Yang Zhou, Coote J H
Division of Neuroscience, The Medical School, University of Birmingham, Birmingham B15 2TT, UK.
Exp Physiol. 2007 Jan;92(1):109-17. doi: 10.1113/expphysiol.2006.034884. Epub 2006 Sep 28.
In Wistar rats, an increase in renal sympathetic activity is induced by activation of presympathetic neurones in the paraventricular nucleus (PVN) and reflexly by a mild venous haemorrhage. Both stimuli are dependent on the release of vasopressin and glutamate at spinal synapses. The significance of the supraspinal pathway and the co-operative interaction of vasopressin with an excitatory amino acid is unclear. The present study examines this in Brattleboro rats, which have a natural vasopressin gene deletion. The responses were compared with Long-Evans rats, from which Brattleboro rats are derived. All rats were anaesthetized with a mixture of urethane (650 mg kg(-1) i.v.) and chloralose (50 mg kg(-1) i.v.). Recordings were made of blood pressure, heart rate and renal sympathetic nerve activity (RSNA). Microinjection of d,l-homocysteic acid (DLH, 0.2 m, 100 nl) at sites restricted to the PVN elicited significant increases in RSNA (P < 0.001) in both strains of rats. These changes were significantly reduced (P < 0.01) in Long-Evans rats by intrathecal application to the spinal cord of either a V(1a) antagonist or a glutamate antagonist (kynurenic acid), whereas in Brattleboro rats the changes were significantly reduced (P < 0.05) only by kynurenic acid. Removal of 1 ml of venous blood in Long-Evans rats increased RSNA by 28 +/- 4% (P < 0.01), which was significantly reduced (P < 0.05) by prior intrathecal application of either the V(1a) antagonist or by kynurenic acid. The same test in Brattleboro rats caused a significantly greater (P < 0.05) increase (63 +/- 14.7%) in RSNA which, in contrast to Long-Evans rats, was unchanged by intrathecal application of the V(1a) antagonist, being significantly reduced (P < 0.01) only by intrathecal kynurenic acid. Thus, in Brattleboro rats, the lack of vasopressin in the brain sympathetic pathways appears to be compensated, acutely, by glutamate-releasing pathways. This might indicate that, in normal rats, vasopressin is more important in maintaining longer term adjustments to stressors.
在Wistar大鼠中，室旁核（PVN）中交感神经节前神经元的激活以及轻度静脉出血引起的反射均可导致肾交感神经活动增加。这两种刺激均依赖于脊髓突触处血管加压素和谷氨酸的释放。脊髓上通路的意义以及血管加压素与兴奋性氨基酸的协同相互作用尚不清楚。本研究在遗传性血管加压素基因缺失的Brattleboro大鼠中对此进行了研究。将这些反应与Brattleboro大鼠的起源品系Long-Evans大鼠进行了比较。所有大鼠均用乌拉坦（650 mg·kg⁻¹静脉注射）和氯醛糖（50 mg·kg⁻¹静脉注射）的混合物麻醉。记录血压、心率和肾交感神经活动（RSNA）。在仅限于PVN的部位微量注射d，l-高半胱氨酸（DLH，0.2 m，100 nl）可使两种品系大鼠的RSNA显著增加（P<0.001）。在Long-Evans大鼠中，鞘内注射V₁a拮抗剂或谷氨酸拮抗剂（犬尿氨酸）可使这些变化显著降低（P<
