ABSTRACT

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, HCO₃⁻ transporters and Rhesus proteins. Consequently, renal acid output in the form of protons and NH₄⁺ 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 HCO₃⁻ 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⁺, HCO₃⁻, NH₃/NH₄⁺) for each tubule segment in C. auratus kidney. While the proximal tubule appears to play a major role in both H⁺ secretion and HCO₃⁻ reabsorption, the distal and connecting tubules seem to mainly serve for HCO₃⁻ reabsorption and NH₃/NH₄⁺ secretion.