title: Does chronic stress enhance the risk of diseases?
abstract: OBJECTIVE
  In the everyday life, stress is deemed as something unfavorable that may enhance the risk for the development or worsen a disease. However, in its nature, stress is adaptive reaction of the body. Its main characteristic is the activation of the hypothalamic-pituitary-adrenocortical (HPA) axis. Previously, we have shown that activation of the HPA axis plays a gastroprotective role during acute stress. The aim of our study was to clarify the effects of chronic stress and chronically elevated basal corticosterone levels on the gastric ulceration and cardiovascular vulnerability in rats.
  
  
  METHODS
  Male Wistar rats were repeatedly restrained 60 min daily for 14 days and examined on day 15th. The gastric ulceration was induced by a s.c. injection of indomethacin (35 mg/kg). The cardiovascular vulnerability was examined in urethane-anaesthetized rats in an experimental angina pectoris model (epinephrine, 10 µg/kg, 30 s later phentolamine, 15 mg/kg, both i.v.).
  
  
  RESULTS
  We confirmed the development of chronic stress consequences by changes in several somatic parameters (body weight decrease, thymus involution, adrenal gland hypertrophy), and elevated resting corticosterone levels. However, the gastroprotective effect of chronic stress was not manifested and there was no aggravation of indomethacin-induced gastric ulceration, either. In the experimental angina pectoris model, previous chronic stress did not have any profound effect on the blood pressure, heart rate, and electrocardiogram changes.
  
  
  CONCLUSIONS
  In contrast to the general view on the harmfulness nature of the stress, we were unable to find a harmful effect of chronic stress on the internal diseases (gastric ulceration and angina pectoris). However, its protective effect was also missing among present experimental conditions.
authors.forename: L
authors.initials: L
authors.lastname: Filaretova
authors.forename: O
authors.initials: O
authors.lastname: Morozova
authors.forename: F
authors.initials: F
authors.lastname: Laszlo
authors.forename: E
authors.initials: E
authors.lastname: Morschl
authors.forename: D
authors.initials: D
authors.lastname: Zelena
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000787:Angina Pectoris / Q000139:chemically induced / Q000453:epidemiology* / Q000503:physiopathology*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D002908:Chronic Disease; D004195:Disease Models, Animal; D004837:Epinephrine / Q000494:pharmacology; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000503:physiopathology; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D010646:Phentolamine / Q000494:pharmacology; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D012149:Restraint, Physical; D012307:Risk Factors; D013276:Stomach Ulcer / Q000139:chemically induced / Q000453:epidemiology* / Q000503:physiopathology*; D013312:Stress, Physiological / Q000502:physiology*; D013566:Sympathomimetics / Q000494:pharmacology
chemical_list: D000317:Adrenergic alpha-Antagonists; D000894:Anti-Inflammatory Agents, Non-Steroidal; D013566:Sympathomimetics; D007213:Indomethacin; D004837:Epinephrine; D010646:Phentolamine