title: Interactive effects of growth hormone and oestrogen on vascular responses in hypophysectomised female rats.
abstract: OBJECTIVE
  Growth hormone (GH) and oestrogen (E(2)) are associated with beneficial effects on the cardiovascular system and it is therefore of great interest to study their interactive effects on haemodynamics and vascular function.
  
  
  METHODS
  Female hypophysectomised (Hx) rats were treated for seven days with GH, E(2) or a combination of the hormones. Systolic blood pressure (SBP), heart rate (HR) and plasma insulin-like growth factor-I (IGF-I) were measured. Contractile properties and endothelial function were studied in isolated resistance arteries using the wire-myograph technique.
  
  
  RESULTS
  Hypophysectomy, per se, caused a fall in SBP and HR, while vascular adrenergic reactivity (sensitivity to applied noradrenaline) was enhanced. Impaired acetylcholine-induced relaxation and basal release of nitric oxide, suggests endothelial dysfunction after Hx. After supplementation with GH, SBP remained low while HR increased towards the control level. GH increased plasma IGF-I, but had no effect on vascular contractility or endothelial responses. E(2) replacement resulted in blunted plasma IGF-I, while the vascular adrenergic and serotonergic responses were reinforced. Endothelial function was not improved after E(2) treatment. When GH and E(2) were given in combination, the GH-induced increase in body weight, plasma IGF-I levels and HR were counteracted by E(2). Moreover, the anticipated reinforcement of the vascular serotonergic response by E(2) was reduced. Neither E(2) nor GH+E(2) affected SBP.
  
  
  CONCLUSIONS
  The results suggest that GH and E(2) might have interactive effects on haemodynamic and metabolic parameters, but not on the contractility or endothelial function of resistance arteries, in Hx female rats.
authors.affiliation: Clinical Experimental Research Laboratory, Heart and Lung Institute, Sahlgrenska University Hospital/Ostra, Goteborg, Sweden. helena.gustafsson@hjl.gu.se
authors.forename: Helena
authors.initials: H
authors.lastname: Gustafsson
authors.forename: Anna Wickman
authors.initials: AW
authors.lastname: Tordby
authors.forename: Lisa
authors.initials: L
authors.lastname: Brandin
authors.forename: Lars
authors.initials: L
authors.lastname: Hedin
authors.forename: Ingibjorg H
authors.initials: IH
authors.lastname: Jonsdottir
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001808:Blood Vessels / Q000187:drug effects* / Q000502:physiology; D004347:Drug Interactions; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D013006:Growth Hormone / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D007016:Hypophysectomy; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009569:Nitric Oxide / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012701:Serotonin / Q000494:pharmacology; D014655:Vascular Resistance
chemical_list: D009569:Nitric Oxide; D012701:Serotonin; D004958:Estradiol; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D000109:Acetylcholine; D009638:Norepinephrine