Bhaskaran D, Freed C R
Department of Medicine, University of Colorado Health Sciences Center, Denver.
J Pharmacol Exp Ther. 1989 May;249(2):660-6.
Catechol and indole metabolism in rostral ventrolateral medulla (RVLM or C1) was studied in response to changes in blood pressure across different rat strains. Sprague-Dawley, Wistar Kyoto normotensive and spontaneously hypertensive rats were anesthetized with urethane and had a 250 mu carbon paste in vivo electrochemical electrode implanted in RVLM area. Two electrochemical peaks were detected in this region. The first was at 0.12 V and the second at 0.28 V. To identify the electrochemical peaks, inhibitors of monoamine metabolism were administrated. alpha-Methylparatyrosine (tyrosine hydroxylase inhibitor), fusaric acid (dopamine-beta-hydroxylase inhibitor), pargyline (monoamine oxidase inhibitor) and LY 134046 (phenylethanolamine-N-methyltransferase inhibitor) showed that the first peak measured in the RVLM is likely to have multiple components including epinephrine, norepinephrine and 3,4-dihydroxyphenylacetic acid. The second peak most likely represents 5-hydroxyindole acetic acid. Phenylephrine or nitroprusside was infused to increase or decrease the blood pressure. Phenylephrine-induced hypertension reduced the catechol peak and increased the indole peak. By contrast, nitroprusside-induced hypotension produced reciprocal results. Hypotension led to an increase in the catechol peak and a reduction in the indole peak. The same pattern was observed in all three rat strains. We conclude that catechol and serotonin metabolism in RVLM changes in close relation to changes in blood pressure.
研究了延髓头端腹外侧区(RVLM或C1区)的儿茶酚和吲哚代谢对不同大鼠品系血压变化的反应。将Sprague-Dawley大鼠、Wistar Kyoto正常血压大鼠和自发性高血压大鼠用乌拉坦麻醉,并在RVLM区域植入一个250微米的碳糊体内电化学电极。在该区域检测到两个电化学峰。第一个峰在0.12 V,第二个峰在0.28 V。为了鉴定这些电化学峰,给予了单胺代谢抑制剂。α-甲基对酪氨酸(酪氨酸羟化酶抑制剂)、富马酸(多巴胺-β-羟化酶抑制剂)、帕吉林(单胺氧化酶抑制剂)和LY 134046(苯乙醇胺-N-甲基转移酶抑制剂)表明,在RVLM中测得的第一个峰可能有多个成分,包括肾上腺素、去甲肾上腺素和3,4-二羟基苯乙酸。第二个峰很可能代表5-羟吲哚乙酸。输注去氧肾上腺素或硝普钠以升高或降低血压。去氧肾上腺素诱导的高血压降低了儿茶酚峰并增加了吲哚峰。相比之下,硝普钠诱导的低血压产生了相反的结果。低血压导致儿茶酚峰增加和吲哚峰降低。在所有三种大鼠品系中都观察到了相同的模式。我们得出结论,RVLM中的儿茶酚和5-羟色胺代谢与血压变化密切相关。