ObjectivesTo test the effects of chronic angiotensin II administration on blood pressure and small artery biomechanics in the female sex hormone-depleted state (proposed to increase cardiovascular vulnerability) and with hormone replacement.DesignBiomechanical properties of saphenous artery segments from ovariectomized (n= 10), ovariectomized + chronically angiotensin II infused-(n= 10), and ovariectomized + chronically angiotensin II-infused + sex hormone-replaced (n= 10) rats were studied.MethodsSurgical ovariectomy was performed. Osmotic minipumps were used for chronic angiotensin II infusion (100 ng/min per kg). For hormone replacement therapy, oestradiol-propionate, 450 μg/kg for 7 days + medroxyprogesterone-acetate, 15 mg/kg for 14 days were given, intramuscularly. After 4 weeks, cylindrical segments of the saphenous artery were prepared and subjected to in-vitro microarteriographic measurements. Pressure – diameter curves (0–200 mmHg) were recorded in Krebs–Ringer solution, with smooth muscle contracted (norepinephrine, 16 μmol/l) and with relaxed (papaverine, 28 μmol/l).ResultsChronic angiotensin II infusion significantly reduced the inner radius (at 100 mmHg: 298 ± 17 μm versus 347 ± 7 μm,P< 0.001), while wall-thickness did not change. Hormone replacement restored the morphological radius (333 ± 7 μm). Angiotensin II infusion slightly increased the full contraction range of the segments (defined as the percentage difference between fully contracted and fully relaxed diameters), which was further significantly increased by hormone replacement (39 ± 4%, 46 ± 8%, 62 ± 7% at 100 mmHg, in the three groups, respectively;P< 0.05). Despite unaltered stiffness in relaxed state, elastic moduli computed for the contracted segments decreased after hormone replacement.ConclusionsThese observations give further experimental support to the hypothesis that sex hormone replacement might be useful in preventing the development and/or stabilization of postmenopausal hypertension, as well as in treating existing disease.