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

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Huerta-Bahena J, Villalobos-Molina R, Garcia-Sainz JA

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

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

PubMed ID

6135146 [ View in PubMed

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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.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Chlorpromazine	Alpha-1 adrenergic receptors (Protein Group)	Protein group	Humans	Unknown	Inhibitor	Details
Trifluoperazine	Alpha-1A adrenergic receptor	Protein	Humans	Yes	Antagonist	Details