The paraventricular nucleus of the hypothalamus (PVH) plays a pivotal role in body fluid homeostasis and in autonomic regulation of cardiovascular function, particularly under conditions of high salt intake-induced hypertension. Here, we investigated, in an animal model of short-term high salt exposure, its impact on baroreflex function, cardiac autonomic balance, and the pattern and phenotype of PVH neuronal activation in response to baroreflex challenge in adult rats. Salt loading significantly increased mean arterial pressure and heart rate, indicating the development of hypertension. This was accompanied by impaired baroreflex function, characterized by a reduced functional range and autonomic imbalance marked by enhanced cardiac sympathetic tone, without changes in the vagal component. During pharmacologically induced baroreflex activation, salt-loaded animals exhibited greater c-Fos expression within the PVH compared with euhydrated controls. Notably, baroreflex stimulation in euhydrated and salt-loaded animals recruited oxytocinergic neurons, whereas in salt-loaded rats, it additionally engaged vasopressinergic neurons, revealing an atypical pattern of neuronal recruitment. Together, these findings demonstrate that short-term high salt intake induces hypertension, impairs baroreflex function, and increases cardiac sympathetic tone. These functional alterations are associated with enhanced PVH activation and the recruitment of vasopressinergic neurons during baroreflex loading, highlighting the central role of PVH in salt-induced hypertension and autonomic dysregulation.