Objective: We tested the hypothesis that female sex hormone depletion and estradiol replacement therapy significantly influences the biomechanical properties of intramural coronary resistance arteries. Design: 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 µm 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<HIGHWIRE EXLINK_ID="61:2:317:1" VALUE="U46619" TYPEGUESS="GEN, PIRDB, SPROT">, a thromboxane (TX) A 2 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 A 2 agonist induced the largest contraction in the ovariectomized group, whereas bradykinin-induced relaxation was the largest in the estrogen replacement group ( p <0.05). Conclusion: 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.
Copyright (C) 2004, European Society of Cardiology
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