Paraventricular nucleus of the hypothalamus activation and forebrain neuroinflammation in salt-loaded rats.

Salt loading (SL) in rats for 7 days raises mean arterial pressure (MAP) and induces astrogliosis in the paraventricular nucleus of the hypothalamus (PVN). However, the exact role of the PVN in elevating MAP and sympathetic nerve activity (SNA), as well as its effects on astrocytes in forebrain osmosensitive areas, remain unclear. Male Holtzman and Wistar rats (300-320 g) received only 2% NaCl solution (SL) to drink for 7 days, while controls drank water (WT). Daily fluid and food intake, body weight, urinary volume, and MAP were recorded. On day 7, blood and cerebrospinal fluid (CSF) were collected, and GFAP immunoreactivity (an astrocyte marker) was measured in the PVN, SFO, and the preoptic region of the hypothalamus containing the organum vasculosum of the lamina terminalis (OVLT) and the medial preoptic area (MPO). In anesthetized rats, MAP and splanchnic SNA (SSNA) responses were recorded after bilateral injections of muscimol (1 nmol/50 nL; each side) into the PVN. SL increased NaCl intake, urinary volume, plasma osmolality, CSF sodium, and MAP, while decreasing food intake and body weight. Bilateral muscimol injections into the PVN lowered MAP and SSNA more in SL than in WT rats. SL induced astrogliosis in the PVN and OVLT/MPO but not in the SFO. These results indicate that the PVN plays a critical role in cardiovascular responses during SL.