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A recent study demonstrated that in response to a feeding-induced metabolic acidosis, goldfish ( Carassius auratus ) adjust epithelial protein and/or mRNA expression in their kidney tubules for multiple transporters known to be relevant for acid-base regulation. These include Na + /H + exchanger (NHE), V-type H + -ATPase (V-ATPase), cytoplasmic carbonic anhydrase, HCO 3  - transporters and Rhesus proteins. Consequently, renal acid output in the form of protons and NH 4  + increases. However, little is known about the mechanistic details of renal acid-base regulation in C. auratus and teleost fishes in general. The present study applied the scanning ion-selective electrode technique (SIET) to measure proton flux in proximal, distal and connecting tubules of goldfish. We detected increased H + efflux into the extracellular fluid from the tubule in fed animals, resulting from paracellular back-flux of H + through the tight junction. By applying inhibitors for selected acid-base regulatory epithelial transporters, we found that cytosolic carbonic anhydrase and HCO 3  - transporters were important in mediating H + flux in all three tubule segments of fed goldfish. Contrastingly, V-ATPase seemed to play a role in H + flux only in proximal and distal tubules, and NHE in proximal and connecting tubules. We developed working models for transport of acid-base relevant equivalents (H + , HCO 3  - , NH 3 /NH 4  + ) for each tubule segment in C. auratus kidney. While the proximal tubule appears to play a major role in both H + secretion and HCO 3  - reabsorption, the distal and connecting tubules seem to mainly serve for HCO 3  - reabsorption and NH 3 /NH 4  + secretion.

Section-specific H+ fluxes in renal tubules of fasted and fed goldfish