Saigusa Takeshi, Granger Naomi S, Godwin Shirley J, Head Geoffrey A
Department of Physiology, Faculty of Medicine, University of Yamanashi, Tamaho, Nakakoma, Yamanashi 409-3898, Japan.
Auton Neurosci. 2003 Aug 29;107(1):20-31. doi: 10.1016/S1566-0702(03)00104-8.
The present study examined the role of the rostral ventrolateral medulla (RVLM) in mediating the pressor and renal sympathetic baroreflex effects of intraventricularly administered angiotensin II (Ang II) in urethane anaesthetised rabbits. Microinjection of Ang II over a wide range of medullary sites showed that pressor responses were observed only in the RVLM. Ang II was particularly potent in producing a transient pressor response at this site with a half maximal dose of 9 fmol. The administration of the Ang II antagonist Sar(1)-Ile(8)-Ang II (10 pmol) bilaterally into the RVLM inhibited the pressor response to local and fourth ventricular Ang II, but not the pressor response to RVLM applied glutamate. To determine the contribution of the RVLM to the renal sympathetic baroreflex effects of Ang II, blood pressure-renal sympathetic nerve activity (RSNA) curves were constructed with intravenous infusion of phenylephrine or nitroprusside before and after Ang II, vehicle or glutamate infusions into the RVLM. Ang II infusion of 4 pmol/min into the RVLM increased blood pressure by 8+/-3 mm Hg and shifted the renal sympathetic baroreflex curve to the right. The maximum RSNA evoked by lowering blood pressure increased by 36+/-6%, similar to the effect seen with fourth ventricular Ang II and RVLM glutamate. These studies suggest that the major medullary pressor site of action of Ang II when injected into the hindbrain cerebro-spinal fluid of anaesthetized rabbits is the RVLM where it facilitates baroreflex control of RSNA.
本研究探讨了延髓头端腹外侧区（RVLM）在介导脑室注射血管紧张素II（Ang II）对乌拉坦麻醉家兔的升压及肾交感压力反射效应中的作用。在广泛的延髓部位微量注射Ang II显示，仅在RVLM观察到升压反应。Ang II在此部位产生短暂升压反应的效力特别强，半数最大剂量为9飞摩尔。双侧向RVLM注射Ang II拮抗剂Sar(1)-Ile(8)-Ang II（10皮摩尔）可抑制对局部及第四脑室Ang II的升压反应，但不影响对RVLM应用谷氨酸的升压反应。为确定RVLM对Ang II肾交感压力反射效应的作用，在向RVLM注入Ang II、赋形剂或谷氨酸之前及之后，通过静脉输注去氧肾上腺素或硝普钠构建血压-肾交感神经活动（RSNA）曲线。以4皮摩尔/分钟的速度向RVLM注入Ang II可使血压升高8±3毫米汞柱，并使肾交感压力反射曲线右移。通过降低血压诱发的最大RSNA增加了36±6%，类似于第四脑室注入Ang II和RVLM注入谷氨酸时的效应。这些研究表明，当向麻醉家兔的后脑脑脊液中注射Ang II时，其主要的延髓升压作用部位是RVLM，在此处它促进对RSNA的压力反射控制。
