A role for a pertussis toxin-sensitive trimeric G-protein in store-operated Ca super(2+) inflow in hepatocytes

The mechanism of store-operated Ca super(2+) inflow in hepatocytes was investigated using fluo-3 and fura-2 to monitor changes in the concentration of intracellular free Ca super(2+) in single cells, and 1-( alpha -glycerophosphoryl)-myo-inositol 4,5-diphosphate. P super(4(5))-1(2-nitrophenyl)ethyl ester ('caged' GPIP sub(2)) and 'caged' guanosine 5'-[ gamma thio]triphospate (GTP gamma S) (introduced into the cytoplasmic space by microinjection), thapsigargin and 2,5-di-tertbutylhydroquinone (DBHQ) to stimulate Ca super(2+) inflow. Photolysis of 'caged' GPIP sub(2) or 'caged' GTP gamma S stimulated Ca super(2+) inflow. The abilities of GPIP sub(2), thapsigargin and DBHQ to stimulate Ca super(2+) inflow were inhibited by the pre-treatment of hepatocytes with pertussis toxin in vivo for 36 h. Thapsigargin-stimulated Ca super(2+) inflow was also inhibited by guanosine 5'-[ beta -thio]diphosphate (GDP beta S) (introduced by microinjection). It is concluded that, in hepatocytes, store-operated Ca super(2+) inflow induced by the actions of either inositol 1,4,5-trisphosphate, thapsigargin or DBHQ requires a pertussis toxin-sensitive trimeric G-protein.