Anti-anaphylactic action in the mouse of thyrotropin-releasing hormone (TRH) is mediated through beta 1-adrenoceptive effectors.

Intravenous or intracerebroventricular administration of thyrotropin-releasing hormone (TRH) significantly improved survival in immunized mice subjected to fatal anaphylaxis by intravenous challenge with an antigen. This protective action of TRH was blocked by pretreatment with the beta-adrenergic antagonist propranolol (5 mg/kg), or by prior administration of the cardioselective beta 1-antagonist, metoprolol (5 mg/kg), but not by pretreatment with the beta 2-selective antagonist, butoxamine (5 mg/kg). It is suggested, based on the present and previous findings that the anti-anaphylactic effect of TRH in the mouse is mediated through activation of beta 1-adrenoceptive effectors, secondary to central stimulation of sympathomedullary release of catecholamines.