The effects of administration of thyrotrophic-releasing hormone (TRH) into the lateral cerebral ventricle on cardiovascular functions were assessed in both urethane-anesthetized and unanesthetized rats. Intracerebroventricular administration of TRH (10-60 micrograms in 5.0 microliters volume) caused a dose-dependent increase in both the heart rate and the mean arterial pressure. For example, both the heart rate and the arterial pressure rose almost immediately and reached their maximal levels about 4 min after an injection of 40 micrograms TRH. The cardiovascular responses recovered about 10 min after the TRH injection. In addition, reflex bradycardia was produced by intravenous infusion of epinephrine (1.0-5.0 micrograms/kg) in rats. Over the dose range of epinephrine used, a dose-dependent bradycardia was obtained. It was found that intracerebroventricular pretreatment of animals with TRH, although causing no change in the epinephrine-induced pressor effect, did reduce the epinephrine-induced reflex bradycardia in rats. However, intravenous pretreatment of animals with the same dose of TRH had no effect on the epinephrine-induced bradycardia. Thus, the data indicate that TRH acts through a central mechanism to inhibit reflex bradycardia mediated through baroreceptor reflexes in response to acute increase in blood pressure.