Inoue A, Buñag R D
Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
J Cardiovasc Pharmacol. 1989 Jun;13(6):902-7. doi: 10.1097/00005344-198906000-00013.
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 bradycardic 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 bradycardic) 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.
为了研究中枢给予血清素产生心血管效应的潜在机制，我们记录了在乌拉坦麻醉的大鼠中，对脑室内（i.c.v.）注射血清素的反应。持续引发了与剂量相关的血压升高，同时伴有心率降低和交感神经放电减少。交感神经活动的减弱意味着，虽然交感神经抑制可能导致心动过缓，但仅交感神经激活不能解释升压反应。升压和心动过缓反应一定是由脑中特定血清素能受体的激活引起的，因为在i.c.v.注射麦角新碱产生血清素阻断后，这两种反应均受到抑制。相比之下，静脉注射血管加压素拮抗剂选择性地抑制了升压反应，从而表明升压反应（而非心动过缓反应）的外周介导涉及内源性血管加压素的释放。总体而言，我们的结果符合以下解释：i.c.v.注射的血清素作用于脑内的血清素能受体，通过释放内源性血管加压素升高血压，并通过交感神经抑制使心率减慢。
