The hypothalamic paraventricular nucleus (PVN) plays a critical role in cardiovascular and neuroendocrine regulation. Angiotensin II (ANG) acts throughout the periphery in the maintenance of fluid-electrolyte homeostasis and has also been demonstrated to act as a neurotransmitter in PVN exerting considerable influence on neuronal excitability in this nucleus. The mechanisms underlying the ANG mediated excitation of PVN magnocellular neurons have yet to be determined. We have used whole cell patch clamp techniques in hypothalamic slices to examine the effects of ANG on magnocellular neurons. Application of ANG resulted in a depolarization of magnocellular neurons, a response which was abolished in tetrodotoxin (TTX) suggesting an indirect mechanism of action. Interestingly, ANG also increased the frequency of EPSP/Cs in magnocellular neurons an effect which was abolished following application of the glutamate antagonist kynurenic acid. ANG was without effect on the amplitude of EPSCs suggesting a pre-synaptic action on an excitatory interneuron within PVN. The ANG induced depolarization was shown to be sensitive to kynurenic acid revealing the requisite role of glutamate in mediating the ANG induced excitation of magnocellular neurons. These observations indicate that the ANGergic excitation of magnocellular PVN neurons are dependent upon an increase in glutamatergic input and thus highlight the importance of a glutamate interneuron in mediating the effects of this neurotransmitter.