Sampson S R, Aminoff M J, Jaffe R A, Vidruk E H
J Pharmacol Exp Ther. 1976 Apr;197(1):119-25.
Experiments were performed to determine the mechanism by which centrifugal impulses in the carotid sinus nerve (CSN) reduce the frequency of impulse traffic in afferent chemoreceptor fibers from the carotid body in cats. Recordings of chemoreceptor activity were made from single- or few-fiber preparations dissected off the CSN, while the remainder of the CSN was stimulated electrically to produce neurally induced inhibition of chemoreceptor activity. Various drugs were injected either intravenously or directly into the arterial blood supply to the carotid body. We found that catecholamines (dopamine, norepinephrine and epinephrine) inhibited spontaneous chemoreceptor activity, and that alpha adrenergic antagonists abolished both this inhibition and that produced by electrical stimulation of the CSN in the same preparation. Atropine, but not nicotinic antagonists of acetylcholine, consistently blocked neurally induced inhibition but not that produced by catecholamines. Muscarinic agonists had no effect on spontaneous chemoreceptor activity. We conclude that centrifugal activity in the CSN causes release of endogenous catecholamines in the carotid body, and that these catecholamines mediate neurally induced inhibition of chemoreceptor activity is due to the vasomotor effects of acetylcholine.
进行了实验以确定猫的颈动脉窦神经（CSN）中的离心冲动降低来自颈动脉体的传入化学感受器纤维中冲动传输频率的机制。从CSN分离出的单纤维或少数纤维制剂记录化学感受器活动，同时对CSN的其余部分进行电刺激以产生神经诱导的化学感受器活动抑制。将各种药物静脉注射或直接注入颈动脉体的动脉血液供应中。我们发现儿茶酚胺（多巴胺、去甲肾上腺素和肾上腺素）抑制自发化学感受器活动，并且α肾上腺素能拮抗剂消除了同一制剂中这种抑制以及CSN电刺激产生的抑制。阿托品而非乙酰胆碱的烟碱拮抗剂始终阻断神经诱导的抑制，但不阻断儿茶酚胺产生的抑制。毒蕈碱激动剂对自发化学感受器活动没有影响。我们得出结论，CSN中的离心活动导致颈动脉体内内源性儿茶酚胺的释放，并且这些儿茶酚胺介导神经诱导的化学感受器活动抑制是由于乙酰胆碱的血管运动作用。
