Renal proximal tubules absorb HCO3- by secretion of H+ into the tubular lumen. This paper focuses on the mechanisms of HCO3- exit across the basolateral cell membrane. The major exit pathway is rheogenic sodium bicarbonate co-transport. This system transports Na+ and HCO3-, but not Cl-, in obligatory coupling at a fixed overall stoichiometry of three HCO3- to one Na+. The fact that HCO3- flux is reduced after inhibition of cytoplasmic and/or membrane-bound peritubular carbonic anhydrase indicates that HCO3- is not transported as such but is split during permeation into its buffer subspecies from which it is regenerated on the other side of the membrane. Since flow of OH- or of H+ (in opposite directions) can be excluded, it appears most likely that one HCO3- and one CO3(2-) move together with one Na+. Besides carbonic anhydrase inhibitors, disulphonic stilbenes and harmaline are known to block the co-transporter. In addition to rheogenic Na+ (HCO3-)3 co-transport, Na+-dependent and Na+-independent electroneutral Cl-/HCO-3 exchange have been identified. The latter mechanisms are particularly important in S3 segments of proximal tubule where Na+ (HCO3-)3 co-transport is missing. Further mechanisms which operate in parallel, but at lower rates, are electroneutral SO4(2-)/HCO3- exchange and, in some species, lactate/HCO3- exchange. Moreover, there may be some uncoupled OH- flux and it is reasonable to assume that OH- (or H+) flux is involved in the transport of dicarboxylic acids across the basolateral cell membrane.