Weinstock M, Thoa N B, Kopin I J
Eur J Pharmacol. 1978 Feb 1;47(3):297-302. doi: 10.1016/0014-2999(78)90237-6.
Superior cervical ganglia of rats grown in organ culture were used to study the effect of beta-receptor stimulants and antagonists on 3H-noradrenaline release in response to stimulation by KC1 (75 mM). (--)-Isoprenaline 1X 10(-9)--1 X 10(-7) M) increased 20--25% the release of 3H-noradrenaline from cultured ganglia exposed to KC1. Isoprenaline did not modify either the spontaneous (non-calcium dependent) release of 3H-noradrenaline from cultured ganglia, or the KC1-stimulated release from fresh ganglia. The effect of (--)-isoprenaline was blocked by (--)-propranolol 5 X 10(-9) -- 1 X 10(-8) M and by butoxamine 10(-6) M, but not by (+)-propranolol (1 -- 5 X 10(-8) M), practolol (1 X 10(-8) -- 1 X 10(-6) M), or sotalol (1 X 10(-7) -- 1 X 10(-6) M). Isoprenaline induced augmentation of 3H-noradrenaline release and its antagonism by (--)-propranolol still occurred in the presence of DMI. It is suggested that presynaptic beta-receptors in sympathetic nerve terminals may be involved in a positive feedback of noradrenaline release.
利用在器官培养中生长的大鼠颈上神经节，研究β受体激动剂和拮抗剂对3H-去甲肾上腺素在75 mM氯化钾刺激下释放的影响。（-）-异丙肾上腺素（1×10^(-9) - 1×10^(-7) M）使暴露于氯化钾的培养神经节中3H-去甲肾上腺素的释放增加20%-25%。异丙肾上腺素既不改变培养神经节中3H-去甲肾上腺素的自发（非钙依赖性）释放，也不改变新鲜神经节中氯化钾刺激的释放。（-）-异丙肾上腺素的作用被5×10^(-9) - 1×10^(-8) M的（-）-普萘洛尔和10^(-6) M的丁氧胺阻断，但不被（+）-普萘洛尔（1 - 5×10^(-8) M）、心得宁（1×10^(-8) - 1×10^(-6) M）或索他洛尔（1×10^(-7) - 1×10^(-6) M）阻断。在存在DMI的情况下，异丙肾上腺素仍能诱导3H-去甲肾上腺素释放增加及其被（-）-普萘洛尔拮抗。提示交感神经末梢的突触前β受体可能参与去甲肾上腺素释放的正反馈。
