Acute handling stress resulted in significant elevation of plasma cortisol and lactate concentrations within 30 min in both fed and food-deprived rainbow trout (Oncorhynchus mykiss), indicating a typical stress response. Plasma glucose levels rose immediately (30 min) poststress in the food-deprived group, while there was a delayed response (2 h) in the fed group. The low liver glycogen content and total glycogen phosphorylase (GPase) and glycogen synthase (GSase) activities in the food-deprived group indicated an overall depression in glycogen metabolism. Acute handling stress maintained liver glycogen stores for up to 4 h in the food-deprived group, but the combined effects of limited substrate and increased energy demand necessitated mobilization of liver glycogen in the food-deprived group, but not in the fed group. This increased glycogen mobilization in the food-deprived group coincided with a secondary elevation in plasma cortisol concentration 4 h poststress. The results indicated that food-deprived rainbow trout were more sensitive to stress of handling and mobilized glycogen stores to meet the energy demand imposed by the stressor. The elevated plasma cortisol levels noted during acute handling stress could play an important role in energy partitioning, metabolically adapting the fish to handling stress.

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This study examined the effects of pituitary-interrenal hormones on catecholamine storage and release in the rainbow trout Oncorhynchus mykiss. An extract of trout pituitary elicited the release of adrenaline, but not noradrenaline, using an in situ perfusion preparation. A variety of doses of adrenocorticotropic hormone (2-2000 mU) caused the release of both catecholamines in situ which was unaffected by pre-treatment with the ganglion blocker, hexamethonium, or the serotonergic receptor antagonist, methysergide, but was abolished in calcium-free media. Intra-arterial injections of adrenocorticotrophic hormone in vivo caused an elevation of plasma adrenaline but not noradrenaline levels. Injections of cortisol in situ did not elicit catecholamine release. Trout given an intraperitoneal implant of cortisol (50 mg.kg-1 body weight) had significantly higher plasma cortisol concentrations when compared to controls after 7 days of implantation. Increases in the levels of stored catecholamines were observed in various regions of the kidney and posterior cardinal vein following 3 and 7 days of cortisol treatment. The ability of the chromaffin cells to release catecholamines in response to cholinergic stimulation was assessed in situ after 7 days of treatment. Basal (non-stimulated) adrenaline outflowing perfusate levels were greater in the cortisol-treated fish. Cortisol treatment increased the responsiveness of the catecholamine release process to low doses of the cholinoceptor agonist carbachol. Three or 7 days of cortisol treatment did not alter the in vitro activity of the enzyme phenylethanolamine-N-methyl transferase. The results of this study demonstrate that interactions within the pituitary-adrenal axis can influence both catecholamine storage and release in the rainbow trout.

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We examined the in vivo effect of acute hypoxemia on myocardial cell-surface (sarcolemmal) β-adrenoreceptor density (Bmax) and binding affinity ( K D) and on stress protein 70 (sp70) expression by exposing rainbow trout ( Oncorhynchus mykiss; 2.1–2.7 kg) to hypoxic water (3 mg/l O2) at 15°C for 6 h. This degree of hypoxia was the minimum O2 level that these trout could tolerate without losing equilibrium and struggling violently. Hypoxic exposure reduced arterial [Formula: see text]([Formula: see text]) from 98 to 26 mmHg and arterial oxygen content ([Formula: see text]) from 10.8 to 7.4 vol/100 vol, but did not elevate epinephrine and norepinephrine levels above 10 and 30 nM, respectively. Despite the substantial reduction in blood oxygen status, the Bmax and K D of myocardial cell-surface β-adrenoreceptors were unaffected by 6 h of hypoxic exposure. In addition, acute hypoxemia did not increase myocardial sp70 expression. The failure of short-term hypoxia to decrease trout myocardial β-adrenoreceptor density clearly contrasts with the established hypoxia-mediated downregulation shown for mammals. To further investigate the influence of low[Formula: see text] on salmonid myocardial β-adrenoreceptors, binding studies were performed on the spongy (continuously exposed to deoxygenated venous blood) and compact (perfused by oxygenated blood supplied by the coronary artery) myocardia of chinook salmon. The spongy myocardium has adapted to its microenvironment of continuous low[Formula: see text] by having 14% more cell-surface β-adrenoreceptors compared with the compact myocardium. There was no tissue-specific difference in K D and no evidence of sexual dimorphism in Bmax or K D. We conclude from our studies that the salmonid heart is well adapted for sustained performance under hypoxic conditions. We found that wild chinook salmon had 2.8× more cell-surface β-adrenoreceptors compared with hatchery-reared rainbow trout. This difference suggests a significant degree of plasticity exists for fish myocardial β-adrenoreceptors. The signals underlying such differences await further study, but are not likely to include moderate hypoxia and sexual dimorphism.

Rainbow trout (Oncorhynchus mykiss) fasted for 4 months had lower plasma glucose concentration and hepatocyte glycogen content than the fed fish. Gluconeogenesis from alanine in the fasted fish was not significantly different from that of the fed fish, whereas both alanine glyconeogenesis and oxidation increased with fasting by 400% and 300%' respectively. Glyconeogenesis from glucose was not significantly different with fasting, whereas glucose oxidation decreased significantly with fasting. The presence of glucose (10 mM) in the medium did not modify alanine glyconeogenesis or gluconeogenesis in either the fed or the fasted groups. However, glucose did increase alanine oxidation in the fed group but not in the fasted group, this response being further stimulated in the presence of insulin. Alanine (2 mM) in the medium had no effect on glyconeogenesis from glucose in either fed or fasted trout hepatocytes. Insulin significantly decreased glucose oxidation in the fed fish, whereas the insulin effect on glucose oxidation in the fasted fish occurred only in the presence of alanine. The results indicate that nutritional state affects hepatocyte responsiveness to substrate utilization and insulin stimulation in trout. Specifically, the hepatocyte potential for glyconeogenesis is enhanced in the fasted fish, although this increased glycogen production is not due to an increased glucose utilization. o 1995 Wiley-Liss, Inc.