Dedeoğlu A, Fisher L A
Department of Physiology, Ohio State University College of Medicine, Columbus 43210
Am J Physiol. 1996 Sep;271(3 Pt 2):R569-78. doi: 10.1152/ajpregu.1996.271.3.R569.
The present studies investigated the mechanisms mediating the cardiovascular changes induced by intracerebroventricular injection of serotonin (5-HT; 100 nmol) in conscious rats. At 5 min after 5-HT injection, arterial pressure and plasma levels of epinephrine were elevated and heart rate was reduced. The pressor response was abolished either by bilateral adrenalectomy or by pretreatment with chlorisondamine plus vasopressin V1 receptor antagonist. The bradycardic response was attenuated by pretreatment with chlorisondamine or a combination of methylatropine, propranolol, and vasopressin V1 receptor antagonist. At 20 min postinjection, arterial pressure and heart rate were both decreased. The reduction of heart rate at this time point was not blocked by the following pretreatments given alone or in combination: methylatropine, propranolol, vasopressin V1 and V2 receptor antagonists, adenosine A1 receptor antagonist, angiotensin-converting enzyme inhibitor, and chlorisondamine. These results suggest that immediately after intracerebroventricular injection of 5-HT, arterial pressure is elevated through the release of epinephrine and vasopressin and that heart rate is reduced via reciprocal changes in cardiac parasympathetic and sympathetic tone. In contrast, adrenergic, cholinergic, vasopressinergic, purinergic, and angiotensinergic mechanisms do not mediate the bradycardia observed at 20 min postinjection.
本研究探讨了在清醒大鼠中，脑室内注射5-羟色胺（5-HT；100 nmol）引起心血管变化的介导机制。注射5-HT后5分钟，动脉压和肾上腺素血浆水平升高，心率降低。双侧肾上腺切除术或用氯异吲哚胺加血管加压素V1受体拮抗剂预处理可消除升压反应。用氯异吲哚胺或甲基阿托品、普萘洛尔和血管加压素V1受体拮抗剂联合预处理可减弱心动过缓反应。注射后20分钟，动脉压和心率均降低。此时单独或联合给予以下预处理均不能阻断心率的降低：甲基阿托品、普萘洛尔、血管加压素V1和V2受体拮抗剂、腺苷A1受体拮抗剂、血管紧张素转换酶抑制剂和氯异吲哚胺。这些结果表明，脑室内注射5-HT后立即通过肾上腺素和血管加压素的释放使动脉压升高，心率通过心脏副交感神经和交感神经张力的相互变化而降低。相反，肾上腺素能、胆碱能、血管加压素能、嘌呤能和血管紧张素能机制并不介导注射后20分钟观察到的心动过缓。
