Please use this identifier to cite or link to this item:
|Title:||Functional characterization of renal ammonia transport and acid-base regulation in teleost and elasmobranch fishes|
|Authors:||Lawrence, Michael J.|
|Advisor:||Wood, Chris M.|
Wright, Patricia A.
|Keywords:||Ammonia;Renal ammonia transport;Kidney;Sodium;Rhesus glycoproteins;Acid-base regulation;Teleost fish;Elasmobranch fish;Comparative and Evolutionary Physiology;Systems and Integrative Physiology;Biology;Cellular and Molecular Physiology;Metabolic Acidosis;Gills;Amino acid metabolism;H+ ATPase|
|Abstract:||Teleost fishes incorporate renal ammonia excretion as part of a greater acid-base regulatory system. However, the transport mechanisms employed by the renal epithelium to excrete ammonia are relatively unknown. I hypothesized that, under metabolic acidosis, increased renal ammonia excretion would be the product of tubular secretion and involve a Na+/NH4+ exchange metabolon mediated through Rhesus (Rh) glycoproteins. To induce metabolic acidosis, goldfish (Carassius auratus) were exposed to a low pH environment (pH 4.0; 48-h). There was a clear signal of metabolic acidosis: a reduction in both plasma [HCO3-] and blood pH with no influence on plasma PCO2. Goldfish demonstrated an elevation in total plasma [ammonia] with a reduction in PNH3 under acidosis. Metabolic acidosis induced higher rates of urinary excretion of acidic equivalents in the form of both NH4+ and titratable acidity-HCO3- (TA-HCO3-) excretion. Urinary Na+ excretion was not affected by acidosis and urine [Na+] did not correlate with urinary [ammonia]. Alanine aminotransferase activity in the kidney was higher in acidotic goldfish. Glomerular filtration rate and urine flow rate were not affected by acidosis. Increased renal NH4+ excretion was due to increased secretion, and not increased filtration, of ammonia. There was a corresponding elevation in Rhcg1b mRNA expression but no change in renal Na+ reabsorption. My data support a secretion-based mechanism of teleost renal ammonia transport. This system is Na+ independent and is likely mediated by Rh glycoproteins and H+ ATPase, involving a parallel H+/NH3 secretion mechanism. To investigate effects of metabolic acidosis on elasmobranch fish, Pacific spiny dogfish (Squalus acanthias suckleyi) were infused with an acidic saline (125 mM HCl/375 mM NaCl; 3 ml/kg/h; 24-h). The results are preliminary, with no marked effects of HCl infusion on plasma acid-base or N-status, but increased branchial NHE2 and lower renal NHE3 protein expressions. These data are summarized in an Appendix.|
|Appears in Collections:||Open Access Dissertations and Theses|
Files in This Item:
|Functional Characterization of renal ammonia transport and acid base regulation in teleost and elasmobranch fish Michael J Lawrence.pdf||Compiled Thesis||1.03 MB||Adobe PDF||View/Open|
Items in MacSphere are protected by copyright, with all rights reserved, unless otherwise indicated.