Abstract Body: Hypertension remains a global health concern. Studies have shown a correlation with the loss of normal 24-hour blood pressure patterns and hypertension with a high salt diet. However, the mechanisms behind this are not fully known. The nucleus of the solitary tract (nTS), a key medullary nucleus involved in cardiorespiratory regulation, is known to modulate sympathetic outflow and blood pressure alterations.When blood pressure increases, baroreceptors in peripheral vessels detect these changes and send signals to the nTS through the neurotransmitter glutamate. Increased nTS glutamatergic signaling decreases blood pressure via efferent signals to the heart and blood vessels. The nTS integrates these signals and initiates responses through the baroreflex to counteract changes in blood pressure. Thus, baroreflex sensitivity (BRS), or a measure of how the baroreflex adjusts, serves as an indicator of the regulation of this feedback loop. An increased BRS indicates a more robust ability of the body to respond to blood pressure changes. Conversely, a reduced BRS is associated with hypertension, and autonomic dysfunction. Studies have shown that those with diet-induced hypertension also have a decreased BRS, however, the mechanism is not clear. We hypothesize that dysregulation of the 24-hour circadian glutamatergic signaling within the nTS may cause BRS decrease and hypertension. Salt-sensitive rats were subjected to either a normal salt diet (NSD, 0.4 % NaCl) or high salt diet (HSD, 4% NaCl) for 7 weeks. To determine nTS changes related to HSD, we measured blood pressure using 24/7 telemetry, and activation of glutamatergic neurons via immunohistochemistry (IHC). Antibodies against glutamate (CAMKII) and neuronal activation (cFos) were used to detect neuronal activation 6 hours apart, at the end of the NSD or HSD. Our preliminary findings reveal near significant decreases in glutamate signaling during the active period (at 9pm), suggesting a potential shift in the excitatory signaling in the nTS. Additionally, HSD over 7 weeks caused a significant increase in blood pressure and a decrease in BRS during the active period. Our preliminary data shows a connection between 24-hour regulation of glutamate within the nTS, diet-induced hypertension, and loss of BRS. This dysregulation in the blood pressure regulation underscores the importance of understanding the molecular mechanisms linking diet and development of disease.