In rat mast cells Ca2+ entry is modified by the presence or absence of othe
r ions in the external medium. HCO3- ions, which modify mast cell degranula
tion, seemed to modulate the Ca2+ entry elicited by the intracellular Ca2+-
ATPase inhibitor thapsigargin. In this work we studied the regulation of th
e Ca2+ entry by HCO3- and its relationship with exocytosis, The Ca2+ entry
was activated by thapsigargin and Ca2+ in mast cells bathed by a HCO3--buff
ered medium or a HCO3--free medium, Both Ca2+ entry and exocytosis were enh
anced by the presence of HCO3- ions. Nondegranulated mast cells showed a lo
w Ca2+ entry either in the presence or absence of HCO3-. Thus, mast cells w
ith a high [Ca2+](i) increase in a HCO3--buffered medium undergo degranulat
ion. In the same cells a second Ca2+ entry was significantly higher than th
e first Ca2+ entry in a HCO3--free medium, while in a HCO3--buffered medium
the first and second Ca2+ entries reached similar [Ca2+](i) levels. Althou
gh the second Ca2+ entry is high in a HCO3--free medium, degranulation is s
till low. Our results demonstrate that HCO3- ions increase the capacitative
Ca2+ entry and the sensitivity of mast cells to intracellular Ca2+ in orde
r to induce degranulation. (C) 2001 Academic Press.