Display Settings:

Format

Send to:

Choose Destination
    Mol Pharmacol. 1983 Jan;23(1):67-70.

    Trifluoperazine and chlorpromazine antagonize alpha 1- but not alpha2- adrenergic effects.

    Abstract

    Trifluoperazine and chlorpromazine inhibited in a dose-dependent manner the stimulation of glycogenolysis, gluconeogenesis, and ureogenesis due to alpha 1-adrenergic stimulation in rat hepatocytes. In contrast, the antipsychotic agents were unable to block the inhibition of adenylate cyclase due to alpha 2-adrenergic activation in hamster adipocytes. Binding experiments showed that trifluoperazine and chlorpromazine at low concentrations displaced tritiated dihydroergocryptine binding from rat liver membranes (alpha 1-adrenergic sites), whereas very large concentrations of the phenothiazine derivatives were required to displace dihydroergocryptine from hamster adipocyte membranes (alpha 2-adrenergic sites). It is concluded that chlorpromazine and trifluoperazine are much more potent at alpha 1- than at alpha 2-adrenergic receptors. The use of rat hepatocytes and hamster adipocytes to study the alpha-adrenergic subtype selectivity of drugs is proposed.

    PMID:
    6135146
    [PubMed - indexed for MEDLINE]

      Supplemental Content

      Icon for HighWire Press

      Save items

      loading

      Recent activity

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      Write to the Help Desk