Increased dietary salt sensitizes vasomotor neurons of the rostral ventrolateral medulla.
Increased dietary salt sensitizes vasomotor neurons of the rostral ventrolateral medulla.
复制标题
饮食中盐的增加会使延髓头端腹外侧的血管运动神经元变得敏感。
DOI：
10.1161/01.hyp.22.6.929
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Gordon,FJ
中科院分区：
文献类型：
--
作者：
Pawloski-Dahm,CM;Gordon,FJ
饮食中过量的钠是高血压发病率和严重程度的主要因素。然而，盐导致高血压严重程度的确切机制尚不清楚。延髓头端腹外侧区(RVLM)是交感神经系统调节动脉血压的主要脑干部位。这项研究的目的是确定过量的食盐是否会改变RVLM中神经元的功能或反应。雄性SD大鼠饮用自来水或0.9%氯化钠溶液，连续饮用10~14天。过量的氯化钠不会影响基线血压。然而，当微量注射L谷氨酸刺激RVLm神经元时，氯化钠引起的大鼠动脉压升高的作用增强。由于两组患者对静脉注射苯肾上腺素和去甲肾上腺素的反应相似，因此血管反应性的增强不能解释升压反应增强的原因。此外，电刺激脊髓下行交感神经兴奋性轴突在两组中产生相同的升压反应，表明RVLM远端中枢或外周神经效应器接头突触传递的改变不能解释直接刺激RVLM细胞体细胞所产生的增强的升压反应。最后，动脉压力感受器反射受损不能解释增强的RVLM升压反应，因为在摄入过量氯化钠的大鼠中，电刺激主动脉压力感受器传入所产生的降压和心动过缓反应并没有减少。
Excess dietary sodium is a major contributing factor to the incidence and severity of hypertension. However, the precise mechanism or mechanisms by which salt contributes to the severity of hypertension are unknown. The region of the rostral ventrolateral medulla (RVLM) is a principal brain stem locus critical for the regulation of arterial blood pressure by the sympathetic nervous system. The purpose of this study was to determine if excess dietary sodium chloride might alter the function or responsiveness of neurons in the RVLM. Male Sprague-Dawley rats were given either tap water or 0.9% sodium chloride solution to drink for 10 to 14 days. Excess sodium chloride did not affect baseline blood pressure. However, when neurons of the RVLM were stimulated by microinjections of L-glutamate, evoked increases in arterial pressure were potentiated in rats given sodium chloride. Augmented pressor responses could not be accounted for by increased vascular reactivity because both groups responded similarly to intravenously administered phenylephrine and norepinephrine. Additionally, electrical stimulation of descending spinal sympathoexcitatory axons produced identical pressor responses in both groups, indicating that altered synaptic transmission at central or peripheral neuroeffector junctions distal to the RVLM could not explain enhanced pressor responses produced by direct stimulation of RVLM cell somata. Finally, impaired arterial baroreceptor reflexes could not account for augmented RVLM pressor responses, as depressor and bradycardic responses produced by electrical stimulation of aortic baroreceptor afferents were not reduced in rats given excess dietary sodium chloride.(ABSTRACT TRUNCATED AT 250 WORDS)