Dart A M, Dietz R, Hieronymus K, Kübler W, Mayer E, Schömig A, Strasser R
Br J Pharmacol. 1984 Mar;81(3):475-8. doi: 10.1111/j.1476-5381.1984.tb10100.x.
beta-Adrenoceptor blockade by propranolol (4 X 10(-6)M) was without effect on the overflow of endogenous noradrenaline from the isolated heart of the rat induced by stimulation of sympathetic nerves for 1 min at 1 and at 4 Hz. The increase in heart rate in response to such stimulation was abolished by propranolol treatment. alpha 2-Adrenoceptor blockade by yohimbine (10(-6)M) induced approximately a two fold increase in the overflow of endogenous noradrenaline induced by stimulation of sympathetic nerves for 1 min at 1 and at 4 Hz. A combination of yohimbine (10(-6)M) and desipramine (10(-7)M) induced a more than 3 fold increase in the overflow of endogenous noradrenaline produced by sympathetic nerve stimulation at 1 and at 4 Hz. Heart rate increases produced by such stimulation were intensified. These results provide no evidence for the feedback stimulation of presynaptic beta-adrenoceptors in this preparation. The action of alpha-2-blockade was equipotent at stimulation frequencies of 1 and 4 Hz.
普萘洛尔（4×10⁻⁶M）对大鼠离体心脏交感神经刺激1分钟（频率为1赫兹和4赫兹）所诱导的内源性去甲肾上腺素溢出无影响。普萘洛尔处理可消除此类刺激引起的心率增加。育亨宾（10⁻⁶M）对α₂肾上腺素能受体的阻断作用，使交感神经刺激1分钟（频率为1赫兹和4赫兹）所诱导的内源性去甲肾上腺素溢出增加约两倍。育亨宾（10⁻⁶M）与地昔帕明（10⁻⁷M）联合使用，使交感神经刺激（频率为1赫兹和4赫兹）所产生的内源性去甲肾上腺素溢出增加超过三倍。此类刺激引起的心率增加增强。这些结果并未为此制剂中突触前β肾上腺素能受体的反馈刺激提供证据。α₂阻断作用在1赫兹和4赫兹的刺激频率下效力相当。
