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动脉血压的变化导致大鼠孤束核中压力感受器介导的去甲肾上腺素和5-羟吲哚乙酸的变化。

Changes in arterial blood pressure lead to baroreceptor-mediated changes in norepinephrine and 5-hydroxyindoleacetic acid in rat nucleus tractus solitarius.

作者信息

Bhaskaran D, Freed C R

机构信息

Department of Medicine, University of Colorado Health Sciences Center, Denver.

出版信息

J Pharmacol Exp Ther. 1988 Apr;245(1):356-63.

PMID:2452247
Abstract

Catecholamine and indoleamine metabolism in nucleus tractus solitarius were studied during drug-induced hypertension and hypotension. Urethane-anesthetized normotensive male Sprague-Dawley rats implanted with a 250-mu carbon paste in vivo electrochemical electrode were infused with phenylephrine to raise blood pressure 50 mm Hg. Other animals were given nitroprusside to lower pressure 20 mm Hg. Phenylephrine-induced hypertension was associated with a 30% reduction in the electrochemical peak corresponding to norepinephrine. The electrochemical peak which was identified as 5-hydroxyindoleacetic acid (5-HIAA) was increased 25% with the onset of hypertension and remain elevated after the phenylephrine infusion was stopped. Nitroprusside-induced hypotension resulted in a 20% reduction in the norepinephrine peak during the infusion followed by an additional 10% reduction after the infusion. 5-HIAA concentration did not change during the hypotensive phase but showed a 40% increase after the nitroprusside was stopped as blood pressure rebounded to levels higher than the control period. Direct tissue assays of norepinephrine and 5-HIAA confirmed the electrochemical findings. These experiments were repeated in rats which had undergone sinoaortic denervation. The electrochemical changes in norepinephrine and 5-HIAA associated with hypertension and hypotension were attenuated in these animals indicating that the brain neurotransmitter changes were a consequence of baroreceptor input to the brain. We conclude that 5-HIAA in nucleus tractus solitarius appears to be a marker for elevated blood pressure, whereas norepinephrine falls with either an increase or a decrease in pressure.

摘要

在药物诱导的高血压和低血压过程中,对孤束核中的儿茶酚胺和吲哚胺代谢进行了研究。给植入了250微米碳糊剂体内电化学电极的氨基甲酸乙酯麻醉的正常血压雄性Sprague-Dawley大鼠输注去氧肾上腺素,使血压升高50毫米汞柱。给其他动物注射硝普钠以降低血压20毫米汞柱。去氧肾上腺素诱导的高血压与对应于去甲肾上腺素的电化学峰降低30%有关。被鉴定为5-羟吲哚乙酸(5-HIAA)的电化学峰在高血压发作时增加25%,并且在停止输注去氧肾上腺素后仍保持升高。硝普钠诱导的低血压导致输注期间去甲肾上腺素峰降低20%,输注后再降低10%。5-HIAA浓度在低血压阶段没有变化,但在硝普钠停止后随着血压反弹至高于对照期水平而增加40%。去甲肾上腺素和5-HIAA的直接组织测定证实了电化学研究结果。在接受了窦主动脉去神经支配的大鼠中重复了这些实验。在这些动物中,与高血压和低血压相关的去甲肾上腺素和5-HIAA的电化学变化减弱,表明大脑神经递质的变化是压力感受器向大脑输入的结果。我们得出结论,孤束核中的5-HIAA似乎是血压升高的标志物,而去甲肾上腺素在血压升高或降低时都会下降。

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1
Changes in arterial blood pressure lead to baroreceptor-mediated changes in norepinephrine and 5-hydroxyindoleacetic acid in rat nucleus tractus solitarius.动脉血压的变化导致大鼠孤束核中压力感受器介导的去甲肾上腺素和5-羟吲哚乙酸的变化。
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引用本文的文献

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Blood pressure changes modify the release rates of catecholamines in the intermediate nucleus of the solitary tract.血压变化会改变孤束核中间神经元中儿茶酚胺的释放速率。
Naunyn Schmiedebergs Arch Pharmacol. 1992 Feb;345(2):176-80. doi: 10.1007/BF00165733.