GABA_B receptor function is upregulated in the paraventricular nucleus (PVN) of the hypothalamus in spontaneously hypertensive rats (SHR), but it is unclear whether this upregulation occurs pre- or postsynaptically. We determined pre- and postsynaptic GABA_B receptor function in retrogradely labeled spinally projecting PVN neurons using whole-cell recording in brain slices in SHR and Wistar-Kyoto (WKY) rats. Bath application of the baclofen decreased the spontaneous firing activity of labeled PVN neurons in both SHR and WKY rats. However, the magnitude of reduction in the firing rate was greater in SHR than in WKY rats. Furthermore, baclofen produced larger membrane hyperpolarization and outward currents in labeled PVN neurons in SHR than in WKY rats. The baclofen-induced current was abolished by either including G-protein inhibitor GDP--s in the pipette solution or bath application of the GABA_B receptor antagonist. Blocking NMDA receptors had no significant effect on baclofen-elicited outward currents in SHR. In addition, baclofen caused greater inhibition of glutamatergic excitatory postsynaptic currents in labeled PVN neurons in SHR than in WKY rats. By contrast, baclofen produced less inhibition of GABAergic inhibitory postsynaptic currents in labeled PVN neurons in SHR than in WKY rats. These findings suggest that postsynaptic GABA_B receptor function is upregulated in PVN presympathetic neurons in SHR. While presynaptic GABA_B receptor control of glutamatergic synaptic inputs is enhanced, presynaptic GABA_B receptor control of GABAergic inputs in the PVN is attenuated in SHR. Changes in both pre- and postsynaptic GABA_B receptors in the PVN may contribute to the control of sympathetic outflow in hypertension.