AJP - Renal Physiology, Vol 244, Issue 6 712-F718, Copyright © 1983 by American Physiological Society
Intracellular pH, transepithelial pH gradients, and ADH-induced water channels
M. Parisi, J. Wietzerbin and J. Bourguet
Urinary bladders of frogs were exposed to a transepithelial proton and
osmotic gradient (serosal pH 8.1, Tris or bicarbonate buffer; mucosal pH
5.8, unbuffered) while the alkalinization rate of the mucosal bath and the
net water movement were simultaneously monitored. It was observed that 1)
the mucosal alkalinization rate was dependent on serosal pH and buffer; 2)
oxytocin increased the mucosal alkalinization rate only when serosal
bicarbonate was employed, whereas the net water movement augmented both
when serosal bicarbonate or Tris buffers were used; 3) amiloride did not
modify the mucosal alkalinization rate either before or after oxytocin; 4)
the increases in the mucosal alkalinization rate and in the net water
movement induced by oxytocin (serosal bicarbonate) were negatively
correlated. In other experiments intracellular pH (pHi) was estimated with
the DMO distribution technique with the following results. 1) Oxytocin
increased the pHi when either serosal bicarbonate or Tris buffers was used
and even in the presence of a low mucosal pH (Tris buffer, pH 5.8). 2)
Important cellular acidification was observed when CO2 was bubbled (to pH
5.8), whereas the hydrosmotic response to 8-bromo-cAMP was clearly
inhibited. These results indicate that cellular alkalinization could play a
pivotal role in action of ADH, show that ADH can modify the transepithelial
pH equilibrium mechanism, and suggest that intracellular pH regulation and
water permeability control can be linked regulatory processes.
