OBJECTIVE: To determine the effects of oestrogen deficiency and hormone replacement therapy on the biomechanical properties of a small artery. SAMPLE: 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. MAIN OUTCOME MEASURES: 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.
OBJECTIVE: To determine the effects of oestrogen deficiency and hormone replacement therapy on the biomechanical properties of a small artery. SAMPLE: 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. MAIN OUTCOME MEASURES: 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.