Qin S L, Lin M Z
Department of Physiology, Dalian Medical College.
Sheng Li Xue Bao. 1994 Jun;46(3):217-25.
In anesthetized and bilateral sinoaortic denervated rabbits with either intact or ascorbic acid injected paraventricular nucleus (PVN), the inhibition of renal sympathetic nerve activity (RSNA) induced by blood volume expansion (VE) all decreased by approximately 48%. However, 3-4 h and 3-4 d after kainic acid lesion of PVN, the inhibition of RSNA was attenuated respectively to -28.0 +/- 4.5% and -25.7 +/- 4.1% (P < 0.05) with considerably shortened time course (P < 0.01). Also such inhibition could be significantly attenuated (P < 0.05) by intrathecal injection of vasop ressinergic V1 receptor antagonist in spinal T10-T12 segments. There was no significant difference with the slight and brief increase of mean arterial pressure induced by VE in the control and the experimental group. Thus it can be concluded that the inhibition of RSNA induced by VE is partly mediated by a vagal afferent triggered PVN-spinal pathway.
在麻醉且双侧窦主动脉去神经支配的家兔中，无论是室旁核（PVN）完整还是注射了抗坏血酸的家兔，血容量扩张（VE）诱导的肾交感神经活动（RSNA）抑制均降低了约48%。然而，在PVN经海人藻酸损伤后3 - 4小时和3 - 4天，RSNA的抑制分别减弱至-28.0±4.5%和-25.7±4.1%（P<0.05），且时间进程显著缩短（P<0.01）。此外，在脊髓T10 - T12节段鞘内注射血管加压素能V1受体拮抗剂可使这种抑制显著减弱（P<0.05）。对照组和实验组中，VE引起的平均动脉压轻微且短暂升高无显著差异。因此可以得出结论，VE诱导的RSNA抑制部分是由迷走神经传入触发的PVN -脊髓通路介导的。
