scholarly journals Control of Catecholamine Release In Vivo and In Situ in the Atlantic Cod (Gadus Morhua) During Hypoxia

1991 ◽  
Vol 155 (1) ◽  
pp. 549-566 ◽  
Author(s):  
STEVE F. PERRY ◽  
REGINA FRITSCHE ◽  
RICHARD KINKEAD ◽  
STEFAN NILSSON
Keyword(s):  
Gadus Morhua ◽  
Atlantic Cod ◽  
Head Kidney ◽  
Plasma Catecholamine ◽  
Plasma Adrenaline ◽  
Catecholamine Levels ◽  
Chromaffin Tissue ◽  
Stimulation Of

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 Blood withdrawn from pre-branchial (ventral aortic) and post-branchial (dorsal aortic) cannulae after 30 min revealed pronounced reductions in POO2 and O2 content (CO2) as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.

scholarly journals Circulating Catecholamines and Swimming Performance in the Atlantic Cod, Gadus Morhua

1989 ◽  
Vol 141 (1) ◽  
pp. 377-387 ◽  
Author(s):  
P. J. BUTLER ◽  
M. AXELSSON ◽  
F. EHRENSTROM ◽  
J. D. METCALFE ◽  
S. NILSSON
Keyword(s):  
Critical Velocity ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Swimming Performance ◽  
Operative Procedure ◽  
Plasma Catecholamine ◽  
Spinal Nerves ◽  
Performance Results ◽  
Catecholamine Levels

Sectioning the first four pairs of spinal nerves prevents the large increase in circulating catecholamine concentrations seen in Atlantic cod swimming at their critical velocity (Ucrit). There is also a significant reduction in the swimming performance of the fish. To test whether this reduced performance results from the lack of increase in plasma catecholamine levels or from the fact that other organs are also denervated by the operative procedure, a mixture of adrenaline and noradrenaline was infused into swimming, denervated fish. This caused a significant increase in their Ucrit. It is concluded, therefore, that the rise in plasma catecholamine levels seen in Atlantic cod swimming at their maximum sustainable velocity enhances the swimming performance of these fish.

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

2009 ◽  
Vol 36 (4) ◽  
pp. 883-891 ◽  
Author(s):  
Carlo C. Lazado ◽  
Christopher Marlowe A. Caipang ◽  
Sanchala Gallage ◽  
Monica F. Brinchmann ◽  
Viswanath Kiron
Keyword(s):  
Gadus Morhua ◽  
Atlantic Cod ◽  
Head Kidney

Increased ventricular stiffness and decreased cardiac function in Atlantic cod (Gadus morhua) at high temperatures

2013 ◽  
Vol 305 (8) ◽  
pp. R864-R876 ◽  
Author(s):  
Douglas A. Syme ◽  
A. Kurt Gamperl ◽  
Gordon W. Nash ◽  
Kenneth J. Rodnick
Keyword(s):  
Stroke Volume ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Isometric Force ◽  
Full Range ◽  
Large Strains ◽  
High Heart Rate ◽  
Ventricular Filling ◽  
Ventricular Trabeculae

We employed the work loop method to study the ability of ventricular and atrial trabeculae from Atlantic cod to sustain power production during repeated contractions at acclimation temperatures (10°C) and when acutely warmed (20°C). Oxygen tension (Po2) was lowered from 450 to 34% air saturation to augment the thermal stress. Preparations worked under conditions simulating either a large stroke volume (35 contractions/min rate, 8–12% muscle strain) or a high heart rate (70 contractions/min, 2–4% strain), with power initially equal under both conditions. The effect of declining Po2 on power was similar under both conditions but was temperature and tissue dependent. In ventricular trabeculae at 10°C (and atria at 20°C), shortening power declined across the full range of Po2 studied, whereas the power required to lengthen the muscle was unaffected. Conversely, in ventricular trabeculae at 20°C, there was no decline in shortening power but an increase in lengthening power when Po2 fell below 100% air saturation. Finally, when ventricular trabeculae were paced at rates of up to 115 contractions/min at 20°C (vs. the maximum of 70 contractions/min in vivo), they showed marked increases in both shortening and lengthening power. Our results suggest that although elevated heart rates may not impair ventricular power as they commonly do isometric force, limited atrial power and the increased work required to expand the ventricle during diastole may compromise ventricular filling and hence, stroke volume in Atlantic cod at warm temperatures. Neither large strains nor high contraction rates convey an apparent advantage in circumventing this.

Dissociation between plasma, urine, and renal papillary cyclic AMP content following vasopressin and DDAVP

1979 ◽  
Vol 237 (3) ◽  
pp. F218-F225 ◽  
Author(s):  
M. J. Bia ◽  
S. Dewitt ◽  
J. N. Forrest
Keyword(s):  
Cyclic Amp ◽  
Urine Osmolality ◽  
Brattleboro Rats ◽  
Renal Papilla ◽  
Brattleboro Rat ◽  
Clearance Studies ◽  
Urinary Cyclic Amp ◽  
Stimulation Of

The effects of in vivo physiologic doses of vasopressin and 1-deamino-8-D-arginine vasopressin (DDAVP) on the cyclic AMP content of plasma, urine, and renal papillary tissue were determined in the ADH-deficient Brattleboro rat. During clearance studies, plasma cyclic AMP concentrations and both total and nephrogenous urinary cyclic AMP excretion in vasopressin- and DDAVP-treated rats were similar to the values in time-matched controls. In contrast, in situ renal papillary cyclic AMP content was higher (P less than 0.001) in both vasopressin- (35.7 +/- 3.6 pmol/mg protein) and DDAVP- (29.7 +/- 2.2 pmol/mg protein) treated rats compared to controls (15.1 +/- 1.3 pmol/mg protein). Endogenous stimulation of vasopressin by dehydration in normal rats increased both papillary cyclic AMP content (27.1 +/- 2.7 pmol/mg protein) and urine osmolality, whereas no change in papillary cyclic AMP was observed following dehydration in Brattleboro rats (13.6 +/- 0.8 pmol/mg protein) despite an increase in urine osmolality. The results demonstrate that changes in cyclic AMP following in vivo vasopressin are best demonstrated by measurement of in situ cyclic AMP content of the renal papilla, whereas total urinary cyclic AMP and nephrogenous cyclic AMP are not useful indices of tubular sensitivity to this hormone.

Dogfish pressor response to potassium blocked by magnesium and phentolamine

1982 ◽  
Vol 242 (3) ◽  
pp. R185-R188
Author(s):  
R. G. Carroll ◽  
D. F. Opdyke ◽  
N. E. Keller
Keyword(s):  
Adrenergic Receptor ◽  
Pressor Response ◽  
In Vitro Experiments ◽  
Spontaneous Release ◽  
Alpha Adrenergic Receptor ◽  
Receptor Sites ◽  
Catecholamine Levels ◽  
Chromaffin Tissue

In vivo infusion of MgCl2 blocks the dogfish pressor response to K+. This action of Mg2+ was contrasted to phentolamine in in vivo and in vitro experiments. Mg2+ blocks the spontaneous release of catecholamines from dogfish chromaffin tissue but does not alter the norepinephrine-induced contraction of the isolated dogfish artery. In vivo infusion of Mg2+ causes a significant decrease in resting catecholamine levels and diminishes the catecholamine release caused by K+ challenge. Both Mg2+ and phentolamine block the pressor action of K+, Mg2+ by preventing the K+-induced release of catecholamines and phentolamine by preventing the circulating catecholamines from interacting with alpha-adrenergic receptor sites.

Localization and In Situ Activities of Homoacetogenic Bacteria in the Highly Compartmentalized Hindgut of Soil-Feeding Higher Termites (Cubitermes spp.)

1999 ◽  
Vol 65 (10) ◽  
pp. 4497-4505 ◽  
Author(s):  
Anne Tholen ◽  
Andreas Brune
Keyword(s):  
Detection Limit ◽  
Companion Paper ◽  
Homoacetogenic Bacteria ◽  
Appl Environ ◽  
Partial Pressures ◽  
Almost All ◽  
Stimulation Of

ABSTRACT Methanogenesis and homoacetogenesis occur simultaneously in the hindguts of almost all termites, but the reasons for the apparent predominance of methanogenesis over homoacetogenesis in the hindgut of the humivorous species is not known. We found that in gut homogenates of soil-feeding Cubitermes spp., methanogens outcompete homoacetogens for endogenous reductant. The rates of methanogenesis were always significantly higher than those of reductive acetogenesis, whereas the stimulation of acetogenesis by the addition of exogenous H2 or formate was more pronounced than that of methanogenesis. In a companion paper, we reported that the anterior gut regions of Cubitermes spp. accumulated hydrogen to high partial pressures, whereas H2 was always below the detection limit (<100 Pa) in the posterior hindgut, and that all hindgut compartments turned into efficient H2 sinks when external H2 was provided (D. Schmitt-Wagner and A. Brune, Appl. Environ. Microbiol. 65:4490–4496, 1999). Using a microinjection technique, we found that only the posterior gut sections P3/4a and P4b, which harbored methanogenic activities, formed labeled acetate from H14CO3 −. Enumeration of methanogenic and homoacetogenic populations in the different gut sections confirmed the coexistence of both metabolic groups in the same compartments. However, the in situ rates of acetogenesis were strongly hydrogen limited; in the P4b section, no activity was detected unless external H2 was added. Endogenous rates of reductive acetogenesis in isolated guts were about 10-fold lower than the in vivo rates of methanogenesis, but were almost equal when exogenous H2 was supplied. We conclude that the homoacetogenic populations in the posterior hindgut are supported by either substrates other than H2 or by a cross-epithelial H2transfer from the anterior gut regions, which may create microniches favorable for H2-dependent acetogenesis.

scholarly journals Heat-shock responsive genes identified and validated in Atlantic cod (Gadus morhua) liver, head kidney and skeletal muscle using genomic techniques

BMC Genomics ◽  
2010 ◽  
Vol 11 (1) ◽  
pp. 72 ◽  
Author(s):  
Tiago S Hori ◽  
A Kurt Gamperl ◽  
Luis OB Afonso ◽  
Stewart C Johnson ◽  
Sophie Hubert ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Head Kidney

In vivo modulation by α2-adrenoceptors of adrenal catecholamine release in the anaesthetized dog

1988 ◽  
Vol 66 (3) ◽  
pp. 380-384 ◽  
Author(s):  
Sylvain Foucart ◽  
Jacques de Champlain ◽  
Reginald Nadeau
Keyword(s):  
Electrical Stimulation ◽  
Splanchnic Nerve ◽  
Catecholamine Release ◽  
Agonist Stimulation ◽  
Control Stimulation ◽  
Anaesthetized Dog ◽  
Splanchnic Nerve Stimulation ◽  
Stimulation Of

In this study, the reversal of the potentiating effect of idazoxan, a selective α2-antagonist, on adrenal catecholamine release elicited by splanchnic nerve stimulation in anaesthetized and vagotomized dogs, was investigated with the use of oxymetazoline, a selective α2-agonist. Stimulation of the left splanchnic nerve (5.0-V pulses of 2 ms duration for 3 min at a frequency of 2 Hz) was applied before and 20 min after the i. v. injection of each drug. Blood samples were collected in the adrenal vein before and at the end of each stimulation. The results show that the release of catecholamines induced by electrical stimulation was potentiated by 50% after idazoxan injection (0.1 mg/kg). This enhanced response was significantly antagonized by the subsequent injection of oxymetazoline (2 μg/kg). The α2-modulating effect appears to be related to the amount of catecholamines released during the stimulation, since by subgrouping of the data on the basis of the degree of potentiation by idazoxan, it was observed that this drug was more efficient when catecholamine release was higher during control stimulation. In contrast, the reversing effect of oxymetazoline was found to be more pronounced when catecholamine release was lower. These results thus suggest that the sensitivity of the α2-adrenoceptor mechanism may depend upon the in situ concentration of adrenal catecholamine release during electrical stimulation and that the potentiating effect of α2-blockade can be reversed by activation of those receptors by a selective α2-agonist.

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