Metabolic responses to epinephrine stimulation in goldfish hepatocytes: evidence for the presence of alpha-adrenoceptors

Gen Comp Endocrinol. 2001 Feb;121(2):205-13. doi: 10.1006/gcen.2000.7587.


The effect of epinephrine on various aspects of cellular metabolism was studied in hepatocytes from the goldfish Carassius auratus. Epinephrine increased cytosolic free calcium ([Ca2+](i)) from a baseline value of 108 +/- 22 nM to a peak value of 577 +/- 127 nM in suspensions of hepatocytes. Responses of single cells ranged from a single spike (66% of hepatocytes) to variable oscillatory patterns (34%). The increase in [Ca(2+)](i) was independent of the presence of extracellular Ca2+ and was prevented by the alpha-adrenergic antagonist phentolamine. Cellular glucose release induced by epinephrine (1.7- to 3.2-fold) was significantly reduced in Ca2+-depleted cells and in the presence of phentolamine, providing evidence for the co-occurrence of alpha-adrenoceptors and a Ca2+-independent, presumably beta-adrenergic, system in these cells. Furthermore, epinephrine stimulated oxygen consumption in a Ca2+-dependent manner, which was not due to stimulated Na(+) pump activity. An increased rate of acid secretion of 50%, evoked by epinephrine, appears to be mediated by enhanced Na(+)/H(+) exchange but did not result in intracellular alkalization.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acids / metabolism
  • Adrenergic alpha-Agonists / pharmacology*
  • Animals
  • Calcium / metabolism
  • Epinephrine / pharmacology*
  • Glucose / metabolism
  • Goldfish / physiology*
  • Hepatocytes / drug effects*
  • Hydrogen-Ion Concentration
  • Lactic Acid / metabolism
  • Oxygen Consumption / drug effects
  • Receptors, Adrenergic, alpha / drug effects*


  • Acids
  • Adrenergic alpha-Agonists
  • Receptors, Adrenergic, alpha
  • Lactic Acid
  • Glucose
  • Calcium
  • Epinephrine