It is well established that the increased sympathetic tone may contribute to initiation and progression of various forms of hypertension. Several lines of evidence suggest a link between the renin-angiotensin system and sympathetic nerve activity in hypertension, and the previous studies in animal models demonstrated increased sympathetic output in the presence of Angiotensin II (AngII). To elucidate potential underlying molecular mechanisms of such phenomenon, we compared the effect of AngII on the whole-cell potassium channel currents in superior cervical ganglia (SCG) neurons isolated from hypertensive (mRen2)27 rats with overexpression of renin gene, and control Sprague Dawley® (SD) rats. In both groups, the whole-cell potassium channel currents were identified as rapidly-activating, 4-Aminopyridine-sensitive transient A-type currents, as well as slowly-activating tetraethylammonium-sensitive delayed rectifier currents. When the cell membrane was depolarized to -40, -30 and -20 mV from a holding potential of -80 mV, AngII (100 nM) profoundly inhibited A-type current, but the magnitude of such inhibition was not significantly different between neurons isolated from (mRen2)27 (38.1±6.2%, 47.8±5.7% and 52.1±5.7%; n=11) and SD rats (37.2±4.6%, 44.±4.5% and 46.1±4.8%; n = 13). Delayed rectifier potassium channel currents were isolated by holding cells at -40 mV, which resulted in complete elimination of the transient A-type current. In contrast to transient current, inhibition of the delayed rectifier current by AngII in the range of membrane potentials between +20 and +80 mV was significantly greater (p<0.05) in neurons obtained from (mRen2)27 rats (11.0±3.2% to 25.0±2.9%, n=12) when compared to SD rats (4.7±1.5% to 16.3±2.7%, n = 12). In both groups, inhibition of both channel types was completely abolished by 10 uM Losartan, indicating involvement of AT1 receptors. Our results suggest that in (mRen2)27 hypertensive rats, the increased inhibitory effect of AngII on delayed rectifier potassium channel currents could possibly lead to lowering spike threshold, which, in turn, could elevate sympathetic outflow and lead to sustained blood pressure elevation.