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通过向大鼠延髓尾端腹外侧微注射L-谷氨酸所引发的升压反应。

Pressor responses evoked by microinjections of L-glutamate into the caudal ventrolateral medulla of the rat.

作者信息

Gordon F J, McCann L A

机构信息

Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322.

出版信息

Brain Res. 1988 Aug 9;457(2):251-8. doi: 10.1016/0006-8993(88)90693-2.

DOI:10.1016/0006-8993(88)90693-2
PMID:2905917
Abstract

The caudal medulla of the rat was mapped for cardiovascular sensitive regions by recording changes in mean arterial pressure (MAP) and heart rate evoked by microinjections of L-glutamate (1 nmol/50 nl). Using this technique to selectively activate cell soma in the brainstem, a new pressor area in the caudal ventrolateral medulla has been identified. Several sites located approximately 1-1.5 mm posterior to the caudal medullary depressor zone were found where L-glutamate evoked pressor responses of 10-45 mm Hg. The most responsive area was located just dorsal to the lateral aspect of the lateral reticular nucleus at the level of the pyramidal decussation and the caudalmost pole of the inferior olives. Pressor responses at this site averaged 37 +/- 2 mm Hg. Changes in heart rate were inconsistent and both tachycardia and bradycardia were observed. Increases in arterial pressure elicited from the caudal pressor area (CPA) were abolished by ganglionic blockade. Pressor responses evoked from the CPA were also eliminated after functional inactivation of vasopressor neurons in the rostral ventrolateral medulla (RVM) was produced by microinjections of muscimol. Inhibition of CPA neurons by microinjections of GABA had no effect on MAP while GABA markedly reduced MAP when injected into the RVM. These studies demonstrate that a circumscribed region of the caudal ventrolateral medulla contains a population of 'vasopressor' neurons distinct from those located in the rostral medulla. No evidence was obtained to suggest that neural activity in the CPA contributes to the maintenance of arterial pressure. The precise functional role of the CPA in central cardiovascular regulation remains to be determined.

摘要

通过记录微量注射L-谷氨酸(1纳摩尔/50纳升)诱发的平均动脉压(MAP)和心率变化,对大鼠延髓尾部进行心血管敏感区域定位。利用该技术选择性激活脑干中的细胞体,已在延髓尾端腹外侧确定了一个新的升压区。在延髓尾端降压区后方约1-1.5毫米处发现了几个位点,L-谷氨酸在这些位点诱发了10-45毫米汞柱的升压反应。反应最强烈的区域位于锥体交叉和下橄榄最尾端水平的外侧网状核外侧的背侧。该位点的升压反应平均为37±2毫米汞柱。心率变化不一致,观察到心动过速和心动过缓。来自尾端升压区(CPA)的动脉压升高被神经节阻断所消除。在通过微量注射蝇蕈醇使延髓头端腹外侧(RVM)的血管升压神经元功能失活后,CPA诱发的升压反应也被消除。微量注射GABA对CPA神经元的抑制对MAP无影响,而当注射到RVM中时,GABA可显著降低MAP。这些研究表明,延髓尾端腹外侧的一个特定区域含有一群与延髓头端不同的“血管升压”神经元。未获得证据表明CPA中的神经活动有助于维持动脉压。CPA在中枢心血管调节中的精确功能作用仍有待确定。

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Pressor responses evoked by microinjections of L-glutamate into the caudal ventrolateral medulla of the rat.通过向大鼠延髓尾端腹外侧微注射L-谷氨酸所引发的升压反应。
Brain Res. 1988 Aug 9;457(2):251-8. doi: 10.1016/0006-8993(88)90693-2.
2
Vasopressor and depressor areas in the rat medulla. Identification by microinjection of L-glutamate.大鼠延髓中的升压和降压区域。通过微量注射L-谷氨酸进行鉴定。
Neuropharmacology. 1983 Sep;22(9):1071-9. doi: 10.1016/0028-3908(83)90027-8.
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The caudal pressor area of the rat: its precise location and projections to the ventrolateral medulla.大鼠的尾侧加压区:其精确位置及向延髓腹外侧区的投射。
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A fall in arterial blood pressure produced by inhibition of the caudalmost ventrolateral medulla: the caudal pressor area.通过抑制延髓尾端腹外侧部产生的动脉血压下降:尾端加压区。
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Cardiovascular effects of L-glutamate and gamma-aminobutyric acid injected into the rostral ventrolateral medulla in normotensive and spontaneously hypertensive rats.
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Putative pathways involved in cardiovascular responses evoked from the caudal pressor area.参与尾侧升压区诱发的心血管反应的潜在途径。
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Caudal ventrolateral medulla. A region responsible for the mediation of vasopressin-induced pressor responses.延髓尾端腹外侧。一个负责介导血管加压素诱导的升压反应的区域。
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Spinal NMDA receptors mediate pressor responses evoked from the rostral ventrolateral medulla.
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Blockade of excitatory amino acid receptors in the ventrolateral medulla does not abolish the cardiovascular actions of L-glutamate.阻断延髓腹外侧区的兴奋性氨基酸受体并不能消除L-谷氨酸的心血管作用。
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AT(1) receptors mediate excitatory inputs to rostral ventrolateral medulla pressor neurons from hypothalamus.血管紧张素Ⅱ1型受体介导来自下丘脑的对延髓头端腹外侧加压神经元的兴奋性输入。
Hypertension. 1999 Dec;34(6):1301-7. doi: 10.1161/01.hyp.34.6.1301.

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