Role of tubular secretion and carbonic anhydrase in vertebrate renal sulfate excretion

Abstract

The renal proximal tubule of vertebrates performs an essential role in controlling plasma SO42−concentration ([SO42−]). Although net tubular SO42−reabsorption is the predominate control process in terrestrial vertebrates, a facilitated secretory flux is also present. In contrast, marine teleosts obtain excess SO42−from drinking, and increased plasma [SO42−] is prevented predominately through net tubular secretion. Tubular SO42−secretion is accomplished by at least two electroneutral anion exchange processes in series. Movement of SO42−into the cell across the basolateral membrane is pH dependent, suggesting SO42−/OH−exchange. Luminal HCO3−and Cl−can facilitate SO42−movement out of the cell across the brush-border membrane. The molecular identities of the anion exchangers are unknown but are probably homologues of SO42−transporters in the mammalian SLC26 gene family. In all species tested, glucocorticoids increase renal SO42−excretion. Whereas glucocorticoids downregulate SO42−reabsorptive mechanisms in terrestrial vertebrates, they may also stimulate a mediated secretory flux. In the marine teleost, cortisol increases the level of SO42−/HCO3−exchange at the brush-border membrane, tubular carbonic anhydrase (CA) activity, CAII protein, and a proportion of tubular SO42−secretion that is CA dependent. CA activity is required for about one-half of this net SO42−secretion but is also required for about one-half of the net reabsorption in bird proximal epithelium. A CA-SO42−/anion exchanger metabolon arrangement is proposed that may speed both the secretory and reabsorptive processes.