In a non-isotonic environment, cells can shrink or swell and return to thei
r normal shape by activating ion transport pathways. Changes in intracellul
ar pH (pHi) after osmotic stress have been identified in several cells. In
order to study the mechanisms that regulate cytosolic pH of rat mast cells
in a hypertonic medium, we used the pH sensitive dye, BCECF. Under these hy
pertonic conditions, pHi undergoes an alkalinization following an initial a
cidification. The alkalinization is mediated by a Na+/H+ exchanger, since i
t is inhibited by amiloride and lack of extracellular sodium. Under these c
onditions, the alkalinization is increased with the PKC activators, TPA and
GAG, and partially blocked with trifluoperazine, an unspecific protein kin
ase C (PKC) and Ca+2 calmodulin-dependent protein kinases (Ca+2/CaM Ii) inh
ibitor. There is also an anion exchanger, blocked with DIDS but not activat
ed by PKC, that participates in the observed alkalinization. However, Na+/M
+ exchanger is the main mechanism involved in the alkalinization of pHi of
mast cells in a hyperosmotic environment. (C) 2000 Elsevier Science Inc. Al
l rights reserved.