Naden R P, Rosenfeld C R
Am J Physiol. 1985 Mar;248(3 Pt 2):H339-44. doi: 10.1152/ajpheart.1985.248.3.H339.
Estradiol-17 beta (E2) produces vasodilation in several systemic vascular beds, but most extensively in the nonpregnant uterus. It has been postulated that E2 induces this vasodilation via blockade of vascular alpha-adrenergic receptors. This hypothesis was tested in six chronically instrumented, nonpregnant sheep by comparing the systemic and uterine hemodynamic responses to intravenous E2, to an alpha-adrenergic receptor blocker, phentolamine, and to both agents given together. Uterine blood flow (UBF) increased significantly after E2 administration, from 20 +/- 7 to 233 +/- 37 (SE) ml/min. In contrast, phentolamine had no detectable effect on UBF or on the UBF response to E2 when both were given together. Similar contrasting responses were observed in the effects of E2 and/or phentolamine on the systemic vasculature. When responses to alpha-agonists were evaluated, there was no evidence of alpha-blockade following E2 despite the substantial vasodilation; in contrast, alpha-blockade was present during phentolamine administration when no vasodilation was noted. Therefore, we conclude that E2-induced vasodilation in chronically instrumented sheep is not mediated through blockade of vascular alpha-adrenergic receptors.
17β-雌二醇（E2）可使多个体循环血管床产生血管舒张，但在未孕子宫中最为显著。据推测，E2通过阻断血管α-肾上腺素能受体诱导这种血管舒张。通过比较静脉注射E2、α-肾上腺素能受体阻滞剂酚妥拉明以及两者联合使用时的体循环和子宫血流动力学反应，在六只长期植入仪器的未孕绵羊中对这一假设进行了验证。给予E2后，子宫血流量（UBF）显著增加，从20±7 ml/min增至233±37（标准误）ml/min。相比之下，酚妥拉明对UBF或两者联合使用时对E2的UBF反应均无明显影响。在E2和/或酚妥拉明对体循环血管系统的影响方面也观察到了类似的对比反应。当评估对α-激动剂的反应时，尽管有明显的血管舒张，但E2给药后没有α-阻断的证据；相反，在酚妥拉明给药期间出现了α-阻断，此时未观察到血管舒张。因此，我们得出结论，长期植入仪器的绵羊中E2诱导的血管舒张不是通过阻断血管α-肾上腺素能受体介导的。
