title: Effects of chemical anoxia on adrenergic responses of goldfish hepatocytes and the contribution of alpha- and beta-adrenoceptors.
abstract: Adrenergic responses during normoxia and chemical anoxia were investigated in anoxia-tolerant hepatocytes from the goldfish, Carassius auratus. Epinephrine-stimulated glucose release was unaltered after 1 hr of chemical anoxia, the concentration of epinephrine required for half maximal stimulation of glucose release (K0.5(GLU)) ranging from 0.62 x 10(-8) to 2.05 x 10(-8) M. Similarly, the maximum rate of glucose release caused by hormonal stimulation was not affected by chemical anoxia. In anoxic goldfish hepatocytes [Ca2+](i) remained constant in nonstimulated cells but could be elevated by addition of epinephrine. The magnitude of this [Ca(2+)](i)-increase was dependent on the concentration of the catecholamine and this dependency was similar under normoxia (K0.5(Ca2+) = 1.17 x 10(-8) M) and chemical anoxia (K0.5(Ca2+) = 1.15 x 10(-8) M), as was the percentage of cells responding (77%) and displaying oscillatory [Ca2+]i response patterns (60%) after epinephrine addition, although the frequency of [Ca2+]i oscillations was significantly lower in anoxic cells. To analyze a possible shift in the importance of alpha- and beta-adrenoceptors during chemical anoxia, the effect of phentolamine and propranolol, alpha- and beta-adrenergic antagonists respectively, on epinephrine-stimulated glucose release was studied. Application of the alpha-antagonist caused a dose-dependent reduction of glucose-release which was similar under both conditions, whereas the sensitivity to the beta-antagonist was lowered after chemical anoxia. Taken together these results provide evidence that during chemical anoxia goldfish hepatocytes remain responsive to adrenergic stimulation and that there is a partial shift regarding the contribution of alpha- and beta-adrenergic pathways to the induction of cellular glucose release stimulated by epinephrine.
authors.affiliation: Institut für Zoologie und Limnologie, Abteilung für Okophysiologie, Universität Innsbruck, A-6020 Innsbruck, Austria.
authors.forename: Claudia
authors.initials: C
authors.lastname: Manzl
authors.forename: Markus
authors.initials: M
authors.lastname: Schubert
authors.forename: Pablo J
authors.initials: PJ
authors.lastname: Schwarzbaum
authors.forename: Gerhard
authors.initials: G
authors.lastname: Krumschnabel
mesh_terms: D000818:Animals; D004837:Epinephrine / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism; D006054:Goldfish / Q000502:physiology*; D022781:Hepatocytes / Q000502:physiology; D000860:Hypoxia / Q000503:physiopathology*; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology*
chemical_list: D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D005947:Glucose; D004837:Epinephrine