Suppression of the pressor effect of centrally administered thyrotropin-releasing hormone under halothane, pentobarbital and flunitrazepam anaesthesia.

Intracerebroventricular (i.c.v.) administration of thyrotropin-releasing hormone (TRH) caused an increase in blood pressure (BP) and heart rate (HR) in conscious rats. The pressor effect was greatly diminished by adrenalectomy as well as after pretreatment with phentolamine, an alpha-receptor antagonist or with mecamylamine, a ganglion blocker, suggesting that centrally administered TRH increases BP mainly by stimulating sympathetic activity. Under halothane (0.8%), pentobarbital (33 mg/kg, i.p.) and flunitrazepam (0.8 mg/kg, i.v.) anaesthesia, the pressor effect of TRH was almost completely blocked. The increase in BP induced by peripheral alpha-receptor stimulation with phenylephrine was not affected by the anaesthetics at these doses. Pretreatment with atropine (50 micrograms, i.c.v.) significantly reduced the pressor effect of TRH. Intracerebroventricularly administered haloperidol and bicuculline also partially diminished the increase in BP produced by TRH, while other neurotransmitter blockers such as phentolamine, propranolol and naloxone did not. These results indicate that the anaesthetics at the doses employed interfere with the central neuronal pathway(s), probably cholinergic pathways, through which TRH exerts its pressor effect.