title: Sex differences in the coronary vasodilation induced by 17 β-oestradiol in the isolated perfused heart from spontaneously hypertensive rats.
abstract: OBJECTIVE
  The relaxation induced by oestrogen in the coronary vascular bed from normotensive rats has been well described. However, almost nothing is known about this action in spontaneously hypertensive rats (SHR). We investigated the effect of 17 β-oestradiol (E(2) ) in coronary arteries from SHR as well as the contribution of the endothelium and the vascular smooth muscle to this action.
  
  
  METHODS
  Coronary arteries from male and female rats were used. Mean arterial pressure (MAP) and baseline coronary perfusion pressure (CPP) were determined. The effects of 10 μm E(2) were assessed by in bolus administration before and after endothelium denudation (0.25 μm sodium deoxycholate) or perfusion with 100 μm N(ω)-nitro-L-arginine methyl ester (L-NAME), 2.8 μm indomethacin, 0.75 μm clotrimazole, 100 μm L-NAME after endothelium denudation (0.25 μm sodium deoxycholate), 100 μm L-NAME plus 2.8 μm indomethacin, 0.75 μm clotrimazole plus 2.8 μm indomethacin and 4 mm tetraethylammonium (TEA).
  
  
  RESULTS
  MAP was higher in the male group, while CPP was higher in the female group (P<0.05). There were no differences in E(2)-induced relaxation between females and males (-17±1.6 vs. -17±2% respectively). Only in the female group the E(2) response was significantly attenuated after endothelium removal or perfusion with clotrimazole. The response to E(2) was reduced in both groups with L-NAME, L-NAME plus indomethacin, L-NAME after endothelium removal or TEA.
  
  
  CONCLUSIONS
  Nitric oxide, endothelium-derived hyperpolarizing factor and potassium channels may have the most important role to E(2) response in the female group, whereas nitric oxide and potassium channels may have the most important role in the male group.
authors.affiliation: Department of Physiological Sciences, Biomedical Center, Federal University of Espírito Santo, Vitória, ES, Brazil.
authors.forename: R L
authors.initials: RL
authors.lastname: Santos
authors.forename: E B
authors.initials: EB
authors.lastname: Marin
authors.forename: W L S
authors.initials: WL
authors.lastname: Gonçalves
authors.forename: N S
authors.initials: NS
authors.lastname: Bissoli
authors.forename: G R
authors.initials: GR
authors.lastname: Abreu
authors.forename: M R
authors.initials: MR
authors.lastname: Moysés
mesh_terms: D000818:Animals; D001685:Biological Factors / Q000378:metabolism; D001794:Blood Pressure; D003331:Coronary Vessels / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004958:Estradiol / Q000378:metabolism*; D005260:Female; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D010477:Perfusion; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D012737:Sex Factors; D014664:Vasodilation / Q000187:drug effects
chemical_list: D001685:Biological Factors; D016861:Cyclooxygenase Inhibitors; D004791:Enzyme Inhibitors; D026902:Potassium Channel Blockers; D015221:Potassium Channels; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide; D004958:Estradiol; D019001:Nitric Oxide Synthase