Salt Loading Impairs Baroreflex, Elevates Cardiac Sympathetic Tone, Activating PVH Vasopressinergic Neurons in Rats

The paraventricular nucleus of the hypothalamus (PVH) is a critical brain region for body fluid homeostasis and autonomic regulation of cardiovascular function, particularly in salt-induced hypertension. Current understanding of how high salt intake specifically alters PVH neuronal activity during baroreflex challenges, leading to autonomic imbalance, remains incomplete. Identifying the precise neuronal phenotypes involved could reveal novel targets for managing hypertension and autonomic dysregulation.

Researchers investigated the impact of short-term high salt exposure on baroreflex function, cardiac autonomic balance, and PVH neuronal activation in adult rats. Animals were divided into salt-loaded and euhydrated control groups. Key parameters measured included mean arterial pressure (MAP), heart rate (HR), and baroreflex function. Following pharmacologically induced baroreflex activation, c-Fos expression within the PVH was assessed to identify activated neurons, and their phenotype (e.g., oxytocinergic, vasopressinergic) was determined.

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. Autonomic imbalance was evident, marked by enhanced cardiac sympathetic tone, with no observed 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, while baroreflex stimulation in both euhydrated and salt-loaded animals recruited oxytocinergic neurons, in salt-loaded rats, it additionally engaged vasopressinergic neurons.