...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Dorsal hippocampus cholinergic and nitrergic neurotransmission modulates the cardiac baroreflex function in rats
【24h】

Dorsal hippocampus cholinergic and nitrergic neurotransmission modulates the cardiac baroreflex function in rats

机译：背部海马胆碱能和Nitrergic神经递质调节大鼠心脏肾病功能

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Hippocampus is a limbic structure involved in the baroreflex and chemoreflex control that receives extensive cholinergic input from basal forebrain. Hippocampal muscarinic receptors activation by acetylcholine might evoke nitric oxide synthesis, which is an important neuromodulator of cardiovascular responses. Thus, we hypothesize that cholinergic and nitrergic neurotransmission within the DH modulates the baroreflex and chemoreflex function. We have used vasoactive drugs (phenylephrine and sodium nitroprusside), and potassium cyanide infused peripherally to induce, respectively, baroreflex or chemoreflex responses in awake animals. Bilateral injection into the DH of the acetylcholinesterase inhibitor (neostigmine) reduced baroreflex responses. Meanwhile, the non-selective muscarinic receptor antagonist (atropine) or the M1-selective muscarinic receptor antagonist increased baroreflex responses (pirenzepine). Furthermore, the neuronal nitric oxide synthase inhibitor (N-propyl) or the intracellular NO scavenger (carboxy-PTIO) increased baroreflex responses, as well as the selective inhibitor of NO-sensitive guanylyl cyclase (ODQ), increased the baroreflex responses. Besides, bilateral administration of an ineffective dose of a neuronal nitric oxide synthase inhibitor abolished the reduction in the baroreflex responses evoked by an acetylcholinesterase inhibitor. On the other hand, we have demonstrated that hippocampal cholinergic neurotransmission did not influence the chemoreflex function. Taken together, our findings suggest that nNOS-derived nitric oxide in the DH participates in acetylcholine-evoked baroreflex responses.
机译：海马是肢体结构，涉及Baroreflex和Chemoreflex控制，从基础前脑中获得广泛的胆碱能输入。通过乙酰胆碱激活的海马毒蕈碱受体可能引起一氧化氮合成，这是心血管反应的重要神经调节剂。因此，我们假设DH内的胆碱能和Nitrergic神经递质调节Baroreflex和ChemoreFlex功能。我们使用了血管活性药物（苯妥啶和硝酸钠），以及外周注入的氰化钾，分别诱导，沼泽射精或化学射精在唤醒动物中的反应。双侧注射到乙酰胆碱酯酶抑制剂的DH（Neostigmine）降低了骨折反应。同时，非选择性毒蕈碱受体拮抗剂（阿托品）或M1选择性毒蕈碱受体拮抗剂增加了Baroreflex反应（Pirenzepine）。此外，神经元一氧化氮合酶抑制剂（N-丙基）或细胞内没有清除剂（羧基-PTIO）增加了Baroreflex反应，以及无敏感的瓜梵烯环化酶（ODQ）的选择性抑制剂，增加了骨折反应。此外，两侧施用无效剂量的神经元一氧化氮合酶抑制剂废除了乙酰胆碱酯酶抑制剂引起的骨折反应的还原。另一方面，我们已经证明海马胆碱能神经递质不会影响化学倒产功能。我们的研究结果表明DH中的NNOS衍生的一氧化氮参与乙酰胆碱诱发的肾射反应。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号