title: Sex differences in the hypothalamo-pituitary-adrenal axis response to inflammatory and neuroendocrine stressors. Evidence for a pituitary defect in the autoimmune disease-susceptible female Lewis rat.
abstract: Susceptibility to inflammatory disease in infantile Lewis (LEW/N) female rats seems to be related to their impaired hypothalamo-pituitary-adrenal (HPA) axis response to different inflammatory stimuli, while the relative resistance to this type of disease in Fischer (F344/N) female rats is apparently due to their potent HPA axis response to the same stimuli. In the present study, we attempted to elucidate whether there is an impairment in the HPA axis response in the juvenile female LEW/N rat to inflammatory and noninflammatory stimuli, and also to determine whether the endogenous sex-steroid environment influences the HPA axis function in both strains of rats. For these purposes, juvenile F344/N and LEW/N rats of both sexes were submitted to different treatments: (a) inhalation of normal atmosphere or ether vapors for 1 min (Ether); (b) i.p. injection of vehicle alone or containing CRH (0.5 microgram/rat), arginine vasopressin (AVP; 5 micrograms/rat, angiotensin II (AII; 5 micrograms/rat), insulin (INS; 0.3 IU/rat), bacterial lipopolysaccharide (LPS; 100 micrograms/rat) or snake venom (SV; 100 micrograms/rat). Rats were then killed at different time intervals (in min) after treatments: 20 for Ether, AVP and CRH, 30 for AII, 45 for INS, 60 for SV and 120 for LPS.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Neurosciences, Multidisciplinary Institute on Cell Biology, La Plata, Argentina.
authors.forename: E
authors.initials: E
authors.lastname: Spinedi
authors.forename: M
authors.initials: M
authors.lastname: Salas
authors.forename: A
authors.initials: A
authors.lastname: Chisari
authors.forename: M
authors.initials: M
authors.lastname: Perone
authors.forename: M
authors.initials: M
authors.lastname: Carino
authors.forename: R C
authors.initials: RC
authors.lastname: Gaillard
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism / Q000494:pharmacology; D001786:Blood Glucose / Q000032:analysis; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism / Q000494:pharmacology*; D004986:Ether / Q000494:pharmacology; D005260:Female; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000502:physiology*; D018836:Inflammation Mediators / Q000008:administration & dosage / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011916:Rats, Inbred F344; D011917:Rats, Inbred Lew; D012727:Sex Characteristics; D012910:Snake Venoms / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D018836:Inflammation Mediators; D007328:Insulin; D008070:Lipopolysaccharides; D012910:Snake Venoms; D004986:Ether; D000804:Angiotensin II; D001127:Arginine Vasopressin; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone