title: Circulating sex hormones modulate vascular contractions and acute response to 17β-estradiol in rat mesenteric arteries.
abstract: OBJECTIVE
  We investigated how modification of levels of the sex hormones 17β-estradiol and testosterone affects vascular contraction and nongenomic vascular effects of 17β-estradiol.
  
  
  METHODS
  Male and female rats were treated with vehicle, 17β-estradiol (25 μg/kg/day) or testosterone (1 mg/kg/day) for 14 consecutive days after sham gonadectomy or gonadectomy was performed. Isometric tensions were then measured from mesenteric arteries of each group of rats.
  
  
  RESULTS
  Contraction to phenylephrine was increased in mesenteric arteries from rats with or without gonadectomy treated with testosterone for 14 days compared to their intact controls. Contraction to phenylephrine was reduced in mesenteric arteries of rats with or without gonadectomy treated with 17β-estradiol for 14 days compared to their intact controls. Incubation of mesenteric arteries with 17β-estradiol (1 nmol/l) for 30 min reduced contraction to phenylephrine in mesenteric arteries of rats that were treated with testosterone for 14 days. This acute incubation of 17β-estradiol had no effect on arteries from rats that were treated with 17β-estradiol for 14 days. The acute effect of 17β-estradiol (1 nmol/l) is preserved in arteries without endothelium.
  
  
  CONCLUSIONS
  Our results suggest that 14 days' testosterone treatment enhances while 14 days' 17β-estradiol treatment suppresses contraction as well as the nongenomic effects of 17β-estradiol in the vascular smooth muscles.
authors.affiliation: Department of Pharmacology and Pharmacy, The University of Hong Kong, Hong Kong, SAR, China. wkeung@ualberta.ca
authors.forename: Wendy
authors.initials: W
authors.lastname: Keung
authors.forename: Ricky Y K
authors.initials: RY
authors.lastname: Man
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D001835:Body Weight; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D004353:Drug Evaluation, Preclinical; D004730:Endothelium, Vascular / Q000502:physiology; D004958:Estradiol / Q000097:blood / Q000494:pharmacology*; D004967:Estrogens / Q000097:blood / Q000494:pharmacology*; D005260:Female; D012739:Gonadal Steroid Hormones / Q000097:blood* / Q000494:pharmacology; D006801:Humans; D008297:Male; D008638:Mesenteric Arteries / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D010656:Phenylephrine / Q000378:metabolism / Q000494:pharmacology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012737:Sex Factors; D013739:Testosterone / Q000097:blood / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D000316:Adrenergic alpha-Agonists; D004967:Estrogens; D012739:Gonadal Steroid Hormones; D010656:Phenylephrine; D013739:Testosterone; D004958:Estradiol