Ethanol, Liver Regeneration and [Ca] i transients. These changes were not due to an effect on the Ins(1,4,5) P 3 receptor on the endoplasmic reticulum or to a decrease in the size of the Ins(1,4,5) P 3 -mobilizable intracellular Ca 2 ϩ store. Further, mobilization of the same Ca 2 ϩ store by 2,5-di-tert -butylhydroquinone or thapsigargin restored the ability of hepatocytes from ethanol-fed rats to proliferate when exposed to EGF. It is concluded that chronic ethanol consumption inhibits liver regeneration by a mechanism that is, at least partly, the result of impaired receptor-operated [Ca 2 ϩ ] i signaling due to reduced generation of