Amino acids injected into the cerebroventricular system induce an enhancement of reflex bradycardia in the rat.

The effects of administration of taurine, GABA and glycine, into the lateral cerebral ventricle, on cardiovascular function were assessed in urethane-anaesthetized rats. Intraventricular administration of either taurine (10-30 micrograms), GABA (5-20 micrograms) or glycine (5-20 micrograms) caused a dose-dependent decrease in both the heart rate and the mean arterial pressure. For example, both the heart rate and the mean arterial pressure fell almost immediately and reached their minimum levels about 5 min after an injection of 20 micrograms of taurine. The cardiovascular responses recovered about 30 min after the injection of taurine. Also, reflex bradycardia was produced in the rats by intravenous infusion of adrenaline (1-5 micrograms/kg). Intraventricular pretreatment of the rats with either taurine, GABA or glycine, although causing no change in the adrenaline-induced pressor effect, did enhance the adrenaline-induced reflex bradycardia. However, pretreatment of the rats intravenously with the same dose of taurine, GABA or glycine had no effect on the adrenaline-induced bradycardia. These data indicate that these amino acids act through a central mechanism to facilitate reflex bradycardia mediated through baroceptor reflexes in response to an acute increase in arterial pressure.