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.

Hydrogen sulfide stimulates catecholamine secretion in rainbow trout (Oncorhynchus mykiss)

2009 ◽  
Vol 296 (1) ◽  
pp. R133-R140 ◽  
Author(s):  
Steve F. Perry ◽  
Brian McNeill ◽  
Eshay Elia ◽  
Ashish Nagpal ◽  
Branka Vulesevic
Keyword(s):  
Hydrogen Sulfide ◽  
Rainbow Trout ◽  
Chromaffin Cells ◽  
Acute Hypoxia ◽  
Electrical Field Stimulation ◽  
Catecholamine Secretion ◽  
Cardinal Vein ◽  
Posterior Cardinal Vein ◽  
Stimulation Of

We tested the hypothesis that endogenously produced hydrogen sulfide (H2S) can potentially contribute to the adrenergic stress response in rainbow trout by initiating catecholamine secretion from chromaffin cells. During acute hypoxia (water Po2 = 35 mmHg), plasma H2S levels were significantly elevated concurrently with a rise in circulating catecholamine concentrations. Tissues enriched with chromaffin cells (posterior cardinal vein and anterior kidney) produced H2S in vitro when incubated with l-cysteine. In both tissues, the production of H2S was eliminated by adding the cystathionine β-synthase inhibitor, aminooxyacetate. Cystathionine β-synthase and cystathionine γ-lyase were cloned and sequenced and the results of real-time PCR demonstrated that with the exception of white muscle, mRNA for both enzymes was broadly distributed within the tissues that were examined. Electrical field stimulation of an in situ saline-perfused posterior cardinal vein preparation caused the appearance of H2S and catecholamines in the outflowing perfusate. Perfusion with the cholinergic receptor agonist carbachol (1 × 10−6 M) or depolarizing levels of KCl (1 × 10−2 M) caused secretion of catecholamines without altering H2S output, suggesting that neuronal excitation is required for H2S release. Addition of H2S (at concentrations exceeding 5 × 10−7 M) to the perfusion fluid resulted in a marked stimulation of catecholamine secretion that was not observed when Ca2+-free perfusate was used. These data, together with the finding that H2S-induced catecholamine secretion was unaltered by the nicotinic receptor blocker hexamethonium, suggest that H2S is able to directly elicit catecholamine secretion via membrane depolarization followed by Ca2+-mediated exocytosis.

Neuronal control of catecholamine secretion from chromaffin cells in the rainbow trout (Oncorhynchus mykiss)

1999 ◽  
Vol 202 (15) ◽  
pp. 2059-2069 ◽  
Author(s):  
C.J. Montpetit ◽  
S.F. Perry
Keyword(s):  
Rainbow Trout ◽  
Muscarinic Receptors ◽  
Chromaffin Cells ◽  
Catecholamine Secretion ◽  
Field Stimulation ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Neuronal Control ◽  
Muscarinic Cholinergic ◽  
Pre Treatment ◽  
Stimulation Technique

The goal of the present investigation was to assess the relative involvement of nicotinic and muscarinic cholinergic receptors in the neuronal control of catecholamine secretion from the chromaffin tissue of rainbow trout (Oncorhynchus mykiss). This was accomplished by first developing and validating a nerve-stimulating technique able specifically to activate the nerve fibres innervating the chromaffin cells in order to elicit secretion of catecholamines. Using an in situ saline-perfused posterior cardinal vein preparation, it was demonstrated that whole-body field stimulation caused specific voltage-dependent neuronal stimulation of adrenaline and noradrenaline secretion. The contribution of non-specific depolarization was negligible. Several experimental results confirmed the specificity of the field stimulation technique. First, pre-treatment with neostigmine (an anticholinesterase) prolonged and more than doubled the amount of adrenaline secreted in response to electrical stimulation. Second, pre-treatment with the nicotinic receptor antagonist hexamethonium inhibited the electrically evoked secretion of adrenaline and noradrenaline. Third, perfusion with Na+-free saline or removal of the spinal cord abolished secretion of both catecholamines in response to the electrical stimulus. By using the field stimulation technique, this study is the first to demonstrate conclusively a role for muscarinic receptors in catecholamine secretion from trout chromaffin cells. Specifically, muscarinic cholinergic stimulation enhances nicotinic-evoked secretion of catecholamines and, under intense stimulation, may directly cause secretion. The results of the present study suggest the presence of muscarinic receptors on rainbow trout chromaffin cells with a functional role in the cholinergic control of catecholamine secretion.

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.

Desensitisation of chromaffin cell nicotinic receptors does not impede catecholamine secretion during acute hypoxia in rainbow trout (Oncorhynchus mykiss)

2000 ◽  
Vol 203 (10) ◽  
pp. 1589-1597 ◽  
Author(s):  
K.N. Lapner ◽  
C.J. Montpetit ◽  
S.F. Perry
Keyword(s):  
Nicotinic Receptor ◽  
Nicotinic Receptors ◽  
Acute Hypoxia ◽  
Plasma Catecholamine ◽  
Cardinal Vein ◽  
Plasma Adrenaline ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Posterior Cardinal Vein ◽  
Receptor Desensitisation

Experiments were performed on adult rainbow trout (Oncorhynchus mykiss) in vivo using chronically cannulated fish and in situ using a perfused posterior cardinal vein preparation (i) to characterise the desensitisation of chromaffin cell nicotinic receptors and (ii) to assess the ability of fish to secrete catecholamines during acute hypoxia with or without functional nicotinic receptors. Intra-arterial injection of nicotine (6.0×10(−)(7)mol kg(−)(1)) caused a rapid increase in plasma adrenaline and noradrenaline levels; the magnitude of this response was unaffected by an injection of nicotine given 60 min earlier. Evidence for nicotinic receptor desensitisation, however, was provided during continuous intravenous infusion of nicotine (1.3×10(−)(5)mol kg(−)(1)h(−)(1)) in which plasma catecholamine levels increased initially but then returned to baseline levels. To ensure that the decline in circulating catecholamine concentrations during continuous nicotine infusion was not related to changes in storage levels or altered rates of degradation/clearance, in situ posterior cardinal vein preparations were derived from fish previously experiencing 60 min of saline or nicotine infusion. Confirmation of nicotinic receptor desensitisation was provided by demonstrating that the preparations derived from nicotine-infused fish were unresponsive to nicotine (10(−)(5)mol l(−)(1)), yet remained responsive to angiotensin II (500 pmol kg(−)(1)). The in situ experiments demonstrated that desensitisation of the nicotinic receptor occurred within 5 min of receptor stimulation and that resensitisation was established 40 min later. The ability to elevate plasma catecholamine levels during acute hypoxia (40–45 mmHg; 5.3-6.0 kPa) was not impaired in fish experiencing nicotinic receptor desensitisation. Indeed, peak plasma adrenaline levels were significantly higher in the desensitised fish during hypoxia than in controls (263+/−86 versus 69+/−26 nmol l(−)(1); means +/− s.e.m., N=6-9). Thus, the results of the present study demonstrate that activation of preganglionic sympathetic cholinergic nerve fibres and the resultant stimulation of nicotinic receptors is not the sole mechanism for eliciting catecholamine secretion during hypoxia.

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 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.

Evidence for an intrarenal renin-angiotensin system in the rainbow trout, Oncorhynchus mykiss

2000 ◽  
Vol 278 (6) ◽  
pp. R1685-R1691 ◽  
Author(s):  
J. Anne Brown ◽  
Richard K. Paley ◽  
Shehla Amer ◽  
Stephen J. Aves
Keyword(s):  
Rainbow Trout ◽  
Renin Angiotensin System ◽  
Aortic Pressure ◽  
Vascular Effects ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Molecular Approaches ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Intrarenal Ras

Physiological and molecular approaches were used to investigate the existence of an intrarenal renin-angiotensin system (RAS) in rainbow trout. Inhibition of angiotensin-converting enzyme by captopril (5 × 10− 4 M) rapidly decreased vascular resistance of the trunk of the trout, perfused at 19 mmHg, resulting in an increased perfusate flow rate and a decreased intrarenal dorsal aortic pressure. A profound diuresis occurred in the in situ perfused kidney and reflected both increased glomerular filtration rates and decreased water reabsorption (osmolyte reabsorption was unchanged). Renal and vascular parameters recovered once captopril treatment was stopped. Diuretic and vascular effects of captopril on the in situ trout kidney concur with an inhibition of known vasoconstrictor and antidiuretic actions of angiotensin II. However, at a higher perfusion pressure (28 mmHg), captopril had no effect on intrarenal aortic pressure or perfusate and urine flow rates, suggesting that the trout intrarenal RAS is activated by low perfusion pressures/flows. Existence of the renal RAS in trout was further supported by evidence for angiotensinogen gene expression in kidney as well as liver.

scholarly journals Cyclical Changes in Interrenal and Chromaffin Cells in Relation to Testicular Activity of Olive Barb, Puntius Sarana (Hamilton)

2014 ◽  
Vol 22 (2) ◽  
pp. 151-158 ◽  
Author(s):  
Padmanabha Chakrabarti ◽  
Saroj Kumar Ghosh
Keyword(s):  
Chromaffin Cells ◽  
Head Kidney ◽  
Staining Intensity ◽  
Annual Reproductive Cycle ◽  
Cardinal Vein ◽  
Distinctive Features ◽  
Testicular Cells ◽  
Post Spawning ◽  
Puntius Sarana ◽  
Posterior Cardinal Vein

Abstract The present study focused on observations of the histological status of adrenocortical tissues and the correlated seasonal changes in testicular activities in Puntius sarana (Hamilton). Interrenal and chromaffin cells were located in the head kidney between the posterior cardinal vein and hemopoietic tissues. Various male germ cells were identified in the testis based on distinctive features, distribution, and staining properties. The cytoplasmic features and the architecture of the interrenal and chromaffin cells varied during different phases of the annual reproductive cycle. The cytoplasm mass was elevated throughout maturation and spawning phases; however, it was weak in the post-spawning and growth phases. The staining intensity changed in the cells showing various phases of secretory efficiency harmonized with the constitution of different testicular cells.

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