title: Rats with steroid-induced polycystic ovaries develop hypertension and increased sympathetic nervous system activity.
abstract: BACKGROUND
  Polycystic ovary syndrome (PCOS) is a complex endocrine and metabolic disorder associated with ovulatory dysfunction, abdominal obesity, hyperandrogenism, hypertension, and insulin resistance.
  
  
  METHODS
  Our objectives in this study were (1) to estimate sympathetic-adrenal medullary (SAM) activity by measuring mean systolic blood pressure (MSAP) in rats with estradiol valerate (EV)-induced PCO; (2) to estimate alpha1a and alpha2a adrenoceptor expression in a brain area thought to mediate central effects on MSAP regulation and in the adrenal medulla; (3) to assess hypothalamic-pituitary-adrenal (HPA) axis regulation by measuring adrenocorticotropic hormone (ACTH) and corticosterone (CORT) levels in response to novel-environment stress; and (4) to measure abdominal obesity, sex steroids, and insulin sensitivity.
  
  
  RESULTS
  The PCO rats had significantly higher MSAP than controls, higher levels of alpha1a adrenoceptor mRNA in the hypothalamic paraventricular nucleus (PVN), and lower levels of alpha2a adrenoceptor mRNA in the PVN and adrenal medulla. After exposure to stress, PCO rats had higher ACTH and CORT levels. Plasma testosterone concentrations were lower in PCO rats, and no differences in insulin sensitivity or in the weight of intraabdominal fat depots were found.
  
  
  CONCLUSIONS
  Thus, rats with EV-induced PCO develop hypertension and increased sympathetic and HPA-axis activity without reduced insulin sensitivity, obesity, or hyperandrogenism. These findings may have implications for mechanisms underlying hypertension in PCOS.
authors.affiliation: Cardiovascular Institute, Wallenberg Laboratory, Sahlgrenska Academy, Göteborg University, SE-413 45 Göteborg, Sweden. elisabet.stener-victorin@wlab.gu.se
authors.forename: Elisabet
authors.initials: E
authors.lastname: Stener-Victorin
authors.forename: Karolina
authors.initials: K
authors.lastname: Ploj
authors.forename: Britt-Mari
authors.initials: BM
authors.lastname: Larsson
authors.forename: Agneta
authors.initials: A
authors.lastname: Holmäng
mesh_terms: D050153:Abdominal Fat / Q000033:anatomy & histology; D000313:Adrenal Medulla / Q000737:chemistry; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure; D003345:Corticosterone / Q000378:metabolism; D004958:Estradiol / Q000031:analogs & derivatives; D005260:Female; D006973:Hypertension / Q000209:etiology*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D007328:Insulin; D007333:Insulin Resistance / Q000502:physiology; D010286:Paraventricular Hypothalamic Nucleus / Q000737:chemistry; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D011085:Polycystic Ovary Syndrome / Q000737:chemistry / Q000503:physiopathology*; D011374:Progesterone / Q000097:blood; D051381:Rats; D011921:Rats, Inbred WKY; D018340:Receptors, Adrenergic, alpha-1 / Q000032:analysis / Q000235:genetics; D018341:Receptors, Adrenergic, alpha-2 / Q000032:analysis / Q000235:genetics; D013315:Stress, Psychological / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013739:Testosterone / Q000097:blood
chemical_list: D007328:Insulin; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone