title: Physiological and molecular responses of the goldfish (Carassius auratus) kidney to metabolic acidosis, and potential mechanisms of renal ammonia transport.
abstract: Relative to the gills, the mechanisms by which the kidney contributes to ammonia and acid-base homeostasis in fish are poorly understood. Goldfish were exposed to a low pH environment (pH 4.0, 48 h), which induced a characteristic metabolic acidosis and an increase in total plasma [ammonia] but reduced plasma ammonia partial pressure (PNH3). In the kidney tissue, total ammonia, lactate and intracellular pH remained unchanged. The urinary excretion rate of net base under control conditions changed to net acid excretion under low pH, with contributions from both the NH4 (+) (∼30%) and titratable acidity minus bicarbonate (∼70%; TA-HCO3 (-)) components. Inorganic phosphate (Pi), urea and Na(+) excretion rates were also elevated while Cl(-) excretion rates were unchanged. Renal alanine aminotransferase activity increased under acidosis. The increase in renal ammonia excretion was due to significant increases in both the glomerular filtration and the tubular secretion rates of ammonia, with the latter accounting for ∼75% of the increase. There was also a 3.5-fold increase in the mRNA expression of renal Rhcg-b (Rhcg1) mRNA. There was no relationship between ammonia secretion and Na(+) reabsorption. These data indicate that increased renal ammonia secretion during acidosis is probably mediated through Rhesus (Rh) glycoproteins and occurs independently of Na(+) transport, in contrast to branchial and epidermal models of Na(+)-dependent ammonia transport in freshwater fish. Rather, we propose a model of parallel H(+)/NH3 transport as the primary mechanism of renal tubular ammonia secretion that is dependent on renal amino acid catabolism.
authors.affiliation: Department of Biology, McMaster University, Hamilton, ON, Canada L8S 4K1 Department of Biology, Carleton University, Ottawa, ON, Canada K1S 5B6 m_lawrence27@live.ca.
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Lawrence
authors.affiliation: Department of Integrative Biology, University of Guelph, Guelph, ON, Canada N1G 2W1.
authors.forename: Patricia A
authors.initials: PA
authors.lastname: Wright
authors.affiliation: Department of Biology, McMaster University, Hamilton, ON, Canada L8S 4K1 Department of Zoology, University of British Columbia, Vancouver, BC, Canada V6T 1Z4.
authors.forename: Chris M
authors.initials: CM
authors.lastname: Wood
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000641:Ammonia / Q000378:metabolism* / Q000652:urine; D000818:Animals; D001692:Biological Transport; D005919:Glomerular Filtration Rate; D006023:Glycoproteins / Q000235:genetics / Q000378:metabolism; D006054:Goldfish / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D007668:Kidney / Q000378:metabolism*; D007684:Kidney Tubules / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism; D010710:Phosphates / Q000652:urine; D012333:RNA, Messenger / Q000378:metabolism; D012964:Sodium / Q000378:metabolism / Q000652:urine; D014508:Urea / Q000378:metabolism / Q000652:urine
chemical_list: D006023:Glycoproteins; D010710:Phosphates; D012333:RNA, Messenger; D019344:Lactic Acid; D000641:Ammonia; D014508:Urea; D012964:Sodium; D000410:Alanine Transaminase
keywords: Acid­–base regulation; Amino acid catabolism; Glomerular filtration rate; Na+ transport; Renal excretion; Renal tubule; Rhesus glycoproteins; Urine flow rate; Urine pH