Purdy R E, Ashbrook D W, Hurlbut D E, Reidy J P, Stratford R E, Watanabe M Y
Blood Vessels. 1981;18(4-5):153-60. doi: 10.1159/000158350.
The contractile effect of propranolol in isolated rabbit ear artery was assessed in reserpinized and in surgically and chemically denervated blood vessels. Reserpinization and surgical denervation either had no effect on or enhanced the ear artery contractile response to 10(-6) to 10(-4) M propranolol. In contrast, the contractile response to propranolol was nearly abolished after denervation of the ear artery in vitro with 6-hydroxydopamine (6-OHDA). Dose-response curves to norepinephrine were shifted to the left by factors of 4.9 in 6-OHDA denervated ear arteries and 15.6 in untreated arteries in the presence of 10(-7) M desipramine. The diluent for 6-OHDA shifted both the norepinephrine and propranolol dose-response curves to the right. It is proposed that propranolol caused a contractile response in ear artery by an action on the postsynaptic tissues of this vessel. 6-OHDA denervation caused nonspecific desensitization in rabbit ear artery leading to the loss of response of this vessel to propranolol.
在利血平化以及手术和化学去神经支配的血管中评估了普萘洛尔对离体兔耳动脉的收缩作用。利血平化和手术去神经支配对耳动脉对10⁻⁶至10⁻⁴M普萘洛尔的收缩反应要么没有影响,要么增强了这种反应。相比之下,用6-羟基多巴胺(6-OHDA)在体外对耳动脉去神经支配后,对普萘洛尔的收缩反应几乎完全消失。在存在10⁻⁷M地昔帕明的情况下,6-OHDA去神经支配的耳动脉中去甲肾上腺素的剂量-反应曲线向左移动了4.9倍,未处理的动脉中向左移动了15.6倍。6-OHDA的稀释剂使去甲肾上腺素和普萘洛尔的剂量-反应曲线都向右移动。有人提出,普萘洛尔通过作用于该血管的突触后组织而引起耳动脉的收缩反应。6-OHDA去神经支配导致兔耳动脉非特异性脱敏,导致该血管对普萘洛尔的反应丧失。