Bhaskaran D, Freed C R
Department of Medicine, University of Colorado Health Sciences Center, Denver.
J Pharmacol Exp Ther. 1988 Apr;245(1):356-63.
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.
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。