Reimann K A, Weaver L C
Am J Physiol. 1980 Sep;239(3):H316-25. doi: 10.1152/ajpheart.1980.239.3.H316.
Afferent neurons within cardiac sympathetic nerves can reflexly excite central sympathetic outflow. However, their contribution to cardiovascular control remains unclear because they are potentially opposed by inhibitory reflexes of cardiac vagal or arterial baroreceptor afferent origin. It was considered that sympathetically mediated, excitatory responses might be more prominent when initiated by chemical stimulation. In chloralose-anesthetized, vagotomized, sinoaortic-denervated cats, epicardial or intracoronary administration of bradykinin or potassium chloride evoked renal nerve excitation and pressor responses mediated by cardiac sympathetic afferent nerves. When upper thoracic sympathetic nerves were severed, and vagal afferent nerves remained intact, bradykinin and potassium chloride produced inhibition of renal nerve activity and depressor responses. When sympathetic and vagal components of cardiac innervation remained intact, these substances produced excitation, inhibition, or no change in sympathetic outflow. Excitation occurred as often as inhibition. A similar pattern was observed when arterial baroreceptor nerves remained intact. These data illustrate that cardiac sympathetic afferent neurons can have significant excitatory influences on the cardiovascular system in spite of opposition by inhibitory afferent groups.
心脏交感神经内的传入神经元可反射性地兴奋中枢交感神经输出。然而，它们对心血管控制的作用仍不清楚，因为它们可能受到心脏迷走神经或动脉压力感受器传入神经的抑制性反射的对抗。有人认为，当由化学刺激引发时，交感神经介导的兴奋性反应可能更为突出。在氯醛糖麻醉、迷走神经切断、窦主动脉去神经的猫中，心外膜或冠状动脉内给予缓激肽或氯化钾可诱发由心脏交感传入神经介导的肾神经兴奋和升压反应。当上胸段交感神经切断而迷走传入神经保持完整时，缓激肽和氯化钾可抑制肾神经活动并产生降压反应。当心脏神经支配的交感和迷走成分保持完整时，这些物质可使交感神经输出产生兴奋、抑制或无变化。兴奋和抑制出现的频率相同。当动脉压力感受器神经保持完整时也观察到类似的模式。这些数据表明，尽管存在抑制性传入神经组的对抗，心脏交感传入神经元对心血管系统仍可产生显著的兴奋性影响。
