scholarly journals The effects of acute hypoxia on chemically or neuronally induced catecholamine secretion in rainbow trout (Oncorhynchus mykiss) in situ and in vivo

2000 ◽  
Vol 203 (9) ◽  
pp. 1487-1495 ◽  
Author(s):  
S.F. Perry ◽  
C.J. Montpetit ◽  
M. Borowska
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Muscarinic Receptor ◽  
Acute Hypoxia ◽  
Catecholamine Secretion ◽  
Cardinal Vein ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Catecholamine Levels

The potential direct and modulating effects of acute hypoxia on catecholamine secretion in rainbow trout (Oncorhynchus mykiss) were assessed in situ, using a perfused cardinal vein preparation, and in vivo, using chronically cannulated fish. Acute (10 min) perfusion with hypoxic (P(O2)<10 mmHg) saline or homologous hypoxic blood did not have a statistically significant effect on basal (non-stimulated) catecholamine secretion. A field stimulation technique was used to excite the sympathetic nerves innervating the chromaffin cells electrically in situ under conditions of high-P(O2) (saline P(O2)=152 mmHg; 1 mmHg=0.133 kPa) or low-P(O2) (saline P(O2)<10 mmHg) perfusion at constant P(CO2) (2.3 mmHg). The results demonstrated that neuronally evoked catecholamine secretion was significantly lowered by 50 % during perfusion with hypoxic saline. To assess whether the inhibitory effect of hypoxia during neuronal stimulation in situ resulted from modulation of nicotinic and/or muscarinic receptor-linked pathways, perfused posterior cardinal vein preparations were injected with selective nicotinic (10(−)(7) or 10(−)(6)mol kg(−)(1) nicotine) or muscarinic (10(−)(3)mol kg(−)(1) methacholine) receptor agonists. For both doses of nicotine, catecholamine secretion was significantly lowered during hypoxia by 55 %. During muscarinic receptor stimulation, perfusion with hypoxic saline caused a 42 % reduction in the rate of catecholamine secretion. In contrast, catecholamine secretion elicited by depolarising levels of KCl (60 mmol l(−)(1)) was unaffected by the oxygen status of the perfusate. In vivo, intra-arterial injections of nicotine (300–600 nmol kg(−)(1)) into normoxic (water P(O2)=155 mmHg) or moderately hypoxic fish (water P(O2)=80 mmHg) caused a dose-dependent elevation of circulating catecholamine levels. However, despite the inhibitory influence of localised hypoxia on chromaffin cell responsiveness previously demonstrated in situ, the increase in plasma catecholamine levels after intra-arterial injection of nicotine was significantly enhanced in the hypoxic fish. The differences between the results from the in vivo and in situ experiments may reflect the contribution of higher control centres and modulating factors in vivo that are absent in situ.

Does blood acid-base status modulate catecholamine secretion in the rainbow trout (Oncorhynchus mykiss)?

1998 ◽  
Vol 201 (22) ◽  
pp. 3085-3095 ◽  
Author(s):  
AE Julio ◽  
CJ Montpetit ◽  
SF Perry
Keyword(s):  
Rainbow Trout ◽  
Receptor Agonist ◽  
Catecholamine Release ◽  
Catecholamine Secretion ◽  
Acid Base ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Acid Base Status ◽  
Catecholamine Levels

The direct and modulating effects of acidosis on catecholamine secretion in rainbow trout (Oncorhynchus mykiss) were assessed in vivo using cannulated fish and in situ using a perfused cardinal vein preparation. In situ, acidosis (a reduction in perfusate pH from 7.9 to 7.4) did not elicit catecholamine release or modulate the secretion of catecholamines evoked by the non-specific cholinergic receptor agonist carbachol (3x10(-7) to 10(-5 )mol kg-1) or the muscarinic receptor agonist pilocarpine (10(-7 )mol kg-1). Acidosis, however, significantly increased the secretion rates of noradrenaline and adrenaline in response to nicotine (10(-8) to 10(-7 )mol kg-1). In vivo, intra-arterial injections of nicotine (300-600 nmol kg-1) into normocapnic or moderately hypercapnic fish (water PCO2=5 mmHg or 0.67 kPa) caused a dose-dependent elevation of circulating catecholamine levels. At the highest dose of nicotine, the rise in plasma catecholamine levels was significantly enhanced in the hypercapnic fish. Acute hypoxia in vivo caused an abrupt release of catecholamines when arterial haemoglobin O2-saturation was reduced to approximately 55-60 %; this catecholamine release threshold during hypoxia was unaltered in hypercapnic fish. However, the hypoxia-induced catecholamine release was significantly greater in hypercapnic fish than in normocapnic fish. The results of this study suggest that blood acid-base status, while not influencing catecholamine secretion directly or influencing the blood O2 content threshold for catecholamine release during hypoxia, may modulate the secretory process specifically in response to nicotinic receptor stimulation of chromaffin cells.

scholarly journals Vasoactive intestinal polypeptide- and pituitary adenylate cyclase activating polypeptide-mediated control of catecholamine release from chromaffin tissue in the rainbow trout, Oncorhynchus mykiss

2000 ◽  
Vol 166 (3) ◽  
pp. 705-714 ◽  
Author(s):  
CJ Montpetit ◽  
SF Perry
Keyword(s):  
Rainbow Trout ◽  
Chromaffin Cells ◽  
Catecholamine Secretion ◽  
Cardinal Vein ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Neuronal Control ◽  
Pituitary Adenylate Cyclase ◽  
Posterior Cardinal Vein ◽  
Chromaffin Tissue

The aim of the present investigation was to assess the relative contributions of cholinergic (acetylcholine) and non-cholinergic vasoactive intestinal polypeptide (VIP), and pituitary adenylate cyclase activating polypeptide (PACAP) neurotransmitters in the neuronal control of catecholamine secretion from the chromaffin tissue lining the posterior cardinal vein of the rainbow trout (Oncorhynchus mykiss). Using an in situ saline-perfused posterior cardinal vein preparation, it was demonstrated that exogenous administration of chicken VIP or human PACAP-27 caused a dose-dependent increase in adrenaline secretion; noradrenaline secretion was unaffected. Analysis of dose-response curves indicated that VIP and PACAP stimulated the secretion of adrenaline with a similar degree of potency (ED(50) for VIP=1.90x10(-11) mol/kg; ED(50) for PACAP=1.03x10(-11) mol/kg). The VIP/PACAP-elicited secretion was diminished in the presence of the VIP receptor antagonist, VIP 6-28, but was unaffected by the PACAP receptor antagonist, PACAP 6-27, or the cholinergic antagonists, hexamethonium and atropine. Thus, this is the first study to demonstrate a direct stimulatory role for VIP or PACAP in catecholamine secretion from piscine chromaffin cells. The relative contribution of cholinergic and non-cholinergic neurotransmitters in the neuronal control of catecholamine secretion from the chromaffin tissue was evaluated using an in situ nerve-stimulating technique previously validated by us in the rainbow trout. This was accomplished by comparing catecholamine secretion in the presence or absence of cholinergic and the VIP and PACAP receptor antagonists during different levels of electrical stimulation. The results demonstrated that cholinergic stimulation predominated during high frequency of electrical stimulation (20 Hz) while the non-cholinergic component prevailed at low frequency (1 Hz). Overall, the results of the present investigation demonstrate that VIP and/or PACAP may directly stimulate adrenaline secretion from trout chromaffin cells at low levels of neuronal activity. Therefore, the neuronal control of catecholamine secretion in teleosts may not be confined to cholinergic-evoked events.

Cardiovascular effects of hypercarbia in rainbow trout (Oncorhynchus mykiss): a role for externally oriented chemoreceptors

2001 ◽  
Vol 204 (1) ◽  
pp. 115-125 ◽  
Author(s):  
J.E. McKendry ◽  
S.F. Perry
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Systemic Resistance ◽  
Rainbow Trout Oncorhynchus Mykiss

In situ and in vivo experiments were performed on rainbow trout (Oncorhynchus mykiss) to examine (i) the direct effect of CO(2) on the systemic vasculature and (ii) the influence of internal versus external hypercapnic acidosis on cardiovascular variables including blood pressure, cardiac output and systemic vascular resistance. Results from in situ saline-perfused trunk preparations indicated that CO(2) (0.6, 1.0 or 2.0% CO(2)) elicited a significant vasodilation, but only in the presence of pre-existing humoral adrenergic tone. In the absence of pre-existing vascular tone, CO(2) was without effect on systemic resistance. In contrast, hypercarbia in vivo triggered a statistically significant increase in systemic resistance (approximately 70 %) that was associated with elevated ventral aortic (approximately 42 %) and dorsal aortic (approximately 43 %) blood pressures and with a significant bradycardia (approximately 12 %); cardiac output was not significantly affected. To determine the potential roles of internal versus external chemoreceptors in mediating the cardiovascular responses to hypercarbia, experiments were performed to elevate the endogenous arterial partial pressure of CO(2) (Pa(CO2)) without an accompanying increase in external P(CO2) (Pw(CO2)). In one series, trout were given a bolus injection of the carbonic anhydrase inhibitor acetazolamide (30 mg kg(−1)) to inhibit CO(2) excretion, and thus raise Pa(CO2), 5–7 h prior to being exposed to an acute increase in Pw(CO2) (maximum Pw(CO2)=6.3+/−0.4 mmHg; 1 mmHg=0.133 kPa). Despite a marked increase in Pa(CO2) (approximately 7 mmHg) after injection of acetazolamide, there was no increase in dorsal aortic blood pressure (P(DA)) or systemic resistance (R(S)). The ensuing exposure to hypercarbia, however, significantly increased P(DA) (by approximately 20 %) and R(S) (by approximately 35 %). A second series of experiments used a 5–7 h period of exposure to hyperoxia (Pw(O2)=643+/−16 mmHg) to establish a new, elevated baseline Pa(CO2) (7.8+/−1.1 mmHg) without any change in Pw(CO2). Despite a steadily increasing Pa(CO2) during the 5–7 h of hyperoxia, there was no associated increase in P(DA) or R(S). Ensuing exposure to hypercarbia, however, significantly increased P(DA) (by approximately 20 %) and R(S) (by approximately 150 %). Plasma adrenaline levels were increased significantly during exposure to hypercarbia and, therefore, probably contributed to the accompanying cardiovascular effects. These findings demonstrate that the cardiovascular effects associated with hypercarbia in rainbow trout are unrelated to any direct constrictory effects of CO(2) on the systemic vasculature and are unlikely to be triggered by activation of internally oriented receptors. Instead, the data suggest that the cardiovascular responses associated with hypercarbia are mediated exclusively by externally oriented chemoreceptors.

scholarly journals SEROTONIN-MEDIATED RELEASE OF CATECHOLAMINES IN THE RAINBOW TROUT ONCORHYNCHUS MYKISS

1993 ◽  
Vol 178 (1) ◽  
pp. 191-204 ◽  
Author(s):  
R. Fritsche ◽  
S. G. Reid ◽  
S. Thomas ◽  
S. F. Perry
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Chromaffin Cells ◽  
Head Kidney ◽  
Catecholamine Release ◽  
Perfusion Fluid ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Dose Dependent

The effects of serotonin (5-hydroxytryptamine; 5-HT) on catecholamine release from chromaffin tissue were investigated in the rainbow trout (Oncorhynchus mykiss) in vivo and in situ. Intra-arterial injections of serotonin in vivo caused dose-dependent (50–250 nmol kg-1) increases in both plasma noradrenaline and adrenaline levels. Pre-treatment of fish with the serotonergic receptor antagonist methysergide did not abolish these increases. An in situ saline-perfused head kidney preparation was developed and validated to study the potential direct effect of serotonin on catecholamine release. The chromaffin cells in the preparation showed a dose-dependent release of catecholamines in response to bolus injections of the cholinergic receptor agonist carbachol (10–7-10-4 mol kg-1). The carbachol-induced release of noradrenaline, but not of adrenaline, was reduced significantly when the nicotinic receptor antagonist hexamethonium (10–4 mol l-1) was present in the perfusion fluid. The removal of calcium from the perfusion fluid prevented the usual release of catecholamines evoked by carbachol. Bolus injections of serotonin (250 nmol kg-1) into the inflowing perfusion fluid resulted in significantly increased levels of adrenaline and noradrenaline in the outflowing perfusate. Addition of hexamethonium to the perfusion fluid did not abolish this serotonin-induced release of catecholamines. The serotonin-induced release of adrenaline, however, was abolished totally by the addition of methysergide. Serotonin is present in high concentrations (44.61+/−5.96 microgram g-1 tissue) in the anterior region of the posterior cardinal vein within the head kidney. Carbachol (10–5 mol kg-1) did not elicit release of the stored serotonin from the perfused head kidney preparation. We conclude that the chromaffin cells in the perfused trout head kidney preparation display characteristics similar to those of other vertebrates and that this preparation is a useful tool for studying the control of catecholamine release in fish. The results demonstrate that serotonin has a direct impact on the chromaffin cells by interacting with methysergide-sensitive receptors to initiate the release of adrenaline. The potential physiological role of serotonin on catecholamine release in trout is discussed.

Myotomal slow muscle function of rainbow trout Oncorhynchus mykiss during steady swimming.

1998 ◽  
Vol 201 (10) ◽  
pp. 1659-1671 ◽  
Author(s):  
L Hammond ◽  
J D Altringham ◽  
C S Wardle
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Body Length ◽  
Muscle Activation ◽  
Activity Patterns ◽  
The Body ◽  
Entire Body ◽  
Negative Power ◽  
Rainbow Trout Oncorhynchus Mykiss

Strain and activity patterns were determined during slow steady swimming (tailbeat frequency 1.5-2.5 Hz) at three locations on the body in the slow myotomal muscle of rainbow trout Oncorhynchus mykiss using sonomicrometry and electromyography. Strain was independent of tailbeat frequency over the range studied and increased significantly from +/-3.3 % l0 at 0.35BL to +/-6 % at 0.65BL, where l0 is muscle resting length and BL is total body length. Muscle activation occurred significantly later in the strain cycle at 0.35BL (phase shift 59 degrees) than at 0.65BL (30 degrees), and the duration of activity was significantly longer (211 degrees at 0.35BL and 181 degrees at 0.65BL). These results differ from those of previous studies. The results have been used to simulate in vivo activity in isolated muscle preparations using the work loop technique. Preparations from all three locations generated net positive power under in vivo conditions, but the negative power component increased from head to tail. Both kinematically, and in the way its muscle functions to generate hydrodynamic thrust, the rainbow trout appears to be intermediate between anguilliform swimmers such as the eel, which generate thrust along their entire body length, and carangiform fish (e.g. saithe Pollachius virens), which generate thrust primarily at the tail blade.

THE EFFECTS OF ACCLIMATION TEMPERATURE ON THE DYNAMICS OF CATECHOLAMINE RELEASE DURING ACUTE HYPOXIA IN THE RAINBOW TROUT ONCORHYNCHUS MYKISS

1994 ◽  
Vol 186 (1) ◽  
pp. 289-307 ◽  
Author(s):  
S. Perry ◽  
S. Reid
Keyword(s):  
Rainbow Trout ◽  
Acute Hypoxia ◽  
Catecholamine Release ◽  
Acclimation Temperature ◽  
Plasma Catecholamine ◽  
Blood Oxygen ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Arterial Blood ◽  
The Difference ◽  
Catecholamine Levels

The response of cannulated rainbow trout (Oncorhynchus mykiss) to acute hypoxia was studied in fish acclimated to two temperatures (5 and 15 °C). Blood/water respiratory variables and plasma catecholamine levels were measured before and 15 min after exposure to hypoxic water varying between 4.0 and 10.7 kPa (30–80 mmHg) oxygen partial pressure (PwO2). Arterial blood PO2 (PaO2) and oxygen content (CaO2) fell during hypoxia in a similar manner at both temperatures, although the changes in CaO2 were often more pronounced in the fish acclimated to 15 °C. Regardless of acclimation temperature, plasma catecholamine levels were consistently elevated at PwO2 values below 8.0 kPa (60 mmHg); the largest increases in plasma catecholamine levels occurred below PwO2=5.3 kPa (40 mmHg). Adrenaline was the predominant catecholamine released into the circulation. Adrenaline was released at PwO2 values of 8.0 kPa or below, whereas noradrenaline was released at PwO2 values of 6.7 kPa or below. The construction of in vivo oxygen dissociation curves demonstrated an obvious effect of acclimation temperature on haemoglobin (Hb) oxygen-affinity; the P50 values at 15 °C and 5 °C were 3.6 kPa (26.7 mmHg) and 1.9 kPa (14.0 mmHg), respectively. At 15 °C, catecholamines were released into the circulation abruptly at a PaO2 threshold of 4.6 kPa (34.5 mmHg) while at 5 °C the catecholamine release threshold was lowered to 3.3 kPa (24.5 mmHg). The difference in the PaO2 catecholamine release thresholds was roughly equivalent to the difference in the P50 values at the two distinct temperatures. Catecholamine release thresholds, calculated on the basis of arterial blood oxygen-saturation (expressed as CaO2/[Hb]), were similar at both temperatures and were approximately equal to 53–55 % Hb O2-saturation. The results support the contention that the lowering of blood oxygen content/saturation rather than PO2 per se is the proximate stimulus/signal causing catecholamine release in rainbow trout during acute hypoxia.

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