Yang T, Levy M N
Department of Investigative Medicine, Mt. Sinai Medical Center, Cleveland, OH 44106.
Circ Res. 1993 Jan;72(1):137-44. doi: 10.1161/01.res.72.1.137.
We studied the effects of intense sympathetic stimulation on the chronotropic responses of the heart to subsequent test stimulations of the cardiac autonomic nerves in dogs anesthetized with alpha-chloralose. Such intense sympathetic stimulations (which we refer to as "release stimulations") are known to release neuropeptide Y as well as norepinephrine. The changes in cardiac cycle length evoked by vagal and sympathetic test stimulations were progressively more attenuated as we increased the frequency and duration of the antecedent sympathetic release stimulations. We found that 2.5 minutes after a maximal release stimulation (30 Hz for 5 minutes), the mean +/- SEM chronotropic responses to the vagal and sympathetic test stimulations were diminished to 36.5 +/- 1.6% and 54.7 +/- 1.3% respectively, of the prestimulation responses. The mean times for the chronotropic responses to the vagal and sympathetic test stimulations to recover to their control values were 52.0 +/- 1.3 and 63.2 +/- 2.9 minutes, respectively. This enduring effect suggests the action of a neuropeptide, such as neuropeptide Y. Phentolamine potentiated the inhibitory effects of the sympathetic release stimulations. The chronotropic responses to isoproterenol infusions were not affected appreciably by antecedent sympathetic release stimulation. We conclude, therefore, that the inhibitory effects of antecedent sympathetic release stimulation on cardiac sympathetic neurotransmission are mediated prejunctionally, probably via an inhibition of the neuronal release of norepinephrine by neuropeptide Y.
我们研究了强烈交感神经刺激对用α-氯醛糖麻醉的犬心脏自主神经后续测试刺激的变时反应的影响。已知这种强烈的交感神经刺激（我们称之为“释放刺激”）会释放神经肽Y以及去甲肾上腺素。随着先前交感神经释放刺激的频率和持续时间增加，迷走神经和交感神经测试刺激引起的心动周期长度变化逐渐减弱。我们发现，在最大释放刺激（30Hz，持续5分钟）后2.5分钟，对迷走神经和交感神经测试刺激的平均±标准误变时反应分别降至刺激前反应的36.5±1.6%和54.7±1.3%。迷走神经和交感神经测试刺激的变时反应恢复到对照值的平均时间分别为52.0±1.3分钟和63.2±2.9分钟。这种持久效应提示了一种神经肽的作用，如神经肽Y。酚妥拉明增强了交感神经释放刺激的抑制作用。先前的交感神经释放刺激对异丙肾上腺素输注的变时反应没有明显影响。因此，我们得出结论，先前交感神经释放刺激对心脏交感神经传递的抑制作用是通过节前介导的，可能是通过神经肽Y抑制去甲肾上腺素的神经元释放。
