Pérgola P E, Alper R H
Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City 66103.
Am J Physiol. 1991 Jun;260(6 Pt 2):R1188-93. doi: 10.1152/ajpregu.1991.260.6.R1188.
Intracerebroventricular administration of serotonin (5-HT) to conscious rats increases mean arterial pressure (MAP) and decreases heart rate. To determine the mechanisms involved, 5-HT (2.5 micrograms) was injected intracerebroventricularly into conscious rats pretreated with various neurotransmitter and hormone antagonists. The selective 5-HT2 antagonist LY 53857 abolished the increase in MAP and the bradycardia elicited by 5-HT. The increase in MAP produced by 5-HT was potentiated by chlorisondamine (a ganglionic antagonist), unaffected by prazosin (an alpha 1-antagonist) or a vasopressin V1 antagonist alone, but eliminated by the combined pretreatment with prazosin plus the vasopressin antagonist. In contrast, the bradycardia was eliminated by either the vasopressin V1 antagonist or chlorisondamine. In conclusion, 5-HT injected into the lateral cerebral ventricle of conscious rats induces sympathoexcitation and the release of vasopressin, which results in an increase in MAP; 5-HT also elicits a bradycardia mediated through an interaction of the autonomic nervous system with circulating vasopressin.
向清醒大鼠脑室内注射血清素（5-羟色胺，5-HT）可使平均动脉压（MAP）升高并使心率降低。为确定其中涉及的机制，将5-HT（2.5微克）脑室内注射到用各种神经递质和激素拮抗剂预处理过的清醒大鼠体内。选择性5-HT2拮抗剂LY 53857消除了5-HT引起的MAP升高和心动过缓。5-HT引起的MAP升高被氯异吲哚铵（一种神经节拮抗剂）增强，单独使用哌唑嗪（一种α1拮抗剂）或血管加压素V1拮抗剂时不受影响，但哌唑嗪与血管加压素拮抗剂联合预处理可消除这种升高。相反，心动过缓可被血管加压素V1拮抗剂或氯异吲哚铵消除。总之，向清醒大鼠侧脑室注射5-HT会引起交感神经兴奋和血管加压素释放，从而导致MAP升高；5-HT还会引发一种通过自主神经系统与循环血管加压素相互作用介导的心动过缓。
