scholarly journals PROPRANOLOL IMPAIRS THE HYPERVENTILATORY RESPONSE TO ACUTE HYPERCAPNIA IN RAINBOW TROUT

1993 ◽  
Vol 175 (1) ◽  
pp. 115-126 ◽  
Author(s):  
R. Kinkead ◽  
S. Aota ◽  
S. F. Perry ◽  
D. J. Randall
Keyword(s):  
Rainbow Trout ◽  
Ventilatory Response ◽  
Respiratory Acidosis ◽  
Fold Increase ◽  
Treated Group ◽  
Antagonistic Activity ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Adrenergic Response

This study investigated the possible role of catecholamines in the ventilatory response of rainbow trout (Oncorhynchus mykiss) to acute external hypercapnia. The ventilatory response to hypercapnia [partial pressure of CO2 in water (PwCO2=0.76 kPa)] of fish pre-treated with the selective beta-adrenoceptor antagonist, d,l-propranolol, was compared with that of d-propranolol (an isomer with minimal beta-antagonistic activity) and saline pre-treated fish (sham). A sustained 3.6- fold increase in gill ventilation volume (V(dot)w) was observed in the sham and d-propranolol-treated groups during the 30 min interval of hypercapnia. Fish pre-treated with d,l-propranolol displayed a blunted hyperventilatory response to hypercapnia (1.9-fold increase at 30 min). These results indicate that the beta-component of an adrenergic response is involved in the usual hyperventilatory response to external hypercapnia. It is suggested that the impaired hyperventilatory response of the d,l- propranolol-treated group reflects an inhibition of central adrenergic mechanism(s) involved in the hyperventilatory reflex to respiratory acidosis.

Effect Of Environmental Water Salinity on Acid-Base Regulation During Environmental Hypercapnia in the Rainbow Trout (Oncorhynchus Mykiss)

1991 ◽  
Vol 158 (1) ◽  
pp. 1-18 ◽  
Author(s):  
GEORGE K. IWAMA ◽  
NORBERT HEISLER
Keyword(s):  
Rainbow Trout ◽  
Respiratory Acidosis ◽  
Environmental Water ◽  
Ammonia Concentration ◽  
Acid Base ◽  
Clear Trend ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Exchange Processes ◽  
Total Ammonia ◽  
Time Courses

Acid-base regulation in rainbow trout acclimated to about 3, 100 and 500 mmol l−1 Na+ and Cl−, at constant water [HCO3−], was assessed during 24h of exposure to 1% CO2 and during recovery. The respiratory acidosis induced by a rise in plasma PCOCO2 to about 1.15kPa (8.5mmHg, 3mmol l−1), 1.33kPa (10mmHg, 100 mmol l−1) or 1.5 kPa (11.2 mmHg, 500 mmol l−1) was partially compensated for by accumulation of plasma HCO3−. The degree of pH compensation depended on the salinity of the environmental water, being about 61, 82 and 88% at 3, 100 and 300 mmol l−1 Na+ and Cl−, respectively. [HCO3−] in animals acclimated to 100 and 500 mmol l−1 rose to higher values than that in fish at 3 mmol l−1. Plasma [Cl−] decreased during hypercapnia as compared to control concentrations in all groups of fish. Plasma [Na+] rose during the first 8 h of hypercapnia in fish acclimated to all three salinities, but recovered towards control values during the remainder of hypercapnia. The rise in plasma [HCO3−] was significantly related to the fall in plasma [Cl−], whereas the changes in plasma [Na+] were unaffected by simultaneous changes in plasma [HCO3−]. Time courses of changes in plasma [Na+] and total ammonia concentration, [Tamm], were similar but in opposite directions. The transepithelial potential (TEP) of blood relative to water was negative, close to zero and positive, averaging −21, −5.8 and +6.2 mV for fish acclimated to 3, 100 and 300 mmol l−1 Na+, respectively. After initiation of hypercapnia, which caused a quite heterogeneous response among groups, a clear trend towards depolarization was observed during the remainder of hypercapnia. These results confirm the role of active HCO3−/Cl− exchange processes for the compensation of extracellular pH during respiratory acidoses in fish.

Possible involvement of somatolactin in the regulation of plasma bicarbonate for the compensation of acidosis in rainbow trout

1997 ◽  
Vol 200 (21) ◽  
pp. 2675-2683
Author(s):  
S Kakizawa ◽  
A Ishimatsu ◽  
T Takeda ◽  
T Kaneko ◽  
T Hirano
Keyword(s):  
Rainbow Trout ◽  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Pituitary Hormone ◽  
Similar Extent ◽  
Acid Infusion ◽  
Control Value ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Blood Ph ◽  
The Difference

Somatolactin is a putative pituitary hormone of the growth hormone/prolactin family in fish. Its function is still unknown. The effects of environmental hypercapnia and hypoxia, acid (HCl) infusion and exhaustive exercise on plasma somatolactin levels were examined in the chronically cannulated rainbow trout to study the possible physiological roles of somatolactin. Respiratory acidosis induced by hypercapnia (2% CO2) did not affect plasma somatolactin level. In contrast, metabolic acidosis induced by acid infusion and exercise increased plasma somatolactin level. Blood pH was depressed to a similar extent by both types of acidosis, whereas plasma [HCO3-] was elevated by respiratory acidosis but reduced by metabolic acidosis. A moderate hypoxia (water PO2 9.3kPa) affected neither acid­base status nor plasma somatolactin level. A more severe hypoxia (water PO2 6.1kPa) resulted in metabolic acidosis accompanied by an apparent rise in plasma somatolactin level, although the difference in somatolactin level from the control value was not statistically significant. Somatolactin immunoneutralization retarded recovery of plasma [HCO3-] following acid infusion. These results indicate that somatolactin is involved in the retention of HCO3- during metabolic acidosis but not in the active accumulation of HCO3- for acid­base compensation of respiratory acidosis in rainbow trout Oncorhynchus mykiss.

Adrenergic Response to Physiological Disturbances in Rainbow Troutf Oncorhynchus mykiss, Exposed to Aluminum at Acid pH

1991 ◽  
Vol 48 (3) ◽  
pp. 414-420 ◽  
Author(s):  
H. E. Witters ◽  
S. Van Puymbroeck ◽  
O. L. J. Vanderborght
Keyword(s):  
Oncorhynchus Mykiss ◽  
Plasma Catecholamines ◽  
Fold Increase ◽  
Low Ph ◽  
Plasma Epinephrine ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Blood Ph ◽  
Fish Exposure ◽  
Adrenergic Response ◽  
Oxygen Carrying Capacity

A 10-fold increase of plasma epinephrine and norepinephrine levels was evident at 46 h of Al exposure in adult rainbow trout, Oncorhynchus mykiss, which were kept for about 2.5 d at pH 5.0 with 60 μg Al/L (Ca2+ = 28 μmol/L). The change of plasma epinephrine levels was related both to the decrease of the blood pH and the decrease of the blood [Formula: see text]. We further observed decreased plasma Na+ concentrations which were accompanied by elevated levels of Cortisol in the plasma of Al-exposed fish. Exposure of fish to pH 6.8 (= control) or pH 5.0 without Al did not yield any changes in plasma Na+ concentrations, plasma Cortisol concentrations, blood pH, blood [Formula: see text], and plasma epinephrine, norepinephrine, and dopamine levels. The release of plasma catecholamines associated with blood acidosis and hypoxia is suggested to be an important factor in maintaining erythrocytic pH to protect the haemoglobin oxygen carrying capacity in fish exposed to low pH and Al.

Covariation in regulation of affinity for branchial zinc and calcium uptake in freshwater rainbow trout.

1998 ◽  
Vol 201 (11) ◽  
pp. 1809-1815 ◽  
Author(s):  
C Hogstrand ◽  
N Webb ◽  
C M Wood
Keyword(s):  
Rainbow Trout ◽  
Fold Increase ◽  
Experimental Period ◽  
Competitive Inhibitor ◽  
Control Fish ◽  
Control Value ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Significant Linear Correlation ◽  
Ca Uptake ◽  
Transport Site

The possible coupling between regulation of the affinities for branchial Zn and Ca influx was investigated in juvenile rainbow trout Oncorhynchus mykiss acclimated to relatively hard fresh water ([Ca]=1.0 mmol l-1). The Km for branchial Ca influx was manipulated experimentally by exposing the fish to 2.3 micromol l-1 waterborne Zn for a total of 28 days. This procedure resulted in rapidly increased Km values for both Ca and Zn influx, an effect that remained through the experimental period. There was a significant linear correlation (r=0.88, P<0.02) between Km values for Ca and Zn measured at the same time points. Zn exposure caused progressively increasing maximum rate of transport, Jmax, values for Zn relative to the control value, but there was little, if any, effect on Jmax for Ca. These results support the idea of a shared transport site for Zn and Ca at the apical membrane of the gill epithelium and suggest that there is a certain degree of coregulation of branchial Zn and Ca uptake in rainbow trout. Removal of Ca from the water resulted in a large (six- to 24-fold) increase in affinity (decreased Km) for Zn influx and a modest (1.1- to 1.8-fold) increase in Jmax for Zn. Thus, Ca is a competitive inhibitor of Zn influx. In water lacking Ca, the Km for Zn in Zn-acclimated fish was no different from that of the control fish, suggesting that the Ca2+/Zn2+ transporter was regulated to improve Ca uptake.

Toxicological mechanisms of a multicomponent agricultural seed protectant in the rainbow trout (Oncorhynchus mykiss) and fathead minnow (Pimephales promelas)

1997 ◽  
Vol 54 (6) ◽  
pp. 1387-1390 ◽  
Author(s):  
Michael W Greene ◽  
Richard M Kocan
Keyword(s):  
Rainbow Trout ◽  
Alcohol Dehydrogenase ◽  
Ethylene Glycol ◽  
Oncorhynchus Mykiss ◽  
Aldehyde Dehydrogenase ◽  
Fathead Minnow ◽  
Pimephales Promelas ◽  
Fold Increase ◽  
Sublethal Concentration ◽  
Rainbow Trout Oncorhynchus Mykiss

Ethylene glycol (EG) and thiram, an aldehyde dehydrogenase inhibitor, are components of the seed protectant Vitavax-200. EG is a common solvent, thought to be nontoxic, whereas thiram, a dithiocarbamate known to be toxic to fish, is an active ingredient in Vitavax-200. When the\i toxicities of EG and thiram were investigated individually and as a mixture in rainbow trout (Oncorhynchus mykiss) and fathead minnow (Pimephales promelas), a strong synergistic toxic effect was observed. Using a constant sublethal concentration of thiram, a 5- to 19-fold increase and a 2- to 2.4-fold increase in EG toxicity was observed in fathead minnow and rainbow trout, respectively. The toxicity of EG following pretreatment of rainbow trout with pyrazole, an alcohol dehydrogenase inhibitor, was decreased by 22% whereas pretreatment with cyanamide, an aldehyde dehydrogenase inhibitor, increased toxicity 3.4-fold. The results indicate that thiram inhibits the complete metabolism of EG, resulting in the buildup of a toxic aldehyde intermediate and increasing the toxicity of EG.

Describing population dynamics for early life stages of rainbow trout (Oncorhynchus mykiss) using a stock synthesis model1This article is a companion to Korman et al. 2011, published this issue.

2011 ◽  
Vol 68 (6) ◽  
pp. 1110-1123 ◽  
Author(s):  
Josh Korman ◽  
S.J.D. Martell ◽  
Carl Walters
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Early Life ◽  
Survival Rates ◽  
Strong Support ◽  
Fold Increase ◽  
Life Stages ◽  
Early Life Stages ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Wide Range

A stock synthesis model was used to assess effects of experimental flows on early life stages of nonnative rainbow trout ( Oncorhynchus mykiss ) in the Colorado River below Glen Canyon Dam (Arizona, USA). The model estimated time-varying survival rates while correcting for entry of new recruits to the age-0 population and changes in vulnerability to capture associated with growth and ontogenetic habitat shifts. A controlled flood, designed in part to enhance native fish habitat, led to an 11-fold increase in early survival rates (fertilization to ~1 month from emergence) of weekly cohorts of trout fertilized after the flood. Effects of increased flow fluctuations during incubation, designed to reduce trout abundance, were not apparent. Age-0 mortality between August and September was over twofold higher in years when there was a 50% reduction in the minimum flow compared with years when flow was stable. There was strong support for models that simulated an ontogenetic shift to deeper habitat in four of five study years. The integration of detailed field information in a stock synthesis model to describe early life history dynamics is a valuable approach that can be applied in a wide range of systems.

Roles of cytosolic and membrane-bound carbonic anhydrase in renal control of acid-base balance in rainbow trout, Oncorhynchus mykiss

2006 ◽  
Vol 291 (2) ◽  
pp. F407-F421 ◽  
Author(s):  
T. Georgalis ◽  
K. M. Gilmour ◽  
J. Yorston ◽  
S. F. Perry
Keyword(s):  
Rainbow Trout ◽  
Carbonic Anhydrase ◽  
Respiratory Acidosis ◽  
Acid Base Balance ◽  
Reading Frame ◽  
Protein Levels ◽  
Bicarbonate Reabsorption ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Urinary Acidification ◽  
Base Balance

We tested the hypothesis that cytosolic and membrane-associated carbonic anhydrase (CA IV) are involved in renal urinary acidification and bicarbonate reabsorption in rainbow trout. With the use of homological cloning techniques, a 1,137-bp cDNA was assembled that included an open reading frame encoding for a deduced protein of 297 amino acids. Phylogenetic analysis revealed that this protein was likely a CA IV isoform. With the use of this sequence and a previously described trout cytosolic isoform [tCAc ( 13 )], tools were developed to quantify and localize mRNA and protein for the two CA isoforms. Unlike tCAc, which displayed a broad tissue distribution, trout CA IV mRNA (and to a lesser extent protein) was highly and preferentially expressed in the posterior kidney. The results of in situ hybridization, immunocytochemistry, and standard histological procedures demonstrated that CA IV was likely confined to epithelial cells of the proximal tubule with the protein being expressed on both apical and basolateral membranes. The CA IV-containing tubule cells were enriched with Na+-K+-ATPase. Similar results were obtained for tCAc except that it appeared to be present in both proximal and distal tubules. The levels of mRNA and protein for tCAc increased significantly during respiratory acidosis (hypercapnia). Although tCA IV mRNA was elevated after 24 h of hypercapnia, tCA IV protein levels were unaltered. By using F3500, a membrane-impermeant (yet filtered) inhibitor of CA, in concert with blood and urine analyses, we demonstrated that CA IV (and possibly other membrane-associated CA isoforms) plays a role in urinary acidification and renal bicarbonate reabsorption.

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