scholarly journals Rapid regulation of Na+ fluxes and ammonia excretion in response to acute environmental hypoxia in the Amazonian oscar, Astronotus ocellatus

2007 ◽  
Vol 292 (5) ◽  
pp. R2048-R2058 ◽  
Author(s):  
Chris M. Wood ◽  
Makiko Kajimura ◽  
Katherine A. Sloman ◽  
Graham R. Scott ◽  
Patrick J. Walsh ◽  
...  

The Amazonian oscar is extremely resistant to hypoxia, and tolerance scales with size. Overall, ionoregulatory responses of small (∼15 g) and large oscars (∼200 g) to hypoxia were qualitatively similar, but the latter were more effective. Large oscars exhibited a rapid reduction in unidirectional Na+ uptake rate at the gills during acute hypoxia (Po2 ∼10 mmHg), which intensified with time (7 or 8 h); Na+ efflux rates were also reduced, so net balance was little affected. The inhibitions were virtually immediate (1st h) and preceded a later 60% reduction (at 3 h) in gill Na+-K+-ATPase activity, reflected in a 60% reduction in maximum Na+ uptake capacity without change in affinity (Km) for Na+. Upon acute restoration of normoxia, recovery of Na+ uptake was delayed for 1 h. These data suggest that dual mechanisms may be involved (e.g., immediate effects of O2 availability on transporters, channels, or permeability, slower effects of Na+-K+-ATPase regulation). Ammonia excretion appeared to be linked indirectly to Na+ uptake, exhibiting a Michaelis-Menten relationship with external [Na+], but the Km was less than for Na+ uptake. During hypoxia, ammonia excretion fell in a similar manner to Na+ fluxes, with a delayed recovery upon normoxia restoration, but the relationship with [Na+] was blocked. Reductions in ammonia excretion were greater than in urea excretion. Plasma ammonia rose moderately over 3 h hypoxia, suggesting that inhibition of excretion was greater than inhibition of ammonia production. Overall, the oscar maintains excellent homeostasis of ionoregulation and N-balance during severe hypoxia.

1989 ◽  
Vol 142 (1) ◽  
pp. 155-175 ◽  
Author(s):  
MARTINE AVELLA ◽  
MICHEL BORNANCIN

The mechanism of ammonia excretion and sodium absorption was re-examined in trout using the isolated-perfused head preparation. Preliminary experiments in which ammonia concentration was increased on the blood side (internal) showed that ammonia and sodium transport was uncoupled. For ammonia excretion, our results showed that gill tissue endogenously produces ammonia. A correlation was demonstrated between ammonia excretion and the internal-external ammonia gradient. We conclude that diffusion in the form of NH3 was responsible for ammonia efflux and we were therefore able to estimate its diffusion coefficient (DNH3 = 1.55×10−6cm2s−1) and permeability coefficient (6×10−3cm s−1). This ammonia diffusion was shown to be modified according to the external proton availability. For sodium absorption, significant changes were caused by indirect modifications of intracellular pH brought about by addition of acetazolamide inside or ammonia outside or by acidification of the internal or external medium. The relationship between sodium and proton transport was further confirmed by the action of the drug amiloride and the measurement of H+ excretion. A possible model representing sodium, proton and ammonia transport through the gill epithelium is proposed.


2021 ◽  
Vol 764 ◽  
pp. 136244
Author(s):  
Elie Farhat ◽  
Maiah E.M. Devereaux ◽  
Hang Cheng ◽  
Jean-Michel Weber ◽  
Matthew E. Pamenter

2020 ◽  
Vol 46 (6) ◽  
pp. 1981-1990
Author(s):  
Hang Li ◽  
Qifang Lai ◽  
Zongli Yao ◽  
Yimeng Liu ◽  
Pengcheng Gao ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Carlos Ricardo Maneck Malfatti ◽  
Leandro Tibiriçá Burgos ◽  
Alexandre Rieger ◽  
Cássio Luiz Rüdger ◽  
Janaína Angela Túrmina ◽  
...  

The essential hypertension has been associated with membrane cell damage. The aim of the present study is investigate the relationship between erythrocyte Na+,K+-ATPase and lipoperoxidation in prehypertensive patients compared to normotensive status. The present study involved the prehypertensive patients (systolic:136±7 mmHg; diastolic:86.8±6.3 mmHg;n=8) and healthy men with normal blood pressure (systolic:110±6.4 mmHg; diastolic:76.1±4.2 mmHg;n=8) who were matched for age (35±4years old). The venous blood samples of antecubital vein (5 mL) were collected into a tube containing sodium heparin as anticoagulant (1000 UI), and erythrocyte ghosts were prepared for quantifying Na+,K+-ATPase activity. The extent of the thiobarbituric acid reactive substances (TBARS) was determined in plasma. The statistical analysis was carried out by Student’st-test and Pearson’s correlation coefficient. AP<0.05was considered significant. The Na+,K+-ATPase activity was lower in prehypertensive patients compared with normotensive subjects (4.9 versus 8.0 nmol Pi/mg protein/min;P<0.05). The Na+,K+-ATPase activity correlated negatively with TBARS content (r=-0.6;P<0.05) and diastolic blood pressure (r=-0.84;P<0.05). The present study suggests that Na+,K+-ATPase activity reduction and elevation of the TBARS content may underlie the pathophysiological aspects linked to the prehypertensive status.


2000 ◽  
Vol 279 (1) ◽  
pp. R161-R168 ◽  
Author(s):  
Akira Takamata ◽  
Hiroshi Nose ◽  
Takashi Kinoshita ◽  
Munetaka Hirose ◽  
Toshiyuki Itoh ◽  
...  

To test the hypothesis that acute hypoxia does not modify the relationship between plasma vasopressin concentration ([AVP]p) and plasma osmolality (Posmol) during exercise and that the increase in [AVP]p during exercise is due mainly to the exercise intensity-dependent increase in Posmol, we examined [AVP]p during a graded exercise in a hypoxic condition (13% O2, N2 balance) in seven healthy male subjects. A graded exercise in a normoxic condition on a separate day served as the control. Hypoxia reduced peak aerobic power (V˙o 2 peak) by 32.4 ± 2.7%. Blood samples obtained during rest and at around 25, 45, 65, 80, and 100% ofV˙o 2 peak of each of the respective conditions were used for analyses of intravascular water and electrolyte balance. The pattern of the changes in fluid and electrolyte balance in response to percentV˙o 2 peak was similar between the two conditions. Plasma volume decreased linearly as percentV˙o 2 peak increased while Posmol increased in a curvilinear fashion with a steep increase occurring at above ∼66%V˙o 2 peak. Above this relative exercise intensity, plasma sodium, potassium, and lactate concentrations also increased, whereas plasma bicarbonate concentration decreased. Thus transvascular fluid movement at above ∼66%V˙o 2 peak was due to the net efflux of hypotonic fluid out of the vascular space in both conditions. The relationship between [AVP]p and Posmol during exercise in response to relative exercise intensity was similar between the two conditions. The results indicate that acute mild hypoxia itself has no direct effect on vasopressin release, and it does not modify the relationship between [AVP]p and Posmol during exercise. The results also support the hypothesis that exercise-induced vasopressin release is primarily stimulated by increased Posmol produced by hypotonic fluid movement out of the vascular space in a relative exercise intensity-dependent manner.


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