A high salt diet can lead to hydromineral imbalance and increases in plasma sodium and osmolality. It is recognized as one of the major contributing factors for cardiovascular diseases such as hypertension. The PVN plays a pivotal role in osmotically-driven sympathoexcitation and high blood pressure, which precise mechanisms are not fully understood. Recent evidence indicates that vasopressin (AVP) released from magnocellular neurons might be involved in this process. Using a combination of in vivo and in situ studies, we sought to investigate whether AVP, acting on PVN neurons, can change mean arterial pressure (MAP) and sympathetic nerve activity (SNA) in euhydrated male rats. Furthermore, we wanted to determine whether V_1a receptors on PVN neurons would be involved in salt-induced sympathoexcitation and hypertension. In rats, 4 days of salt loading (NaCl 2%) elicited a significant increase in plasma osmolality (39±7 mOsm/L), increase in MAP (26±2 mmHg), and sympathoexcitation when compared to euhydrated rats. Microinjection of AVP into the PVN of conscious euhydrated animals (100 nL, 3 µM) elicited a pressor response (14±2 mmHg) and a significant increase in lumbar SNA (100 nL, 1mM) (19±5%). Pre-treatment with a V_1a receptor antagonist, microinjected into the PVN of salt-loaded animals, elicited a decrease in lumbar SNA (-14±5%) and MAP (-19±5 mmHg), when compared with the euhydrated group. Our findings show that AVP plays an important role in modulating the salt-induced sympathoexcitation and high blood pressure, via V_1a receptors, within the PVN, which might contribute to neurogenic hypertension in individuals consuming a high salt diet.