Small conductance Ca2+ activated K+ (SK) channels act as negative feedback regulators of neuronal excitability. We have reported that SK channels expressed in the paraventricular nucleus (PVN) are involved in controlling neuronal activity, sympathetic nerve activity (SNA) and arterial pressure (AP). Blockade of SK channels in the pre‐sympathetic PVN neurons increases neuronal excitability, SNA and AP. Here we investigated the effect of angiotensin II type 1 receptor (AT1R) blockade on the sympathoexcitatory and presser responses elicited by the inhibition of SK channels in the PVN. In anesthetized rats, PVN microinjection of SK channel blocker with apamin (12.5 pmol, 50nl) (n=7) increased splanchnic SNA (SSNA) (278 ± 50%), renal SNA (RSNA) (193 ± 12%), and mean AP (MAP) (32 ± 4mmHg). Pre‐treatment with PVN injection of losartan (20 nmol), an AT1R antagonist, significantly attenuated (n=6) the elevated SSNA (129 ± 37%; p<.05 vs vehicle control), RSNA (84 ± 40%; p<.05 vs vehicle control), and MAP (10 ± 6mmHg; p<.05 vs vehicle control) after PVN injection of apamin. Pre‐treatment with PVN injection of ZD7155 (1.0 nmol), another AT1R antagonist, significantly attenuated (n=5) the elevated SSNA (112 ± 30%; p<.05 vs vehicle control), RSNA (81 ± 23%; p<.05 vs vehicle control) and MAP (7 ± 2mmHg; p<.05 vs vehicle control) elicited by PVN apamin. No significant difference was found between pretreatment with losartan and ZD7155 for SNA and MAP. Our data indicate that sympathoexcitation and pressor responses induced by inhibition of SK channel activity involve the activation of AT1R in the PVN. Support: AHA7420029 (ZYS) 2640130 (QHC).