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大鼠禁水期间,延髓头端腹外侧区的兴奋性氨基酸维持血压。

Excitatory amino acids in rostral ventrolateral medulla support blood pressure during water deprivation in rats.

作者信息

Brooks Virginia L, Freeman Korrina L, Clow Kathy A

机构信息

Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, Oregon 97239-3098, USA.

出版信息

Am J Physiol Heart Circ Physiol. 2004 May;286(5):H1642-8. doi: 10.1152/ajpheart.01004.2003. Epub 2004 Jan 8.

DOI:10.1152/ajpheart.01004.2003
PMID:14715511
Abstract

Water deprivation is associated with regional increases in sympathetic tone, but whether this is mediated by changes in brain stem regulation of sympathetic activity is unknown. Therefore, this study tested the hypothesis that water deprivation increases excitatory amino acid (EAA) drive of the rostral ventrolateral medulla (RVLM), by determining whether bilateral microinjection of kynurenate (Kyn; 2.7 nmol) into the RVLM decreases arterial pressure more in water-deprived than water-replete rats. Plasma osmolality was increased in 48-h water-deprived rats (313 +/- 1 mosmol/kgH2O; P < 0.05) compared with 24-h water-deprived rats (306 +/- 2 mosmol/kgH2O) and water-replete animals (300 +/- 2 mosmol/kgH2O). Kyn decreased arterial pressure by 28.1 +/- 5.2 mmHg (P < 0.01) in 48-h water-deprived rats but had no effect in water-replete rats (-5.9 +/- 1.3 mmHg). Variable depressor effects were observed in 24-h water-deprived animals (-12.5 +/- 2.4 mmHg, not significant); however, in all rats the Kyn depressor response was strongly correlated to the osmolality level (P < 0.01; r2 = 0.47). The pressor responses to unilateral microinjection of increasing doses (0.1, 0.5, 1.0, and 5.0 nmol) of glutamate were enhanced (P < 0.05) during water deprivation, but the pressor responses to intravenous phenylephrine injection were smaller (P < 0.05). These data suggest that water deprivation increases EAA drive to the RVLM, in part by increasing responsiveness of the RVLM to EAA such as glutamate.

摘要

缺水与交感神经张力的局部增加有关,但这是否由脑干对交感神经活动调节的变化介导尚不清楚。因此,本研究通过确定向头端腹外侧延髓(RVLM)双侧微量注射犬尿氨酸(Kyn;2.7 nmol)是否在缺水大鼠中比水充足大鼠更能降低动脉压,来检验缺水增加RVLM兴奋性氨基酸(EAA)驱动的假设。与24小时缺水大鼠(306±2 mosmol/kgH2O)和水充足动物(300±2 mosmol/kgH2O)相比,48小时缺水大鼠的血浆渗透压升高(313±1 mosmol/kgH2O;P<0.05)。Kyn使48小时缺水大鼠的动脉压降低28.1±5.2 mmHg(P<0.01),但对水充足大鼠无影响(-5.9±1.3 mmHg)。在24小时缺水动物中观察到可变的降压作用(-12.5±2.4 mmHg,无显著性差异);然而,在所有大鼠中,Kyn的降压反应与渗透压水平密切相关(P<0.01;r2=0.47)。在缺水期间,对单侧微量注射递增剂量(0.1、0.5、1.0和5.0 nmol)谷氨酸的升压反应增强(P<0.05),但对静脉注射去氧肾上腺素的升压反应较小(P<0.05)。这些数据表明,缺水增加了对RVLM的EAA驱动,部分原因是增加了RVLM对诸如谷氨酸等EAA的反应性。

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