Abstract: The centrally induced hypotensive effects of β-adrenergie blocking agent propranolol in-rabbits were antagonized by the following three ways which attenuated GABA receptor functions: Inhibition of GAB A formation with semicarbazide, inhibition of GABA release from neuron with procaine, and antagonism of GABA effects by picrotoxin. In contrast, the hypotensive effect of propranolol could be enhanced by that pentobarbital increased GABA uptake in the neuron. It is suggested that the hypotensive effect of β-receptor blocker, as that of α-agonists, is mediated via the GABA ergic nervous system.