Is visceral sympathoexcitation to heat stress dependent on activation of ionotropic excitatory amino acid receptors in the rostral ventrolateral medulla?
Is visceral sympathoexcitation to heat stress dependent on activation of ionotropic excitatory amino acid receptors in the rostral ventrolateral medulla?
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DOI：
10.1152/ajpregu.00113.2011
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发表时间：
2011-08-01
影响因子：
2.8
通讯作者：
Fels, R. J.
中科院分区：
文献类型：
--
作者：
Kenney, M. J.;Meyer, C. N.;Fels, R. J.
肯尼MJ，迈耶CN，霍斯金KG，费尔斯RJ.热应激引起的内脏交感兴奋是否依赖于延髓头端腹外侧区离子型兴奋性氨基酸受体的激活？Am J Physiol Regul Integr Comp Physiol 301：R548-R557，2011年。首次发表于2011年6月1日; doi：10.1152/ajpregu.00113.2011。急性热应激激活内脏交感神经放电（SND）在年轻的大鼠，和头端腹外侧延髓（RVLM）的功能完整性是需要维持内脏交感兴奋在内部体温（TC）的峰值增加。然而，RVLM介导SND激活到高热的机制仍然未知。在本研究中，我们调查的作用RVLM离子型兴奋性氨基酸受体介导内脏SND激活热应激在麻醉，年轻大鼠。双侧RVLM犬尿烯酸的作用在最高体温（Tc 41.5 ℃）、进行性体温升高（Tc 40 ℃）和开始加热（Tc从38 ℃增加到38.5 ℃）时测定了微量注射Kyn（2.7和5.4 nmol）、生理盐水或蝇蕈醇（400-800 pmol）对肾SND和脾SND对热应激的反应。RVLM Kyn微量注射没有减少肾和脾SND记录在渐进或高峰高热，并没有减弱SND激活开始加热。事实上，肾和脾的SND往往是或显着增加RVLM Kyn显微注射后，在开始加热和高温（40和41.5摄氏度）。在39、40和41.5摄氏度的RVLM蝇蕈醇微量注射导致SND立即减少。这些数据表明，RVLM离子型谷氨酸受体需要介导内脏交感神经兴奋急性加热，并表明急性加热激活RVLM离子型兴奋性氨基酸受体依赖性抑制输入，这降低了内脏SND加热的水平。
Kenney MJ, Meyer CN, Hosking KG, Fels RJ. Is visceral sympathoexcitation to heat stress dependent on activation of ionotropic excitatory amino acid receptors in the rostral ventrolateral medulla? Am J Physiol Regul Integr Comp Physiol 301: R548-R557, 2011. First published June 1, 2011; doi:10.1152/ajpregu.00113.2011.-Acute heat stress activates visceral sympathetic nerve discharge (SND) in young rats, and the functional integrity of the rostral ventrolateral medulla (RVLM) is required for sustaining visceral sympathoexcitation during peak increases in internal body temperature (T-c). However, RVLM mechanisms mediating SND activation to hyperthermia remain unknown. In the present study, we investigated the role of RVLM ionotropic excitatory amino acid receptors in mediating visceral SND activation to heat stress in anesthetized, young rats. The effects of bilateral RVLM kynurenic acid (Kyn; 2.7 and 5.4 nmol), saline, or muscimol (400-800 pmol) microinjections on renal SND and splenic SND responses to heat stress were determined at peak hyperthermia (T-c 41.5 degrees C), during progressive hyperthermia (T-c 40 degrees C), and at the initiation of heating (Tc increased from 38 to 38.5 degrees C). RVLM Kyn microinjections did not reduce renal and splenic SND recorded during progressive or peak hyperthermia and did not attenuate SND activation at the initiation of heating. In fact, renal and splenic SND tended to be or were significantly increased following RVLM Kyn microinjections at the initiation of heating and during hyperthermia (40 and 41.5 degrees C). RVLM muscimol microinjections at 39, 40, and 41.5 degrees C resulted in immediate reductions in SND. These data indicate that RVLM ionotropic glutamate receptors are required for mediating visceral sympathoexcitation to acute heating and suggest that acute heating activates an RVLM ionotropic excitatory amino acid receptor dependent inhibitory input, which reduces the level of visceral SND to heating.