Russell J A, Bartlett S
J Appl Physiol Respir Environ Exerc Physiol. 1981 Aug;51(2):376-83. doi: 10.1152/jappl.1981.51.2.376.
Superfusion techniques were used to examine the effect of acetylcholine (ACh) on the release of norepinephrine (NE) from isolated canine airways. Trachealis strips and helical strips of intrapulmonary airways were incubated with 3H-labeled NE, rinsed, and mounted in superfusion chambers. The superfusate was collected at timed intervals for estimation of total radioactivity and for column chromatographic separation of NE and its metabolites. Field electrical stimulation (2 Hz) and tyramine perfusion (3 X 10(-5) M) increased the total radioactivity of the perfusate by increasing the amount of intact 3H-labeled NE as well as the amounts of all metabolic fractions. Both extraneuronal and neuronal uptake mechanisms were important in inactivating the NE released by either stimulus. Exogenously administered ACh (10(-6)-10(-5) M) inhibited the release of NE that was caused by nerve stimulation but not that caused by tyramine perfusion. The inhibitory effect of ACh was antagonized by atropine (10(-6) M) but not by hexamethonium (5 X 10(-6) M). We conclude that ACh inhibits the exocytotic nerve-stimulated NE release by activating muscarinic receptors on adrenergic nerve varicosities.
采用灌流技术研究乙酰胆碱（ACh）对离体犬气道去甲肾上腺素（NE）释放的影响。将气管条和肺内气道螺旋条与3H标记的NE一起孵育，冲洗后安装在灌流室中。按一定时间间隔收集灌流液，用于估计总放射性以及对NE及其代谢产物进行柱色谱分离。场电刺激（2Hz）和酪胺灌注（3×10⁻⁵M）通过增加完整的3H标记NE的量以及所有代谢组分的量来增加灌流液的总放射性。神经外摄取机制和神经摄取机制在使两种刺激释放的NE失活方面都很重要。外源性给予ACh（10⁻⁶ - 10⁻⁵M）可抑制神经刺激引起的NE释放，但不抑制酪胺灌注引起的NE释放。ACh的抑制作用可被阿托品（10⁻⁶M）拮抗，但不能被六甲铵（5×10⁻⁶M）拮抗。我们得出结论，ACh通过激活肾上腺素能神经膨体上的毒蕈碱受体来抑制神经刺激引起的NE胞吐释放。
