University of Ottawa Heart Institute, Ottawa, Canada.
Brain Res. 2013 Aug 21;1527:79-86. doi: 10.1016/j.brainres.2013.06.028. Epub 2013 Jun 28.
Central infusion of Na(+)-rich artificial cerebro-spinal fluid (aCSF) activates the brain renin-angiotensin system and causes sympatho-excitatory and pressor responses. We evaluated the role of the subfornical organ (SFO) and angiotensin II type 1 (AT1) receptors in the SFO in mediating the central Na(+)-induced pressor response. In conscious Wistar rats, intra SFO infusions of Na(+)-rich aCSF containing 0.45 and 0.6M Na(+) at 10 nl/min or injection of angiotensin II (Ang II) at 80 ng increased blood pressure (BP) by 15-22 mmHg, whereas mannitol with the same osmolarity as the Na(+)-rich aCSF had no effects. Intra SFO infusion of the AT1 receptor blocker candesartan abolished the pressor response induced by intra SFO administration of Na(+)-rich aCSF or Ang II. Intra cerebro-ventricular (icv) infusion of Na(+)-rich aCSF (0.3M Na(+)) at 3.8 μl/min for 10 min increased BP by 15-20 mmHg. Electrolytic lesion of the SFO attenuated these BP increases by 50-70%. Intra SFO infusion of candesartan also prevented 50% of these pressor responses. These data suggest that SFO neurons are indeed sensitive to Na(+), the SFO is a major - but not only - site in the brain to sense an increase in CSF [Na(+)], and activation of AT1 receptors in the SFO mediates the SFO component of the Na(+)-induced pressor response.
中枢输注富含钠离子的人工脑脊液（aCSF）可激活脑肾素-血管紧张素系统，引起交感兴奋和升压反应。我们评估了穹窿下器官（SFO）和 SFO 中的血管紧张素 II 型 1（AT1）受体在介导中枢钠离子引起的升压反应中的作用。在清醒的 Wistar 大鼠中，以 10nl/min 的速度向 SFO 内输注含有 0.45 和 0.6M Na+的富含钠离子的 aCSF 或注射 80ng 血管紧张素 II（Ang II）可使血压升高 15-22mmHg，而渗透压与富含钠离子的 aCSF 相同的甘露醇则没有作用。SFO 内输注 AT1 受体阻滞剂坎地沙坦可消除 SFO 内输注富含钠离子的 aCSF 或 Ang II 引起的升压反应。向侧脑室（icv）内输注 3.8μl/min 的富含钠离子的 aCSF（0.3M Na+）10min 可使血压升高 15-20mmHg。SFO 电损毁可使这些血压升高减少 50-70%。SFO 内输注坎地沙坦也可防止 50%的这些升压反应。这些数据表明，SFO 神经元确实对钠离子敏感，SFO 是大脑中感应 CSF[Na+]升高的主要部位（但不是唯一部位），而 SFO 中的 AT1 受体的激活介导了 SFO 成分在钠离子引起的升压反应中的作用。
