Marwood J, Tierney G, Stokes G
Clinical Pharmacology Department, Royal North Shore Hospital, St Leonards, New South Wales, Australia.
J Cardiovasc Pharmacol. 1991 Jan;17(1):1-7. doi: 10.1097/00005344-199101000-00001.
Using paired isolated perfused rat tail artery segments, it was found that enalaprilat, an ACE inhibitor, augmented 1.6-fold the contractile responses to phenylephrine (PE), an alpha 1-adrenoceptor agonist. Similarly, enalaprilat potentiated 1.9-fold the alpha 1-adrenoceptor antagonist activity of doxazosin in paired rat tail artery segments. In rats treated with deoxycorticosterone acetate (DOCA) 20 mg/kg i.m. twice weekly for 5 weeks, plasma renin activity fell from a control value of 5.73 +/- 0.93 to 0.04 +/- 0.01 ng of AI/ml/h. The inhibition of circulating renin activity in these animals was associated with a loss of the potentiating effects of enalaprilat upon the alpha 1-adrenoceptor antagonist action of doxazosin. The results are interpreted as indicating that angiotensin II (AII) can modulate the functional activity of alpha 1-adrenoceptors in vascular smooth muscle.
使用成对的离体灌注大鼠尾动脉段，发现血管紧张素转换酶（ACE）抑制剂依那普利拉可使对α1-肾上腺素能受体激动剂去氧肾上腺素（PE）的收缩反应增强1.6倍。同样，在成对的大鼠尾动脉段中，依那普利拉可使多沙唑嗪的α1-肾上腺素能受体拮抗剂活性增强1.9倍。在用醋酸脱氧皮质酮（DOCA）20mg/kg肌肉注射、每周两次、持续5周处理的大鼠中，血浆肾素活性从对照值5.73±0.93降至0.04±0.01ng血管紧张素I/ml/h。这些动物循环肾素活性的抑制与依那普利拉对多沙唑嗪α1-肾上腺素能受体拮抗剂作用的增强效应丧失有关。结果表明，血管紧张素II（AII）可调节血管平滑肌中α1-肾上腺素能受体的功能活性。
