CATECHOLAMINES AND SEROTONIN IN BLOOD PRESSURE CONTROL

脑儿茶酚胺和5-羟色胺已被证明参与了 中枢神经系统对血压的调节。特别是， 下丘脑和脑干核团中含有高浓度的这些物质 神经递质形成血压调节神经元的轴。 临床上重要的抗高血压药物，如α-甲基多巴和 可乐定通过抑制中枢神经系统减少交感神经流出 儿茶酚胺神经元。而去甲肾上腺素能神经元 与中枢作用降压作用机制有关 药物、5-羟色胺能神经元也在血压调节中发挥作用。 我们已经证明，长期输注5-羟色胺前体 5-羟色氨酸增加脑内5-羟色胺的周转和减少血液 正常血压大鼠的血压。我们现在已经适应了体内电化学 研究去甲肾上腺素和5-羟色胺的技术 清醒大鼠脑内特定核团持续释放。 初步实验表明，静脉注射苯肾上腺素 血压升高会导致体内5-羟色胺释放增加 中缝背核。去甲肾上腺素释放最初下降，但随后 随后又增加了。这些结果与假设相符。 大脑通过减少交感神经流出来补偿高血压 通过增加中枢5-羟色胺能张力和降低去甲肾上腺素能 语气。我们计划使用体内电化学来研究去甲肾上腺素能和 5-羟色胺能神经元对急、慢性高血压的反应 低血压。从正常血压和高血压品系唤醒的大鼠 将会被研究。输注的药物会导致高血压 血管加压剂，如苯肾上腺素和低血压，将被诱导 血管扩张剂，如呋喃西林和β受体阻滞剂，如心得安。在……里面 此外，可乐定等中枢降压药将 已评估。拟研究的区域包括下丘脑、蓝斑、 孤束核和中缝背核。这些实验 有助于阐明去甲肾上腺素和5-羟色胺在 血压调节，并指出每一项的相对重要性 单个血管调节核团中的神经递质。

Brain catecholamines and serotonin have been shown to be involved in central nervous system regulation of blood pressure. In particular, hypothalamic and brainstem nuclei containing high concentrations of these neurotransmitters form an axis of blood pressure regulatory neurons. Clinically important antihypertensive agents such as alphamethyldopa and clonidine reduce sympathetic outflow from the brain by inhibiting central catecholamine neurons. While noradrenergic neurons have been most implicated in the mechanism of action of central acting antihypertensive drugs, serotonergic neurons also play a role in blood pressure regulation. We have shown that chronic infusions of the serotonin precursor 5-hydroxytryptophan increase brain serotonin turnover and reduce blood pressure in normotensive rats. We have now adapted in vivo electrochemical techniques to make it possible to study nonrepinephrine and serotonin release continuously from specific nuclei in brain of awake rats. Preliminary experiments have shown that intravenous phenylephrine infusions which increase blood pressure cause an increase in Serotonin release in dorsal raphe nucleus. Norepinephrine release initially falls but then subsequently increases. These results are compatible with the hypothesis that the brain compensates for hypertension by reducing sympathetic outflow through increased central serotonergic tone and reduced noradrenergic tone. We plan to use in vivo electrochemistry to study noradrenergic and serotonergic neuronal responses to acute and chronic hypertension and hypotension. Awake rats from both normotensive and hypertensive strains will be studied. Hypertension will be produced with infusions of vasopressors such as phenylephrine and hypotension will be induced by vasodilators such as hydralazine and beta blockers such as propranolol. In addition, central acting antihypertensive drugs such as clonidine will be evaluated. Regions to be studied include hypothalamus, locus coeruleus, nucleus tractus solitarius and dorsal raphe nucleus. These experiments should help clarify the interactive role of norepinephrine and serotonin in blood pressure regulation and indicate the relative importance of each neurotransmitter in individual vasoregulatory nuclei.