PT  - JOURNAL ARTICLE
AU  - Huerta-Bahena, J
AU  - Villalobos-Molina, R
AU  - García-Sáinz, J A
TI  - Trifluoperazine and chlorpromazine antagonize alpha 1- but not alpha2- adrenergic effects.
DP  - 1983 Jan 01
TA  - Molecular Pharmacology
PG  - 67--70
VI  - 23
IP  - 1
4099  - http://molpharm.aspetjournals.org/content/23/1/67.short
4100  - http://molpharm.aspetjournals.org/content/23/1/67.full
SO  - Mol Pharmacol1983 Jan 01; 23
AB  - 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.