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

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.