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急性血管紧张素II调节肾交感神经活动的动脉压力反射控制的中枢机制。

Central mechanisms of acute ANG II modulation of arterial baroreflex control of renal sympathetic nerve activity.

作者信息

Sanderford Max G, Bishop Vernon S

机构信息

Department of Biological Sciences, Tarleton State University, Stephenville 76401, USA.

出版信息

Am J Physiol Heart Circ Physiol. 2002 May;282(5):H1592-602. doi: 10.1152/ajpheart.00222.2001.

DOI:10.1152/ajpheart.00222.2001
PMID:11959620
Abstract

Short-term intravenous infusion of angiotensin II (ANG II) into conscious rabbits reduces the range of renal sympathetic nerve activity (RSNA) by attenuating reflex disinhibition of RSNA. This action of ANG II to attenuate the arterial baroreflex range is exaggerated when ANG II is directed into the vertebral circulation, which suggests a mechanism involving the central nervous system. Because an intact area postrema (AP) is required for ANG II to attenuate arterial baroreflex-mediated bradycardia and is also required for maintenance of ANG II-dependent hypertension, we hypothesized that attenuation of maximum RSNA during infusion of ANG II involves the AP. In conscious AP-lesioned (APX) and AP-intact rabbits, we compared the effect of a 5-min intravenous infusion of ANG II (10 and 20 ng x kg(-1) x min(-1)) on the relationship between mean arterial blood pressure (MAP) and RSNA. Intravenous infusion of ANG II into AP-intact rabbits resulted in a dose-related attenuation of maximum RSNA observed at low MAP. In contrast, ANG II had no effect on maximum RSNA in APX rabbits. To further localize the central site of ANG II action, its effect on the arterial baroreflex was assessed after a midcollicular decerebration. Decerebration did not alter arterial baroreflex control of RSNA compared with the control state, but as in APX, ANG II did not attenuate the maximum RSNA observed at low MAP. The results of this study indicate that central actions of peripheral ANG II to attenuate reflex disinhibition of RSNA not only involve the AP, but may also involve a neural interaction rostral to the level of decerebration.

摘要

对清醒家兔进行短期静脉输注血管紧张素II(ANG II),通过减弱肾交感神经活动(RSNA)的反射性去抑制作用,从而缩小RSNA的变化范围。当将ANG II注入椎动脉循环时,其减弱动脉压力反射范围的作用会增强,这提示存在一种涉及中枢神经系统的机制。由于ANG II减弱动脉压力反射介导的心动过缓需要完整的最后区(AP),且维持ANG II依赖性高血压也需要AP,因此我们推测,输注ANG II期间最大RSNA的减弱涉及AP。在清醒的AP损伤(APX)和AP完整的家兔中,我们比较了静脉输注5分钟ANG II(10和20 ng·kg⁻¹·min⁻¹)对平均动脉血压(MAP)与RSNA之间关系的影响。向AP完整的家兔静脉输注ANG II,导致在低MAP时观察到的最大RSNA呈剂量依赖性减弱。相比之下,ANG II对APX家兔的最大RSNA没有影响。为了进一步确定ANG II作用的中枢位点,在中脑水平去大脑后评估了其对动脉压力反射的影响。与对照状态相比,去大脑并未改变动脉压力反射对RSNA的控制,但与APX情况一样,ANG II并未减弱在低MAP时观察到的最大RSNA。本研究结果表明,外周ANG II减弱RSNA反射性去抑制作用的中枢作用不仅涉及AP,还可能涉及去大脑水平以上的神经相互作用。

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Central mechanisms of acute ANG II modulation of arterial baroreflex control of renal sympathetic nerve activity.急性血管紧张素II调节肾交感神经活动的动脉压力反射控制的中枢机制。
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