title: Estrogen replacement therapy reverses changes in intramural coronary resistance arteries caused by female sex hormone depletion.
abstract: OBJECTIVE
  We tested the hypothesis that female sex hormone depletion and estradiol replacement therapy significantly influences the biomechanical properties of intramural coronary resistance arteries.
  
  
  METHODS
  Female rats (n=30) were divided into three groups. In group O, rats were subjected to bilateral ovariectomy. Group HRT was subjected to bilateral ovariectomy and estradiol replacement therapy. Rats in group C served as controls. One month after ovariectomy, intramural coronary arteries (approximately 200 microm in diameter) branching from the left anterior descending coronary were isolated, cannulated and studied by microarteriography. Intraluminal pressure was increased in steps between 0 and 90 mm Hg. The steady state diameter at each step was measured. These measurements were repeated in the presence of U46619, a thromboxane (TX) A2 receptor agonist (at a concentration of 10(-6) M), and bradykinin (BK; at 10(-6) M). Finally, Ca2+-free Krebs-induced passive diameter (PD) was measured in each group.
  
  
  RESULTS
  Ovariectomy increased spontaneous myogenic tone of coronary arteries (p<0.05), which was normalized by estrogen replacement. Ovariectomy decreased distensibility observed at low pressure, although passive diameter was not changed. Estrogen replacement decreased wall stress and elastic modulus (p<0.05). The thromboxane A2 agonist induced the largest contraction in the ovariectomized group, whereas bradykinin-induced relaxation was the largest in the estrogen replacement group (p<0.05).
  
  
  CONCLUSIONS
  Estradiol hormone replacement therapy (HRT) may exert a beneficial effect on myocardial perfusion in menopause by opposing the deterioration of biomechanical properties of intramural coronary resistance vessels induced by female sex hormone depletion.
authors.affiliation: Second Department of Obstetrics and Gynecology, Faculty of Medicine, Semmelweis University, H-1082 Budapest, Ulloi u 78, Hungary. mmericli@hotmail.com
authors.forename: Metin
authors.initials: M
authors.lastname: Mericli
authors.forename: György L
authors.initials: GL
authors.lastname: Nádasy
authors.forename: Maria
authors.initials: M
authors.lastname: Szekeres
authors.forename: Szabolcs
authors.initials: S
authors.lastname: Várbíró
authors.forename: Zoltan
authors.initials: Z
authors.lastname: Vajo
authors.forename: Máté
authors.initials: M
authors.lastname: Mátrai
authors.forename: Nándor
authors.initials: N
authors.lastname: Acs
authors.forename: Emil
authors.initials: E
authors.lastname: Monos
authors.forename: Béla
authors.initials: B
authors.lastname: Székács
mesh_terms: D000818:Animals; D003331:Coronary Vessels / Q000503:physiopathology*; D004548:Elasticity; D004730:Endothelium, Vascular / Q000187:drug effects; D004958:Estradiol / Q000494:pharmacology*; D015914:Estrogen Replacement Therapy; D005260:Female; D066298:In Vitro Techniques; D010052:Ovariectomy; D051381:Rats; D017207:Rats, Sprague-Dawley; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D004958:Estradiol