Mechanisms underlying cardioprotective properties of estrogens are not fully understood. We evaluated effects of ovariectomy and estrogen replacement on arterial distensibility and endothelial function in rats. Sprague-Dawley rats were sham operated (Sham) or ovariectomized and treated with 17-estradiol (OVX-E₂) or vehicle (OVX) for 3 wk. Anesthetized rats were instrumented for measurement of central and peripheral arterial blood pressures and carotid and hindquarters blood flows. Arterial distensibility was evaluated in anesthetized rats on the basis of changes in thoracoabdominal pressure pulse wave velocity (PWV). PWV was calculated as the distance between the two central and peripheral cannula tips divided by transit time. Ovariectomy significantly reduced PWV (390 ± 19 and 472 ± 42 cm/s in OVX and Sham, respectively). Estrogen treatment completely normalized PWV (490 ± 37 cm/s). Estrogen-treated rats were associated with left ventricular hypertrophy and increased pulse pressure. Resting hemodynamic parameters were similar in all groups. Estrogen replacement significantly potentiated bradykinin vasodilatory responses in the hindlimb, but not in the carotid vascular bed. Hemodynamic responses to sodium nitroprusside and ANG II were similar in all groups. In conclusion, our results demonstrate for the first time that aortic stiffness determined by PWV is decreased in estrogen-deficient rats. Estrogen treatment increases aortic stiffness and potentiates endothelial vasodilator function in the hindquarters, but not in the carotid vascular bed, suggesting a regional heterogeneity in the modulatory influence of estrogen on vasomotor function.