Echizen H, Freed C R
Life Sci. 1984 Apr 16;34(16):1581-9. doi: 10.1016/0024-3205(84)90613-1.
The effect of drug-induced hypertension on neurotransmitter release from dorsal raphe nucleus was studied by in vivo electrochemical electrodes in urethane anesthetized male Sprague-Dawley rats. Carbon paste electrodes were stereotaxically placed into dorsal raphe nucleus and neurotransmitter release was estimated electrochemically. Blood pressure was recorded from a femoral arterial catheter. Voltammograms taken from dorsal raphe nucleus showed two distinct peaks corresponding to norepinephrine and 5-hydroxyindole acetic acid (5-HIAA). After basal blood pressure and neurotransmitter release were monitored for 30 min, blood pressure was raised 50 mmHg by continuous intravenous infusion of L-phenylephrine hydrochloride. Drug infusion was discontinued after 50 min, but blood pressure and neurotransmitter release were measured for an additional 2 hr. Results showed that the 5-HIAA response increased immediately after the initiation of hypertension and remained elevated. By contrast, norepinephrine release initially decreased, then returned to the basal level and then rose in parallel with 5-HIAA to a level above baseline as drug-induced hypertension was discontinued. The same experimental protocol was used to study the electrochemical response to drug-induced hypotension. Blood pressure was lowered 20 mmHg by intravenous infusion of sodium nitroprusside dihydrate. During hypotension, no changes were seen in either transmitter response. However, as reflex hypertension appeared following discontinuation of the sodium nitroprusside infusion, the 5-HIAA response increased and the norepinephrine response decreased. These results show that drug-induced and reflex hypertension reduce norepinephrine release and increase serotonin turnover in dorsal raphe nucleus in anesthetized normotensive rats. These reciprocal changes appear to be a part of the neural response to hypertension.
采用体内电化学电极，在氨基甲酸乙酯麻醉的雄性Sprague-Dawley大鼠中，研究了药物性高血压对中缝背核神经递质释放的影响。将碳糊电极立体定位至中缝背核，通过电化学方法估算神经递质释放量。通过股动脉导管记录血压。从中缝背核获取的伏安图显示出两个分别对应去甲肾上腺素和5-羟吲哚乙酸（5-HIAA）的明显峰。在监测基础血压和神经递质释放30分钟后，通过持续静脉输注盐酸去氧肾上腺素使血压升高50 mmHg。50分钟后停止药物输注，但额外再测量2小时的血压和神经递质释放量。结果显示，高血压开始后5-HIAA反应立即增加并持续升高。相比之下，去甲肾上腺素释放最初减少，然后恢复至基础水平，随后随着药物性高血压停止，与5-HIAA平行升高至基线以上水平。采用相同的实验方案研究对药物性低血压的电化学反应。通过静脉输注二水合硝普钠使血压降低20 mmHg。在低血压期间，两种递质反应均未出现变化。然而，在停止硝普钠输注后出现反射性高血压时，5-HIAA反应增加而去甲肾上腺素反应减少。这些结果表明，在麻醉的正常血压大鼠中，药物性高血压和反射性高血压均可减少中缝背核去甲肾上腺素释放并增加5-羟色胺周转。这些相反的变化似乎是对高血压神经反应的一部分。
