title: Chronic stress improves NO- and Ca2+ flux-dependent vascular function: a pharmacological study.
abstract: BACKGROUND
  Stress is associated with cardiovascular diseases.
  
  
  OBJECTIVE
  This study aimed at assessing whether chronic stress induces vascular alterations, and whether these modulations are nitric oxide (NO) and Ca(2+) dependent.
  
  
  METHODS
  Wistar rats, 30 days of age, were separated into 2 groups: control (C) and Stress (St). Chronic stress consisted of immobilization for 1 hour/day, 5 days/week, 15 weeks. Systolic blood pressure was assessed. Vascular studies on aortic rings were performed. Concentration-effect curves were built for noradrenaline, in the presence of L-NAME or prazosin, acetylcholine, sodium nitroprusside and KCl. In addition, Ca(2+) flux was also evaluated.
  
  
  RESULTS
  Chronic stress induced hypertension, decreased the vascular response to KCl and to noradrenaline, and increased the vascular response to acetylcholine. L-NAME blunted the difference observed in noradrenaline curves. Furthermore, contractile response to Ca(2+) was decreased in the aorta of stressed rats.
  
  
  CONCLUSIONS
  Our data suggest that the vascular response to chronic stress is an adaptation to its deleterious effects, such as hypertension. In addition, this adaptation is NO- and Ca(2+)-dependent. These data help to clarify the contribution of stress to cardiovascular abnormalities. However, further studies are necessary to better elucidate the mechanisms involved in the cardiovascular dysfunction associated with stressors.
authors.affiliation: Departamento de Farmacologia, Instituto de Biociências de Botucatu, Universidade do Estado de São Paulo, Botucatu, São Paulo, Brazil.
authors.forename: Thiago
authors.initials: T
authors.lastname: Bruder-Nascimento
authors.affiliation: Departamento de Clínica Médica, Faculdade de Medicina de Botucatu, Universidade do Estado de São Paulo, Botucatu, São Paulo, Brazil.
authors.forename: Dijon Henrique Salome
authors.initials: DH
authors.lastname: Campos
authors.affiliation: Departamento de Clínica Médica, Faculdade de Medicina de Botucatu, Universidade do Estado de São Paulo, Botucatu, São Paulo, Brazil.
authors.forename: Antônio Carlose
authors.initials: AC
authors.lastname: Cicogna
authors.forename: Sandra
authors.initials: S
authors.lastname: Cordellini
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism / Q000503:physiopathology*; D001794:Blood Pressure / Q000502:physiology; D002118:Calcium / Q000378:metabolism*; D002122:Calcium Chloride / Q000032:analysis; D002318:Cardiovascular Diseases / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D003345:Corticosterone / Q000097:blood; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000032:analysis; D009569:Nitric Oxide / Q000378:metabolism*; D009638:Norepinephrine / Q000032:analysis; D011189:Potassium Chloride / Q000032:analysis; D017208:Rats, Wistar; D012016:Reference Values; D013315:Stress, Psychological / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology*
chemical_list: D009569:Nitric Oxide; D011189:Potassium Chloride; D002122:Calcium Chloride; D002118:Calcium; D019331:NG-Nitroarginine Methyl Ester; D003345:Corticosterone; D009638:Norepinephrine