Roles of alpha sub(1)-and beta-adrenergic receptors in adrenergic responsiveness of liver cells formed after partial hepatectomy

The adrenergic receptor involved in the action of epinephrine changed dramatically during the process of active proliferation which follows partial hepatectomy. In control or sham-operated animals, the stimulation of glycogenolysis, gluconeogenesis and ureogenesis by epinephrine was mediated through...

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Published inBiochimica et biophysica acta, Protein structure and molecular enzymology Vol. 763; no. 2; pp. 112 - 119
Main Authors Huerta-Bahena, J, Villalobos-Molina, R, Garcia-Sainz, JA
Format Journal Article
LanguageEnglish
Published 01.01.1983
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Summary:The adrenergic receptor involved in the action of epinephrine changed dramatically during the process of active proliferation which follows partial hepatectomy. In control or sham-operated animals, the stimulation of glycogenolysis, gluconeogenesis and ureogenesis by epinephrine was mediated through alpha sub(1)-adrenergic receptors. In contrast, in hepatocytes obtained from animals partially hepatectomized 3 days before experimentation, the receptor involved in the stimulation of these metabolic pathways by epinephrine was of the beta-adrenergic type. Interestingly, the adrenergic receptor involved in the metabolic actions of epinephrine, in hepatocytes from rats partially hepatectomized 7 days before experimentation was again of the alpha sub(1)-subtype. Thus, it appears that during the process of liver regeneration which follows partial hepatectomy there is a transition in the type of adrenergic receptor involved in the hepatic actions of catecholamines from beta in the initial stages to later alpha sub(1). The number and affinity (for epinephrine or prazosin) of alpha sub(1)-adrenergic receptors did not change at any stage of the process, which indicates that the markedly diminished alpha sub(1)-adrenergic sensitivity observed in hepatocytes obtained from rats partially hepatectomized 3 days before experimentation is probably due to defective generation or intracellular processing of the alpha sub(1)-adrenergic signal, rather than to changes at the receptor level.
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ISSN:0167-4838