Increased dietary sodium enhances activation of neurons in the medullary cardiovascular pathway during acute sodium loading in the rat

Increased sodium ingestion diminishes baroreflex-induced bradycardia in animals during acute sodium loading. These experiments studied effects of high sodium diet on activation of central nervous system sites associated with baroreflex activation and cardiovascular responses to hypernatremia during systemic sodium administration. Fos-like (Fos-Li) protein immunoreactivity was measured to estimate activation of neurons in the medullary baroreflex pathway (nucleus tractus solitarius (NTS), caudal ventrolateral medulla (CVLM), and rostral ventrolateral medulla (RVLM)), and in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON) in male Sprague–Dawley rats consuming standard chow and either tap water (TAP) or isotonic saline (ISO) for 2–3 weeks. Fos-Li immunoreactivity in the PVN and SON was similar in rats consuming TAP and ISO infused with 0.6 M NaCl. However, there were significantly more Fos-Li positive cells in NTS and CVLM of animals consuming ISO and infused with 0.6 M NaCl than any other experimental group, while Fos-Li immunoreactivity was similar in the RVLM in all animals. In conclusion, these data demonstrate that activation of neurons in the NTS and CVLM was significantly enhanced by moderate sodium loading in animals consuming high dietary sodium. The increased basal activation of neurons in these medullary sites could account for decreased baroreflex-induced bradycardia observed during ingestion of a high salt diet and acute, moderate sodium loading.