Responses of Atlantic cod Gadus morhua head kidney leukocytes to phytase produced by gastrointestinal-derived bacteria

We 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 (40 mmHg)], whereas noradrenaline levels did not increase significantly in these particular experiments in which PWWOWO2 was lowered gradually over a 30 min period. All subsequent experiments were performed using a more rapid induction of hypoxia to reach a final PWWOWO2 of 5.3 kPa within the first 57–10 min of exposure. Blood withdrawn from pre-branchial (ventral aortic) and post-branchial (dorsal aortic) cannulae after 30 min revealed pronounced reductions in POO2 and O2 content (CO2) as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 17-4 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.

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Antarctic fishes have a limited capacity for catecholamine synthesis

Journal of Experimental Biology ◽

10.1242/jeb.202.24.3623 ◽

1999 ◽

Vol 202 (24) ◽

pp. 3623-3629 ◽

Cited By ~ 1

Author(s):

N.M. Whiteley ◽

S. Egginton

Keyword(s):

Gadus Morhua ◽

Atlantic Cod ◽

Activity Patterns ◽

Stress Hormones ◽

Antarctic Fish ◽

Head Kidney ◽

Catecholamine Synthesis ◽

Primary Stress ◽

Dissostichus Mawsoni ◽

Champsocephalus Gunnari

To determine whether an attenuated stress response is a general feature of Antarctic fish or is dependent on ecotype, the capacity for catecholamine synthesis within the head kidney and plasma levels of the primary stress hormones (catecholamines and cortisol) were determined in species with a range of activity patterns. Tyrosine hydroxylase (TH) activities were similar in both sluggish (Gobionotothen gibberifons, 153+/−22 nmol g(−)(1)h(−)(1), mean +/− s.e.m.) and active (Notothenia rossii, 185+/−39 nmol g(−)(1)h(−)(1), Dissostichus mawsoni, 128+/−31 nmol g(−)(1)h(−)(1)) pelagic nototheniids, but only 30 % of those in Atlantic cod (Gadus morhua, 393+/−88 nmol g(−)(1)h(−)(1)) at the same temperature. TH activities were even lower in white-blooded channichthyids (Chaenocephalus aceratus, 74+/−16 nmol g(−)(1)h(−)(1) and Champsocephalus gunnari, 53+/−17 nmol g(−)(1)h(−)(1)), although values in Chionodraco rastrospinosus were similar to red-blooded species (178+/−45 nmol g(−)(1)h(−)(1)). Circulating catecholamine levels were extremely high in all species after fishing stress, with adrenaline levels 3–4 times higher than noradrenaline levels. Cortisol levels remained low, ranging from 1.33+/−0.58 ng ml(−)(1) in Champsocephalus gunnari to 44.9+/−25.0 ng ml(−)(1)in Dissostichus mawsoni. These data suggest that depressed catecholamine synthesis is typical of Antarctic fish regardless of life style, although they are able to release extensive stores from the chromaffin tissue under conditions of extreme trauma. Cortisol does not appear to be an important primary stress hormone in these species.

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