest that NMDA receptors are putative central control mechanisms that process oxygen chemoreceptor information in fish.
Journal of Experimental Biology 05/2003; 206(Pt 7):1251-9. · 3.00 Impact Factor
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ABSTRACT: Glutamate is a major neurotransmitter of chemoreceptor and baroreceptor afferent pathways in mammals and therefore plays a central role in the development of cardiorespiratory reflexes. In fish, the gills are the major sites of these receptors, and, consequently, the terminal field (sensory area) of their afferents (glossopharyngus and vagus) in the medulla must be an important site for the integration of chemoreceptor and baroreceptor signals. This investigation explored whether fish have glutamatergic mechanisms in the vagal sensory area (Xs) that could be involved in the generation of cardiorespiratory reflexes. The locations of the vagal sensory and motor (Xm) areas in the medulla were established by the orthograde and retrograde axonal transport of the neural tract tracer Fast Blue following its injection into the ganglion nodosum. Glutamate was then microinjected into identified sites within the Xs in an attempt to mimic chemoreceptor- and baroreceptor-induced reflexes commonly observed in fish. By necessity, the brain injections were performed on anaesthetised animals that were fixed by 'eye bars' in a recirculating water system. Blood pressure and heart rate were measured using an arterial cannula positioned in the afferent branchial artery of the 3rd gill arch, and ventilation was measured by impedance probes sutured onto the operculum. Unilateral injection of glutamate (40-100 nl, 10 mmol l(-1)) into the Xs caused marked cardiorespiratory changes. Injection (0.1-0.3 mm deep) in different rostrocaudal, medial-lateral positions induced a bradycardia, either increased or decreased blood pressure, ventilation frequency and amplitude and, sometimes, an initial apnea. Often these responses occurred simultaneously in various different combinations but, occasionally, they appeared singly, suggesting specific projections into the Xs for each cardiorespiratory variable and local determination of the modality of the response. Response patterns related to chemoreceptor reflex activation were predominantly located rostral of obex, whereas patterns related to baroreceptor reflex activation were more caudal, around obex. The glutamate-induced bradycardia was N-methyl-D-aspartate (NMDA) receptor dependent and atropine sensitive. Taken together, our data provide evidence that glutamate is a putative player in the central integration of chemoreceptor and baroreceptor information in fish.
Journal of Experimental Biology 04/2003; 206(Pt 5):867-76. · 3.00 Impact Factor
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ABSTRACT: Little is known of the cardiovascular functions of prostaglandins in non-mammalian vertebrates. There are indications that prostaglandins may have a function in haemostasis by constricting blood vessels in filament arteries in the fish gill after injury. Our aim was to examine the cardiovascular effect of the prostaglandins F(2 alpha) (PGF(2 alpha)) and E(2) (PGE(2)) with emphasis on branchial circulation. Intra-arterial injections of PGF(2 alpha) (10, 40, 160, 400 nmol kg(-1)) in cod caused a dose-dependent increase in ventral aortic blood pressure, a reduction in cardiac output, and an increase in gill vascular resistance. A contraction of filament arteries was observed with in vivo microscopy only seconds after injection. PGF(2 alpha) may therefore possibly be involved in a haemostatic vasoconstriction. In contrast, the most significant effects of PGE(2) appeared to be on the heart. PGE(2) also reduced dorsal aortic blood pressure.
Journal of Comparative Physiology B 08/2002; 172(5):363-9. · 1.97 Impact Factor
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ABSTRACT: Little is known of the cardiovascular functions of prostaglandins in non-mammalian vertebrates. There are indications that prostaglandins may have a function in haemostasis by constricting blood vessels in filament arteries in the fish gill after injury. Our aim was to examine the cardiovascular effect of the prostaglandins F2! (PGF2!) and E2 (PGE2) with emphasis on branchial circulation. Intra-arterial injections of PGF2! (10, 40, 160, 400 nmol kg-1) in cod caused a dose-dependent increase in ventral aortic blood pressure, a reduction in cardiac output, and an increase in gill vascular resistance. A contraction of filament arteries was observed with in vivo microscopy only seconds after injection. PGF2! may therefore possibly be involved in a haemostatic vasoconstriction. In contrast, the most significant effects of PGE2 appeared to be on the heart. PGE2 also reduced dorsal aortic blood pressure.
Journal of Comparative Physiology B 01/2002; 172(5):363-369. · 1.97 Impact Factor
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ABSTRACT: This study examines the effects of lung inflation/deflation with and without CO2 on the entire population of pulmonary receptors in the vagus nerve in two species of snakes and two species of turtles. We asked the question, "how does the response of the entire mixed population of pulmonary stretch receptors (PSR) and intrapulmonary chemoreceptors (IPC) in species possessing both differ from that in species with only PSR"? This was studied under conditions of artificial ventilation with the secondary goal of extending observations on the presence/absence of IPC to a further three species. Our results indirectly illustrate the presence of IPC in the Burmese python and South American rattlesnake but not the side necked turtle, adding support to the hypothesis that IPC first arose in diapsid reptiles. In both species of snake, CO2-sensitive discharge (presumably from IPC) predominated almost to the exclusion of CO2-insensitive discharge (presumably arising from PSR) while the opposite was true for both species of turtle. The data suggest that for animals breathing air under conditions of normal metabolism there is little to distinguish between the discharge profiles of the total population of receptors arising from the lungs in the different groups. Interestingly, however, under conditions of elevated environmental CO2 most volume-related feedback from the lungs is abolished in the two species of snakes, while under conditions of elevated metabolic CO2, it is estimated that volume feedback from the lungs would be enhanced in these same species.
Journal of Comparative Physiology B 04/2001; 171(2):103-11. · 1.97 Impact Factor
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ABSTRACT: Although the branchial and cardiovascular effects of serotonin (5-hydroxytryptamine) have only partially been characterized, a physiological role for serotonin in the cardiorespiratory responses of fish to environmental changes such as reduced Ph has been suggested. Therefore, we have characterized and compared the effects of serotonin and a rapid reduction of Ph in the ambient water (from pH 8.8 to pH 4.0) on ventral and dorsal aortic blood pressures, heart rate, cardiac output, and arterial pH in rainbow trout, Onchorhynchus mykiss. In addition, the circulation in the branchial microvasculature was observed using in vivo epi-illumination microscopy. The fall in water Ph and injection of serotonin (100 nmol/kg) both increased the branchial resistance and reduced the efferent filamental artery (EFA) blood velocity. Nevertheless, quantitatively, the responses to the two stimuli were different. Although acid exposure caused a much more profound increase in branchial resistance compared with serotonin, the blood flow in the observable distal portion of the EFA was only reduced by 60% in acid water, while it stopped with serotonin. Regardless of the marked branchial resistance elevation, a constriction of the efferent filamental vasculature could not be seen during acid exposure, as occasionally was the case with serotonin. While methysergide completely abolished the serotonin-induced branchial events, it only modestly suppressed the acid-induced reduction of EFA blood velocity. In contrast, all of the systemic changes induced by serotonin and acidic water were insensitive to methysergide. In conclusion, acidic water and injected serotonin elevate the branchial resistance, but the involvement of a serotonergic component in the acidic response appears negligible.
Journal of Experimental Zoology 08/2000; 287(2):113-9.
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ABSTRACT: This study examined the location and physiological roles of branchial chemoreceptors involved in the cardiorespiratory responses to hypoxia and hypercarbia in a neotropical fish that exhibits aquatic surface respiration, the tambaqui (Colossoma macropomum). Fish were exposed to abrupt progressive environmental hypoxia (18. 6-1.3 kPa water P(O2)) and hypercarbia (water equilibrated with 5 % CO(2) in air, which lowered the water pH from 7.0 to 5.0). They were also subjected to injections of NaCN into the ventral aorta (to stimulate receptors monitoring the blood) and buccal cavity (to stimulate receptors monitoring the respiratory water). All tests were performed before and after selective denervation of branchial branches of cranial nerves IX and X to the gill arches. The data suggest that the O(2) receptors eliciting reflex bradycardia and increases in breathing frequency are situated on all gill arches and sense changes in both the blood and respiratory water and that the O(2) receptors triggering the elevation in systemic vascular resistance, breathing amplitude, swelling of the inferior lip and that induce aquatic surface respiration during hypoxia are extrabranchial, although branchial receptors also contribute to the latter two responses. Hypercarbia also produced bradycardia and increases in breathing frequency, as well as hypertension, and, while the data suggest that there may be receptors uniquely sensitive to changes in CO(2)/pH involved in cardiorespiratory control, this is based on quantitative rather than qualitative differences in receptor responses. These data reveal yet another novel combination for the distribution of cardiorespiratory chemoreceptors in fish from which teleologically satisfying trends have yet to emerge.
Journal of Experimental Biology 05/2000; 203(Pt 7):1225-39. · 3.00 Impact Factor
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ABSTRACT: To examine the distribution and physiological role of CO2/pH-sensitive chemoreceptors in the gills of the tropical fish, traira (Hoplias malabaricus), fish were exposed to acute environmental hypercarbia (1.25, 2.5 and 5.0% CO2 in air) and subjected to injections of HCl into the ventral aorta and buccal cavity. This was done before and after selective denervation of branchial branches of the IXth and Xth cranial nerves to various gills arches. Hypercarbia produced a significant decrease in heart rate, a mild hypotension as well as increases in both ventilation rate and ventilation amplitude. The data suggest that the hypercarbic bradycardia and increase in ventilation frequency arise from receptors exclusively within the gills but present on more than the first gill arch, while extra-branchial receptors may also be involved in controlling the increase in ventilation amplitude. With the exception of a decrease in heart rate in response to HCl injected into the ventral aorta, the acid injections (internal and external) did not mimic the cardiorespiratory responses observed during hypercarbia suggesting that changes in CO2 are more important than changes in pH in producing cardiorespiratory responses. Finally, the data indicate that chemoreceptors sensitive to CO2/pH and to O2 in the gills of this species involved in producing ventilatory responses are distributed in a similar fashion, but that those involved in producing the bradycardia are not.
Respiration Physiology 04/2000; 120(1):47-59.
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ABSTRACT: The lamellae of the fish gill are the primary sites for oxygen uptake from the water. Here, only two very thin layers of
cells separate the blood from the water. Therefore, energetically costly ion-fluxes will also occur between blood and water,
and it has been hypothesised that the blood flow within the lamellae can be regulated through vasoconstriction, but evidence
for this has been lacking. Through direct observations of the lamellae of rainbow trout (Oncorhynchus mykiss) in vivo, using epi-illumination microscopy, we show here that an endothelium-derived vasoactive peptide, endothelin-1 (ET-1,
0.2 μg kg−1 or 1.0 μg kg−1), is able to completely constrict the vascular sheet in the lamellae, probably by inducing contraction of pillar cells. This
coincided with a dose-dependent increase in ventral aortic blood pressure (rising from 6.6 kPa to 12.0 kPa in response to
the high ET-1 dose). However, blood continued to flow through the marginal channel that circumvents each lamella. Thus, ET-1
caused an intralamellar blood shift from the lamellar sheet towards the marginal channels. Vasoconstriction in the lamellae
is likely to provide the fish with a mechanism for matching its respiratory surface area with its respiratory needs, thereby
minimising ion-fluxes.
Journal of Comparative Physiology B 10/1998; 168(8):619-623. · 1.97 Impact Factor
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ABSTRACT: By cutting gill filaments in anesthetized rainbow trout (Oncorhynchus mykiss), observing the bleeding through a stereomicroscope, and using blockers of various known endogenous filament artery vasoconstrictors, we have here attempted to characterize hemostatic mechanisms in gills. The immediate hemostatic response to a cut in a gill filament artery was a local vasoconstriction, stopping the hemorrhage within approximately 20 s. In heparinized fish, the hemorrhage recommenced after approximately 8 min, suggesting that the vasoconstriction soon subsides and blood clotting becomes responsible for the hemostasis. Antagonists of acetylcholine, adenosine, and serotonin receptors were unable to block the hemostatic vasoconstriction. Also, tetrodotoxin was without effect, indicating a nonnervous origin. By contrast, indomethacin significantly affected the measured bleeding times, suggesting that eicosanoids play a significant role in this process (possibly by stimulating vasoconstriction and/or by inducing local thrombocyte aggregation). By possessing several hundred virtually identical filaments with readily observable vasculature, the fish gill appears to be a good experimental model for studying hemostatic mechanisms.
The American journal of physiology 09/1998; 275(2 Pt 2):R460-5.
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ABSTRACT: This study was conducted to describe the cardiovascular responses to intra-arterial injections of serotonin in the Antarctic fish Pagothenia borchgrevinki and to elucidate the underlying mechanisms. Immunohistochemistry was used to localise serotonin-containing cells within the gills. Simultaneous and continuous recordings of ventral and dorsal aortic blood pressure, heart rate and ventral aortic blood flow (cardiac output) were made using standard cannulation procedures in combination with Doppler flow measurement. An extracorporeal loop with an in-line oxygen electrode allowed continuous measurements of arterial oxygen pressure PaO2. Pre-branchial injection of serotonin (5-hydroxytryptamine, 5-HT) or the 5-HT2 receptor agonist alpha-methylserotonin increased the branchial vascular resistance and ventral aortic pressure, while the 5-HT1 receptor agonist piperazine was without effect. The branchial vasoconstriction produced by serotonin injection was completely blocked by the 5-HT1/5-HT2 receptor antagonist methysergide and the branchial vasoconstriction produced by WIDTH="9" HEIGHT="12" ALIGN="BOTTOM" NATURALSIZEFLAG= alpha-methylserotonin injection was completely blocked by the specific 5-HT2 receptor antagonist LY53857. The results suggest that the 5-HT2 receptor alone mediates the branchial vasoconstriction. Serotonin also mediated a methysergide-sensitive reduction in PaO2, the reduction being greatest when the pre-injection PaO2 value was high. 5-HT-immunoreactive cells and nerve fibres were present within the gill tissues. All the 5-HT-immunoreactive cells were located on the efferent side of the filaments, but 5-HT-immunoreactive nerve fibres were found lining both of the branchial arteries. Our findings demonstrate a potential serotonergic control system for the gills in Pagothenia borchgrevinki. In contrast to its effects on the branchial vasculature, serotonin produced a methysergide-insensitive decrease in the systemic vascular resistance. However, neither the specific 5-HT1 nor 5-HT2 receptor agonists produced a decrease in the resistance of the systemic vasculature. The nature of the serotonergic receptor(s) inducing vasodilation in teleost fish is uncertain.
Journal of Experimental Biology 08/1998; 201(Pt 14):2129-38. · 3.00 Impact Factor
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ABSTRACT: The arrangement of the fish gill vasculature is quite complex, and varies between the different fish groups. The use of vascular casting techniques has greatly enhanced our knowledge of the anatomy of the branchial microcirculation, not least through the contributions of Pierre Laurent and co-workers at Strasbourg. At different physiological situations, the contact surface between water and blood (functional surface area) varies to balance oxygen uptake against osmotic water flow ("respiratory-osmoregulatory compromise"). This is controlled by nerves and by blood-borne or locally released substances that affect blood flow patterns in the gill. Histochemical techniques have been used to demonstrate neurotransmitter substances in the branchial innervation. In combination with physioly-osmoregulatory compromise" at different physiological situations.
Comparative Biochemistry and Physiology - Part A Molecular & Integrative Physiology 02/1998; 119(1):137-47. · 2.23 Impact Factor
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ABSTRACT: In vivo microscopy combined with systemic blood flow and pressure measurements were used to examine the hemodynamic and microcirculatory responses to hypoxia in gills of rainbow trout and to clarify if the underlying mechanisms are adrenergic, cholinergic, serotonergic, or adenosinergic. Hypoxia (P(O2) 1.07-1.33 kPa) reduced, halted, or reversed the blood flow in the distal portion of the efferent filamental artery (EFA). Simultaneously, a large overflow to the central venous system appeared, allowing a continuous flow through many of the secondary lamellae. No vasoconstriction could be observed in this portion of the filament, showing that a vasoconstriction occurred elsewhere, possibly at the EFA sphincter, because the gill resistance (R(G)) increased. These effects were mimicked by prebranchial injection of acetylcholine, a treatment that also strongly constricted the distal efferent filamental vasculature. Atropine blocked most of the hypoxia-induced hemodynamic changes, although a minor increase in R(G) remained. The latter appeared to be of a nonadrenergic noncholinergic origin, being unaffected by additional treatment with an alpha-adrenoreceptor antagonist. It was also unaffected by blockers of serotonin and adenosine-A1 receptors. Other responses seen included a cholinergic maintenance of the systemic resistance during hypoxia and an alpha-adrenoceptor-mediated posthypoxic hypertension. This study demonstrates that hypoxia evoked a cholinergic reflex vasoconstriction located at proximal parts of the efferent filamental vasculature.
The American journal of physiology 03/1997; 272(2 Pt 2):R576-85.
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ABSTRACT: The purinergic branchial vasomotor control in rainbow trout (Oncorhynchus mykiss) was studied using an epi-illumination microscope equipped with a water-immersion objective. Cardiac output (Q), heart rate, and dorsal (PDA) and ventral (PVA) aortic pressures were recorded simultaneously. Prebranchial injection of adenosine or the A1-receptor agonist N6-cyclopentyl-adenosine (CPA) constricted the distal portion of the filament vasculature, which coincided with an increase of PVA. The A2-receptor agonist PD-125944 was without effect. After adenosine and CPA injection, an overflow of blood to the secondary system was repeatedly observed unless blood flow came to a complete stop. The lack of a concomitant reduction of Q suggested a redistribution of blood to the secondary system and to more proximal parts of the filament. The branchial effects of adenosine and CPA were completely blocked by the unspecific adenosine receptor antagonist amino-phylline and the specific A1-receptor antagonist N6-cyclopen-tyltheophylline. The results suggest that A1-receptors alone mediate the branchial vasoconstriction observed. Thus the responses of the branchial vasculature to adenosine include a vasoconstriction of the filament vasculature mediated via specific A1 receptors and a redistribution of blood flow to the secondary system and to proximal parts of the filament. Additional cardiovascular effects of adenosine included decreased systemic vascular resistance and heart rate.
The American journal of physiology 10/1996; 271(3 Pt 2):R661-9.
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ABSTRACT: The effects of exogenously applied serotonin [5-hydroxytryptamine (5-HT)] on the distal arterial vasculature of gill filaments were observed using an epi-illumination microscope equipped with a water-immersion objective and connected to a video camera. In addition, ventral aortic flow (Q) and celiac artery pressure (PCA) were measured. Intra-arterial injection of serotonin (100 nmol/kg) completely stopped the blood flow in the distal part of the filaments and caused a rapid decrease of PCA. Repeatedly, the flow reduction was found to coincide with a constriction of the distal portion of the efferent filamental vasculature. Because there was no concomitant reduction in Q, it is concluded that a redistribution of blood to more proximal parts of the filaments occurred. After treatment with the serotonergic receptor antagonist methysergide, the vasoconstrictor effect of serotonin on the filamental vasculature was eliminated, while a decrease in PCA was still observed. The results demonstrate a specific site(s) for the serotonergic vasoconstriction in the distal portion of the filament.
The American journal of physiology 06/1995; 268(5 Pt 2):R1224-9.
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ABSTRACT: Two species of Antarctic fish were stressed by moving them from seawater at -1 degrees C to seawater at 10 degrees C and holding them for a period of 10 min. The active cryopelagic species Pagothenia borchgrevinki maintained heart rate while in the benthic species Trematomus bernacchii there was an increase in heart rate. Blood pressure did not change in either species. Both species released catecholamines into the circulation as a consequence of the stress. P. borchgrevinki released the greater amounts, having mean plasma concentrations of 177 +/- 54 nmol.l(-1) noradrenaline and 263 +/- 131 nmol.l(-1) adrenaline at 10 min. Pla.sma noradrenaline concentrations rose to 47 +/- 14 nmol.l(-1) and adrenaline to 73 +/- 28 nmol.l(-1) in T. bernacchii. Blood from P. borchgrevinki was tonometered in the presence of isoprenaline. A fall in extracellular pH suggests the presence of a Na+/H+ antiporter on the red cell membrane, the first demonstration of this in an Antarctic fish. Treatment with the beta-adrenergic antagonist drug sotalol inhibited swelling of red blood cells taken from temperature-stressed P. borchgrevinki, suggesting that the antiporter responds to endogenous catecholamines.
