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内源性血管紧张素II支持清醒缺钠大鼠的腰交感神经活动:最后区的作用。

Endogenous ANG II supports lumbar sympathetic activity in conscious sodium-deprived rats: role of area postrema.

作者信息

Xu L, Collister J P, Osborn J W, Brooks V L

机构信息

Department of Physiology and Pharmacology, The Oregon Health Sciences University, Portland, Oregon 97201-3098, USA.

出版信息

Am J Physiol. 1998 Jul;275(1):R46-55. doi: 10.1152/ajpregu.1998.275.1.R46.

DOI:10.1152/ajpregu.1998.275.1.R46
PMID:9688959
Abstract

This study tests the hypothesis that the area postrema (AP) is necessary for endogenous ANG II to chronically maintain lumbar sympathetic nerve activity (LSNA) and heart rate (HR) in conscious sodium-deprived rats. The effect of the ANG II type 1-receptor antagonist, losartan, on LSNA and HR was determined in rats that were either AP lesioned (APX) or sham lesioned. The sham rats were divided into groups, with (SFR) or without (SAL) food restriction, to control for the decreased food intake of APX rats. Before losartan, basal mean arterial pressure (MAP), HR, and baroreflex control of LSNA and HR were similar between groups, with the exception of lower maximal reflex LSNA and higher maximal gain of the HR-MAP curve in APX rats. In all groups, losartan similarly shifted (P < 0.01) the LSNA-MAP curve to the left without altering maximal gain. Losartan also decreased (P < 0.05) minimal LSNA in all groups, and suppressed (P < 0.01) maximal LSNA (% of control) in SFR (240 +/- 13 to 205 +/- 15) and SAL (231 +/- 21 to 197 +/- 26) but not APX (193 +/- 10 to 185 +/- 8) rats. In general, losartan similarly shifted the HR-MAP curve to a lower MAP in all groups. The results suggest that the AP is not necessary for endogenous ANG II to chronically support LSNA and HR at basal and elevated MAP levels in sodium-deprived rats. However, the AP is required for endogenous ANG II to increase maximal reflex LSNA at low MAP levels.

摘要

本研究检验了以下假设

在清醒的缺钠大鼠中,最后区(AP)对于内源性血管紧张素II(ANG II)长期维持腰交感神经活动(LSNA)和心率(HR)是必需的。在接受AP损毁(APX)或假手术损毁的大鼠中,测定了ANG II 1型受体拮抗剂氯沙坦对LSNA和HR的影响。将假手术大鼠分为有(SFR)或无(SAL)食物限制的组,以控制APX大鼠食物摄入量的减少。在给予氯沙坦之前,各组之间的基础平均动脉压(MAP)、HR以及LSNA和HR的压力反射控制相似,但APX大鼠的最大反射性LSNA较低,HR-MAP曲线的最大增益较高。在所有组中,氯沙坦均使LSNA-MAP曲线类似地向左移动(P<0.01),而不改变最大增益。氯沙坦还降低了所有组的最小LSNA(P<0.05),并抑制了SFR组(从240±13降至205±15)和SAL组(从231±21降至197±26)的最大LSNA(相对于对照组的百分比)(P<0.01),但对APX大鼠(从193±10降至185±8)无此作用。总体而言,氯沙坦使所有组的HR-MAP曲线类似地向较低的MAP移动。结果表明,在缺钠大鼠的基础和升高的MAP水平下,内源性ANG II长期维持LSNA和HR并不需要AP。然而,在低MAP水平下,内源性ANG II增加最大反射性LSNA需要AP。

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