title: Expression of Fos in rat brain in relation to sodium appetite: furosemide and cerebroventricular renin.
abstract: Two experiments were performed to investigate the relationship between the expression of sodium appetite and the appearance of Fos-like immunoreactivity (Fos-IR) in the brain of rats. In the first experiment, rats were depleted of sodium by treatment with furosemide 24 h prior to sacrifice and without access to either food or sodium solution. Some rats had access to distilled water, and others had no fluids available during the 24 h. All of the furosemide-treated rats showed Fos-IR in both the subfornical organ (SFO) and around the organum vasculosum laminae terminalis (OVLT). Rats with access to distilled water during the depletion period showed no Fos-IR in the supraoptic (SON) or paraventricular hypothalamic nuclei (PVN) and, in parallel behavioral studies, comparably-treated rats consumed only 0.3 M NaCl solution at the end of the 24 h. In rats that had no fluids during the deprivation period, only about one half showed Fos-IR in SON and PVN and, in parallel behavioral studies, comparably treated rats consumed both water and 0.3 M NaCl solution at the end of 24 h. In a second experiment, cerebroventricular administration of renin stimulated short latency intake of 0.3 M NaCl and water. The relative intakes of water and NaCl were comparable at a low dose of renin, but intake of water exceeded that of NaCl after higher doses. Renin induced Fos-IR in SFO, MnPO, peri-OVLT region, SON and PVN. Both Fos-IR and fluid intake were antagonized by administration of losartan, an angiotensin II type 1 receptor antagonist. Thus, only the circumventricular organs of the lamina terminalis showed Fos-IR during each natriorexigenic regimen in these studies. These data support the view that Ang II of both central and peripheral origin activates the SFO and/or peri-OVLT region and contributes to sodium appetite.
authors.affiliation: Department of Psychology and Physiology, University of Florida, Gainesville 32611-2250, USA. rowland@psych.ufl.edu
authors.forename: N E
authors.initials: NE
authors.lastname: Rowland
authors.forename: M J
authors.initials: MJ
authors.lastname: Fregly
authors.forename: L
authors.initials: L
authors.lastname: Han
authors.forename: G
authors.initials: G
authors.lastname: Smith
mesh_terms: D000818:Animals; D001066:Appetite / Q000187:drug effects; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D004232:Diuretics / Q000494:pharmacology*; D004326:Drinking / Q000187:drug effects; D005665:Furosemide / Q000494:pharmacology*; D007150:Immunohistochemistry; D007276:Injections, Intraventricular; D008297:Male; D009419:Nerve Tissue Proteins / Q000032:analysis*; D010286:Paraventricular Hypothalamic Nucleus / Q000737:chemistry / Q000187:drug effects; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000494:pharmacology; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*; D013495:Supraoptic Nucleus / Q000737:chemistry / Q000187:drug effects
chemical_list: D004232:Diuretics; D009419:Nerve Tissue Proteins; D016760:Proto-Oncogene Proteins c-fos; D017673:Sodium Chloride, Dietary; D005665:Furosemide; D012083:Renin