title: The effect of ovariectomy and oestrogen replacement on small artery biomechanics in the rat.
abstract: OBJECTIVE
  To determine the effects of oestrogen deficiency and hormone replacement therapy on the biomechanical properties of a small artery.
  
  
  METHODS
  Thirty non-pregnant female Sprague-Dawley rats.
  
  
  METHODS
  Twenty animals were pharmacologically ovariectomised by triptorelin and received either oestradiol propionate or its vehicle. Ten other animals received only the vehicle for the same period of time (control group). After 12 weeks of treatment, cylindrical segments of the saphenous artery were isolated and cannulated at both ends. Pressure-diameter curves were recorded from segments in normal Krebs-Ringer, using norepinephrine, and then with papaverine. The vessel segment close to the examined one was histologically evaluated. Serum levels of oestradiol and cortisol were determined.
  
  
  METHODS
  Biomechanical parameters based on the pressure-diameter curves.
  
  
  RESULTS
  Pharmacological ovariectomy decreased the passive diameter of the arteries and oestrogen replacement therapy prevented this. Decreased reactivity to norepinephrine was also restored by oestrogen treatment. Pressure induced myogenic tone was decreased significantly by oophorectomy and increased after oestradiol treatment. No significant changes were found in wall thickness, distensibility, elastic modulus or tangential stress. No significant histological alterations were seen in the vessel wall. Oestradiol levels were significantly decreased in the castrated animals compared with the other two groups.
  
  
  CONCLUSIONS
  These results suggest that oestrogen deficiency decreases and oestrogen replacement increases the passive diameter of small peripheral arteries, and that oestrogen enhances the reactivity of vascular smooth muscle. These responses may provide the background mechanisms for the increased incidence of arterial hypertension and hot flushes during the menopause and the ability of oestrogen substitution to prevent them.
authors.affiliation: 2nd Department of Obstetrics and Gynaecology, Semmelweis University of Medicine, Budapest, Hungary.
authors.forename: N
authors.initials: N
authors.lastname: Acs
authors.forename: B
authors.initials: B
authors.lastname: Székács
authors.forename: G L
authors.initials: GL
authors.lastname: Nádasy
authors.forename: S
authors.initials: S
authors.lastname: Várbíró
authors.forename: R
authors.initials: R
authors.lastname: Kakucs
authors.forename: E
authors.initials: E
authors.lastname: Monos
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D001696:Biomechanical Phenomena; D046508:Culture Techniques; D004958:Estradiol / Q000494:pharmacology*; D015914:Estrogen Replacement Therapy; D004967:Estrogens / Q000172:deficiency* / Q000502:physiology; D005260:Female; D008186:Luteolytic Agents; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology; D010208:Papaverine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017329:Triptorelin Pamoate; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D004967:Estrogens; D008186:Luteolytic Agents; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D017329:Triptorelin Pamoate; D004958:Estradiol; D010208:Papaverine; D009638:Norepinephrine