The octapeptide angiotensin II (ANG II) plays a pivotal role in the maintenance of blood pressure by activating ANG II receptors located in variety of cell types including neurons housed in the central nervous system (CNS) and in the peripheral nervous system (PNS). ANG II (100nM) blocked spike frequency accommodation (SFA) recorded with whole-cell patch technique in acutely isolated nodose ganglion neurons (NGN) from adult rats. ANG II increased the frequency of action potentials (AP) produced by supramaximal 500ms depolarizing currents recorded in both tonic (16Hz vs. 58Hz, control vs. ANG II perfusion respectively, n=9) and phasic (1Hz vs. 38Hz, n=13) NGNs. ANG II produced no significant changes in: the resting membrane potential (−51mV vs. −50mV, n=65), AP overshoot (46mV vs. 41mV, n=25), AP undershoot (−65mV vs. −61mV, n=25), AP duration (1ms vs. 1.2ms, n=25), and AP threshold (−40mV vs. −43mV, n=19). CV-11974 (600nM), a specific AT1 receptor antagonist, prevented ANG II-evoked changes SFA (n=10).ANG II (100nM) had no significant effect on total outward potassium current (I K ) but inhibited a fast activating and fast inactivating I K recorded in the presence of TEA. A kinetically similar I K was also inhibited by 4-AP (3mM). In phasic NGNs, 4-AP occluded the effects of 100nM ANG II on SFA. Our results indicate that ANG II can block an A-type of I K and that this effect may underlie the ANG II-mediated change in SFA.