SYMPATHETIC INHIBITION AND VASOPRESSIN MEDIATION DURING CENTRALLY INDUCED RESPONSES TO SEROTONIN IN RATS
SYMPATHETIC INHIBITION AND VASOPRESSIN MEDIATION DURING CENTRALLY INDUCED RESPONSES TO SEROTONIN IN RATS
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DOI：
10.1097/00005344-198906000-00013
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发表时间：
1989-06-01
影响因子：
3
通讯作者：
BUNAG, RD
中科院分区：
文献类型：
--
作者：
INOUE, A;BUNAG, RD
为了研究中枢应用5-羟色胺的心血管效应的机制，我们记录了脑室内注射5-羟色胺的反应。乌拉坦麻醉大鼠注射5-羟色胺。与剂量相关的血压升高伴随着心率和交感神经放电的降低是一致的。交感神经活动的减少表明，虽然交感神经抑制可能导致心动过缓，但交感神经激活本身并不能解释升压反应。升压和心动过缓反应一定是由大脑中特定的5-羟色胺能受体激活引起的，因为这两种反应在静脉注射5-羟色胺阻断后都被抑制了。注射用甲基舍吉。相比之下，静脉注射加压素拮抗剂选择性地抑制加压反应，从而表明外周调节加压反应(而不是心脏减慢)涉及内源性加压素的释放。总体而言，我们的结果与静脉注射5-羟色胺作用于5-羟色胺能脑受体，通过释放内源性加压素来升高血压，并通过交感神经抑制使心脏减慢的解释是一致的。
To study mechanisms underlying the cardiovascular effects of centrally administered serotonin, we recorded responses to intracerebroventricular (i.c.v.) injections of serotonin in urethane-anesthetized rats. Dose-related increases in blood pressure accompanied by reductions in heart rate and sympathetic nerve firing were elicited consistently. The diminution in sympathetic nerve activity implies that while sympathetic inhibition could contribute to the bradycardia, sympathetic activation alone cannot account for the pressor response. Pressor and bradycardiac responses must have been caused by activation of specific serotonergic receptors in the brain because both responses were inhibited following serotonin blockade produced by i.c.v. injection of methysergide. By contrast, intravenous injection of a vasopressin antagonist inhibited the pressor response selectively, thereby suggesting that peripheral mediation of the pressor (but not the bradycardiac) response involves release of endogenous vasopressin. Collectively, our results are compatible with the interpretation that i.c.v.-injected serotonin acts on serotonergic brain receptors to elevate blood pressure by releasing endogenous vasopressin, and slow the heart through sympathetic inhibition.