scholarly journals Acid-Base and Ionic Regulation in the American Eel (Anguilla Rostrata) During and after Prolonged Aerial Exposure: Branchial and Renal Adjustments

1987 ◽  
Vol 133 (1) ◽  
pp. 429-447 ◽  
Author(s):  
D. A. HYDE ◽  
S. F. PERRY

To whom reprint request should be addressed. The involvement of the gill and kidney in acid-base regulation was examined in the American eel, Anguilla rostrata, during 36h of continuous air-exposure and subsequent return to water. While in air, eels developed a severe mixed respiratory/- metabolic acidosis. Renal acid excretion increased only slightly during the latter stages of air-exposure. A pronounced reduction in urine flow rate was important to minimize dehydration but essentially eliminated the kidney as a route for excess acid excretion. Upon return to the water, eels had accrued an extracellular metabolic acid load of 9.53 mmol 1−1. The metabolic acid was cleared from the extracellular compartment at an exceptionally low rate (approximately 70μmol kg−1 h−1) and about 50 % of the acid load remained after 18 h of recovery in water. The clearance of metabolic acid was accounted for by enhanced branchial acid excretion which was related primarily to adjustments of unidirectional Na+ fluxes. Unidirectional Cl− fluxes were undetectable using radiotracer methods. We speculate that the inefficiency of acid-base regulation in the eel compared to other teleosts is, in part, related to the absence of significant branchial C1−/HCO3− exchange.

1988 ◽  
Vol 134 (1) ◽  
pp. 409-422 ◽  
Author(s):  
R. TYLER-JONES ◽  
E. W. TAYLOR

Exposure of the crayfish Austropotamobius pallipes to air resulted in an acidosis in the postbranchial haemolymph (pHa) and the abdominal muscle. The haemolymph acidosis was subsequently compensated and, after 24 h in air, pHa had returned to the settled, submerged value. The intracellular acidosis remained uncompensated throughout the period of aerial exposure. When crayfish were first removed into air, lactate concentrations in the haemolymph and abdominal muscle increased substantially. After 24 h in air lactate concentrations in both compartments had returned towards submerged levels. Possibilities for the fate of lactate are discussed. Re-analysis of haemolymph acid-base data for crayfish exposed to air (Taylor & Wheatly, 1981) revealed discrepancies between observed and expected base excess. Initially these may arise from exchanges of H+ or HCO3− with other compartments. During long-term air exposure, the removal of lactate from the haemolymph and an independent accumulation of base, probably from the mobilization of an internal source of bicarbonate buffer, result in the observed pH compensation. Determination of base excess for the changes in abdominal muscle acid-base status after 3 h of exposure to air corroborated the results of the haemolymph analysis, suggesting a retention of H+ despite the efflux of lactate.


1992 ◽  
Vol 70 (1) ◽  
pp. 8-12
Author(s):  
Mitchell L. Halperin ◽  
Ching-Bun Chen

The purpose of this study was to explore further the relation between the rates of oxygen consumption and ammonium (NH4+) production in the kidney during chronic metabolic acidosis. The experimental model was the dog with chronic metabolic acidosis because of the extensive background literature in this species. Chronic metabolic acidosis was produced by the ingestion of 10 mmol NH4Cl/kg body weight for 5 days. There was a significant increase in the rate of oxygen extraction when hypernatremia was present. Despite this rise in the rate of oxygen consumption, there was no increase in the rate of NH4+ production nor in the rate of glutamine extraction. These data suggest that hypernatremia might prevent a further augmentation in glutamine extraction when the rate of oxygen consumption rises. In addition, a larger proportion of the NH4+ produced was excreted in the urine during hypernatremia. This increase was associated with a rise in the urine flow rate, but not with a fall in urine pH.Key words: Acid–base, ATP, glutamine, energy metabolism, metabolic acidosis, metabolic regulation, net acid excretion, oxygen consumption.


1988 ◽  
Vol 255 (4) ◽  
pp. F763-F770 ◽  
Author(s):  
A. M. Kaufman ◽  
T. Kahn

Studies were performed to investigate the role of concomitant chloride depletion in potassium-depletion alkalosis in the rat and the relationship between potassium depletion, plasma bicarbonate (PHCO3), and net acid excretion. 1) Selective potassium depletion (K-DEPL), potassium plus chloride depletion (KCl-DEPL), or selective chloride depletion (Cl-DEPL) was produced by administering a selectively potassium-, potassium and chloride-, or selectively chloride-deficient diet. In K-DEPL and KCl-DEPL rat, PHCO3 increased progressively and similarly during a 38-day period of restriction, whereas net acid excretion was similar and not elevated in either group. Cl-DEPL did not result in alkalosis. Chloride administration without potassium in alkalotic KCl-DEPL rats did not result in a sustained significant decrease in PHCO3. Potassium administration without chloride in alkalotic KCl-DEPL rats decreased PHCO3. Thus concomitant chloride depletion plays a minimal role in the alkalosis produced by dietary-induced potassium depletion. 2) Administration of a chronic acid load to alkalotic K-DEPL rats did not decrease PHCO3, and net acid excretion increased similarly as in normals. In K-DEPL rats after PHCO3 was reduced toward normal levels with acetazolamide, net acid excretion increased sharply above base-line values and PHCO3 increased markedly. Thus the alkalotic K-DEPL rat maintains the ability to excrete a chronic acid load, and a reduction in PHCO3 elicits an increase in acid excretion to restore the initial acid-base condition. These studies suggest that potassium depletion alters the set-point at which the kidney maintains PHCO3.


Author(s):  
Sam C. Chin ◽  
John Waldman ◽  
Mike Bednarski ◽  
Merry Camhi ◽  
Jake LaBelle ◽  
...  

1972 ◽  
Vol 15 (4) ◽  
pp. 338-346 ◽  
Author(s):  
Herbert S. Diamond ◽  
Robert Lazarus ◽  
David Kaplan ◽  
David Halberstam

2009 ◽  
Vol 16 (4) ◽  
pp. 306-314 ◽  
Author(s):  
H. M. LAMSON ◽  
D. K. CAIRNS ◽  
J.-C. SHIAO ◽  
Y. IIZUKA ◽  
W.-N. TZENG

Author(s):  
Stanley Yeung ◽  
Antonio Gomes-Neto ◽  
Maryse Osté ◽  
Else van den Berg ◽  
Jenny Kootstra-Ros ◽  
...  

Background and objectives: High dietary acid load may accelerate kidney function decline. We prospectively investigated whether dietary acid load is associated with graft outcomes in kidney transplant recipients and whether venous bicarbonate (HCO3−) mediates this association. Design, setting, participants and measurements: We used data from 642 kidney transplant recipients with a functioning graft ≥1 year after transplantation. Net endogenous acid production (NEAP) was estimated using food frequency questionnaires (FFQ) and, alternatively, 24-hour urinary urea and potassium excretion to estimate NEAPUrine. We defined composite kidney endpoint as doubling of plasma creatinine or graft failure. Multivariable Cox regression analyses, adjusted for potential confounders, were used to study the associations of dietary acid load with kidney endpoint. We evaluated potential mediation effects of venous HCO3− , urinary HCO3− excretion, urinary ammonium (NH4+) excretion, titratable acid excretion, and net acid excretion on the association between NEAP and kidney endpoint. Results: Median NEAPFFQ and NEAPUrine were 40 (Interquartile range [IQR] 35-45) and 54 (IQR 44-66) mEq/day, respectively. During a median follow-up time of 5.3 (IQR 4.1-6.0) years, 121 (19%) participants reached kidney endpoint. After multivariable adjustment, NEAPFFQ and NEAPUrine (per SD higher) were independently associated with higher risk for kidney endpoint (hazard ratio [HR] 1.33; 95% confidence interval [CI] 1.12-1.57, P=0.001 and HR 95%CI, 1.44 [1.24-1.69], P<0.001 resp.). Baseline venous HCO3− mediated 20% of the association between NEAPFFQ and kidney endpoint. Baseline venous HCO3−, urinary NH4+ excretion and net acid excretion mediated 25%, -14% and -18% resp. of the association between NEAPUrine and kidney endpoint. Conclusion: Higher dietary acid load was associated with a higher risk of doubling of plasma creatinine or graft failure, and this association was partly mediated by venous HCO3−, urinary NH4+ and net acid excretion.


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