Neurosecretory parvocellular neurons in the hypothalamic paraventricular nucleus (PVN) exercise considerable influence over the adenohypophysis and thus play a critical role in neuroendocrine regulation. Angiotensin II (AII) has been demonstrated to act as a neurotransmitter in PVN exerting significant impact on neuronal excitability and also influencing CRH secretion from the median eminence and therefore release of ACTH from the pituitary. We have used whole cell patch clamp techniques in hypothalamic slices to examine the effects of AII on the excitability of neurosecretory parvocellular neurons. AII application resulted in a dose-dependent depolarization of neurosecretory neurons, a response which was maintained in tetrodotoxin (TTX) suggesting a direct mechanism of action. The depolarizing actions of this peptide were abolished by losartan demonstrating these effects to be AT₁ receptor mediated. Voltage-clamp analysis using slow voltage ramps revealed that AII activates a voltage independent conductance with a reversal potential of -37.8±3.8mV suggesting effects on a non-selective cationic current. Further, a sustained potassium current characteristic of I_k was significantly reduced (29.1 ± 4.7%) by AII. These studies identify multiple post-synaptic modulatory sites through which AII can influence the excitability of neurosecretory parvocellular PVN neurons and, as a consequence of such actions, control hormonal secretion from the anterior pituitary.