title: Inhibition of neuronal nitric oxide synthase activity does not alter vasopressin secretion in septic rats.
abstract: OBJECTIVE
  During the early phase of sepsis, hypotension is accompanied by increase of plasma vasopressin hormone (AVP) levels, which decline during the late phase. This hypotension is due in part to increase of nitric oxide (NO) synthesis by nitric oxide synthase (NOS) enzyme. Neuronal isoform of this enzyme (nNOS) is present in vasopressinergics neurons of hypothalamus, but its role in vasopressin secretion during sepsis is unknown.
  
  
  METHODS
  We evaluated the role of nNOS in NO production and vasopressin secretion during sepsis. Wistar rats received 7-nitroindazole (50 mg/kg, i.p.), an inhibitor of nNOS activity, or vehicle and were submitted to septic stimulus by cecal ligation and puncture (CLP). At the time points 0, 4, 6, 18 and 24 h after sepsis induction the animals were decapitated and neurohypophysis and hypothalamus were removed for analysis of vasopressin content and NOS activity, respectively. Hematocrit, serum sodium, osmolality, proteins and plasmatic AVP were quantified.
  
  
  RESULTS
  Mortality was not affected by 7-nitroindazole (7-NI). Sodium and plasma proteins levels decreased after CLP and the treatment anticipated the protein loss, and delayed serum sodium decrease. Septic animals treated with 7-NI showed decrease of osmolality 4 h after CLP. Nitric oxide synthase activity in hypothalamus increased at 4 and 24 h after CLP and was reduced with 7-NI. Neurohypophysis content of AVP diminished after CLP and 7-NI did not alter this parameter. Plasma AVP levels increased at 6 h and decreased 18 and 24 h after CLP. Treatment with 7-NI did not alter plasma vasopressin levels.
  
  
  CONCLUSIONS
  We concluded that nNOS does not have a substantial role in vasopressin secretion during experimental sepsis.
authors.affiliation: Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, Avenida do Café s/n CEP, Ribeirão Preto, São Paulo, 14040-904, Brazil. camila.coelho@yahoo.com.
authors.forename: Camila Henriques
authors.initials: CH
authors.lastname: Coelho
authors.affiliation: Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, Avenida do Café s/n CEP, Ribeirão Preto, São Paulo, 14040-904, Brazil.
authors.forename: Thalita Freitas
authors.initials: TF
authors.lastname: Martins
authors.affiliation: Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, Avenida do Café s/n CEP, Ribeirão Preto, São Paulo, 14040-904, Brazil.
authors.forename: Gabriela Ravanelli
authors.initials: GR
authors.lastname: Oliveira-Pelegrin
authors.affiliation: Departamento de Morfologia, Fisiologia e Patologia Básica, Faculdade de Odontologia, Universidade de São Paulo, Ribeirão Preto, São Paulo, Brazil.
authors.forename: Maria José Alves
authors.initials: MJA
authors.lastname: da Rocha
mesh_terms: D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism*; D011863:Radioimmunoassay; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000378:metabolism*; D014667:Vasopressins / Q000378:metabolism*
chemical_list: D014667:Vasopressins; D001127:Arginine Vasopressin; D009569:Nitric Oxide; D052248:Nitric Oxide Synthase Type I
keywords: CLP; Neuronal NOS; Nitric oxide; Polymicrobial sepsis; Vasopressin