Energy cost of NaCl transport in isolated gills of cutthroat trout

Morgan, John D.; Iwama, George K.

doi:10.1152/ajpregu.1999.277.3.r631

Cited by 68 publications

(60 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The fact that hypercapnia did not cause a decline in SMR indicates that there was no anaesthetic effect of CO 2 (Bernier and Randall, 1998). Conversely, the absence of any increase in SMR, which represents the minimum costs of organismal maintenance, may indicate that energetic costs for acid-base and ion regulation are low in the eel, as they appear to be in other teleosts (Morgan and Iwama, 1999).…”

Section: Discussionmentioning

confidence: 92%

Tolerance of chronic hypercapnia by the European eelAnguilla anguilla

McKenzie

Piccolella

Valle

et al. 2003

Journal of Experimental Biology

View full text Add to dashboard Cite

SUMMARYEuropean eels were exposed for 6 weeks to water CO2 partial pressures (PCO2) from ambient (approx. 0.8 mmHg), through 15±1 mmHg and 30±1 mmHg to 45±1 mmHg in water with a total hardness of 240 mg l–1 as CaCO3, pH 8.2, at 23±1°C. Arterial plasma PCO2 equilibrated at approximately 2 mmHg above water PCO2 in all groups, and plasma bicarbonate accumulated up to 72 mmol l–1 in the group at a water PCO2 of 45 mmHg. This was associated with an equimolar loss of plasma Cl–, which declined to 71 mmol l–1 at the highest water PCO2. Despite this, extracellular acid–base compensation was incomplete; all hypercapnic groups tolerated chronic extracellular acidoses and reductions in arterial blood O2 content (CaO2), of progressive severity with increasing PCO2. All hypercapnic eels, however, regulated the intracellular pH of heart and white muscle to the same levels as normocapnic animals. Hypercapnia had no effect on such indicators of stress as plasma catecholamine or cortisol levels, plasma osmolality or standard metabolic rate. Furthermore, although CaO2 was reduced by approximately 50% at the highest PCO2, there was no effect of hypercapnia on the eels' tolerance of hypoxia, aerobic metabolic scope or sustained swimming performance. The results indicate that, at the levels tested, chronic hypercapnia was not a physiological stress for the eel, which can tolerate extracellular acidosis and extremely low Cl–levels while compensating tissue intracellular pH, and which can meet the O2 requirements of routine and active metabolism despite profound hypoxaemia.

show abstract

Section: Discussionmentioning

confidence: 92%

Tolerance of chronic hypercapnia by the European eelAnguilla anguilla

McKenzie

Piccolella

Valle

et al. 2003

Journal of Experimental Biology

View full text Add to dashboard Cite

show abstract

“…The cost of ionoregulation in freshwater fish has been estimated as 2-20% of resting metabolism (reviewed by Febry and Lutz, 1987), and direct measurements of O 2 consumption by perfused gills yield similar values (4-12%) (Wood et al, 1978;Lyndon, 1994;Morgan and Iwama, 1999). The ion-poor nature of Amazonian waters (Sioli, 1984) may exacerbate these costs, so at a time of severe O 2 limitation, it makes sense to turn down active ion uptake at the gills, as long as ion efflux can be similarly reduced.…”

Section: Surface Morphology Of the Gills During Hypoxiamentioning

confidence: 99%

Regulation of gill transcellular permeability and renal function during acute hypoxia in the Amazonian oscar (Astronotus ocellatus): new angles to the osmorespiratory compromise

Wood

Iftikar

Scott

et al. 2009

Journal of Experimental Biology

View full text Add to dashboard Cite

SUMMARYEarlier studies demonstrated that oscars, endemic to ion-poor Amazonian waters, are extremely hypoxia tolerant, and exhibit a marked reduction in active unidirectional Na + uptake rate (measured directly) but unchanged net Na + balance during acute exposure to low P O2 , indicating a comparable reduction in whole body Na + efflux rate. However, branchial O 2 transfer factor does not fall. The present study focused on the nature of the efflux reduction in the face of maintained gill O 2 permeability. Direct measurements of 22 Na appearance in the water from bladder-catheterized fish confirmed a rapid 55% fall in unidirectional Na + efflux rate across the gills upon acute exposure to hypoxia (P O2 =10-20 torr; 1 torr=133.3 Pa), which was quickly reversed upon return to normoxia. An exchange diffusion mechanism for Na + is not present, so the reduction in efflux was not directly linked to the reduction in Na + influx. A quickly developing bradycardia occurred during hypoxia. Transepithelial potential, which was sensitive to water [Ca 2+ ], became markedly less negative during hypoxia and was restored upon return to normoxia. Ammonia excretion, net K + loss rates, and 3 H 2 O exchange rates (diffusive water efflux rates) across the gills fell by 55-75% during hypoxia, with recovery during normoxia. Osmotic permeability to water also declined, but the fall (30%) was less than that in diffusive water permeability (70%). In total, these observations indicate a reduction in gill transcellular permeability during hypoxia, a conclusion supported by unchanged branchial efflux rates of the paracellular marker [ 3 H]PEG-4000 during hypoxia and normoxic recovery. At the kidney, glomerular filtration rate, urine flow rate, and tubular Na + reabsorption rate fell in parallel by 70% during hypoxia, facilitating additional reductions in costs and in urinary Na + , K + and ammonia excretion rates. Scanning electron microscopy of the gill epithelium revealed no remodelling at a macro-level, but pronounced changes in surface morphology. Under normoxia, mitochondria-rich cells were exposed only through small apical crypts, and these decreased in number by 47% and in individual area by 65% during 3 h hypoxia. We suggest that a rapid closure of transcellular channels, perhaps effected by pavement cell coverage of the crypts, allows conservation of ions and reduction of ionoregulatory costs without compromise of O 2 exchange capacity during acute hypoxia, a response very different from the traditional osmorespiratory compromise.

show abstract

“…The primary site of ion exchange is the gill (Evans et al 2005), which has a low capacity for the oxidation of fatty acids or ketones (Segner et al 1997, Crockett et al 1999. Gill ionocytes utilize glucose from adjacent glycogen-rich cells , and collectively the gill may represent only a fraction (3-8%) of the energy demand (Morgan & Iwama 1999), suggesting that other tissues contribute to the bulk of the expenditure (e.g. brain and kidney; Sangiao-Alvarellos et al 2005, Polakof et al 2006, Tseng & Hwang 2008.…”

Section: Introductionmentioning

confidence: 99%

Role for leptin in promoting glucose mobilization during acute hyperosmotic stress in teleost fishes

Baltzegar

Reading

Douros

et al. 2013

Journal of Endocrinology

View full text Add to dashboard Cite

Osmoregulation is critical for survival in all vertebrates, yet the endocrine regulation of this metabolically expensive process is not fully understood. Specifically, the function of leptin in the regulation of energy expenditure in fishes, and among ectotherms, in general, remains unresolved. In this study, we examined the effects of acute salinity transfer (72 h) and the effects of leptin and cortisol on plasma metabolites and hepatic energy reserves in the euryhaline fish, the tilapia (Oreochromis mossambicus). Transfer to 2/3 seawater (23 ppt) significantly increased plasma glucose, amino acid, and lactate levels relative to those in the control fish. Plasma glucose levels were positively correlated with amino acid levels (R 2 Z0.614), but not with lactate levels. The mRNA expression of liver leptin A (lepa), leptin receptor (lepr), and hormone-sensitive and lipoprotein lipases (hsl and lpl) as well as triglyceride content increased during salinity transfer, but plasma free fatty acid and triglyceride levels remained unchanged. Both leptin and cortisol significantly increased plasma glucose levels in vivo, but only leptin decreased liver glycogen levels. Leptin decreased the expression of liver hsl and lpl mRNAs, whereas cortisol significantly increased the expression of these lipases. These findings suggest that hepatic glucose mobilization into the blood following an acute salinity challenge involves both glycogenolysis, induced by leptin, and subsequent gluconeogenesis of free amino acids. This is the first study to report that teleost leptin A has actions that are functionally distinct from those described in mammals acting as a potent hyperglycemic factor during osmotic stress, possibly in synergism with cortisol. These results suggest that the function of leptin may have diverged during the evolution of vertebrates, possibly reflecting differences in metabolic regulation between poikilotherms and homeotherms.

show abstract

Energy cost of NaCl transport in isolated gills of cutthroat trout

Cited by 68 publications

References 57 publications

Tolerance of chronic hypercapnia by the European eelAnguilla anguilla

Tolerance of chronic hypercapnia by the European eelAnguilla anguilla

Regulation of gill transcellular permeability and renal function during acute hypoxia in the Amazonian oscar (Astronotus ocellatus): new angles to the osmorespiratory compromise

Role for leptin in promoting glucose mobilization during acute hyperosmotic stress in teleost fishes

Contact Info

Product

Resources

About