Koyama S, Nishida K, Terada N, Shiojima Y, Takeuchi T
Jpn J Physiol. 1986;36(3):441-50. doi: 10.2170/jjphysiol.36.441.
The present experiments were designed to study effects of neural control mechanisms on renal sympathetic nerve activity during acute portal vein distension in anesthetized dogs. Following the inflation of a balloon placed into the main portal vein of animals with the neuraxis intact (intact group), portal vein pressure at a site of the splanchnic regions increased significantly. Mean blood pressure (MBP) fell significantly and then renal vascular resistance (RVR) increased significantly in parallel with changes in portal venous pressure. In animals with sinoaortic denervation (SAD group), changes in portal venous pressure during the inflation of a balloon did not differ from the intact group. However, decreases in MBP in the SAD group were greater than that in the intact group, and sinoaortic denervation did not alter increases in RVR. In animals with both sinoaortic denervation and cervical vagotomy (vagotomy group), portal vein distension produced more profound hypotension, and significant increases in RVR occurred. This increase in RVR, however, was abolished by renal nerve denervation. The results of the present study indicate that increases in RVR during the portal vein distension, which is associated with systemic hypotension, may be mediated by an activation of efferent sympathetic renal nerves and modified by at least two neural reflex mechanisms such as carotid sinus baroreceptors and cardiopulmonary baroreceptors. In addition, local reflex systems such as stretch receptors in the venous wall of the portal vein may be involved in excitatory response to renal sympathetic nerve, leading to renal vasoconstriction, during the portal vein distension.
本实验旨在研究麻醉犬急性门静脉扩张时神经控制机制对肾交感神经活动的影响。在动物完整神经轴(完整组)的主门静脉内放置球囊并充气后,内脏区域门静脉压力显著升高。平均动脉压(MBP)显著下降,随后肾血管阻力(RVR)随门静脉压力变化而显著升高。在去窦弓神经支配的动物(SAD组)中,球囊充气时门静脉压力变化与完整组无差异。然而,SAD组的MBP下降幅度大于完整组,且去窦弓神经支配并未改变RVR的升高。在去窦弓神经支配并切断颈迷走神经的动物(迷走神经切断组)中,门静脉扩张导致更严重的低血压,且RVR显著升高。然而,这种RVR的升高被肾神经切断所消除。本研究结果表明,门静脉扩张时与全身性低血压相关的RVR升高可能由传出性肾交感神经激活介导,并至少由两种神经反射机制如颈动脉窦压力感受器和心肺压力感受器调节。此外,门静脉壁静脉壁牵张感受器等局部反射系统可能参与门静脉扩张时对肾交感神经的兴奋性反应,导致肾血管收缩。