salusin α在孤束核内的心血管效应可能通过抑制头端延髓腹外侧区前交感神经元活动介导  

Cardiovascular inhibition of salusin α within the nucleus tractus solitarii originated from suppressing the activities of presympathetic neurons in the rostral ventrolateral medulla

作　　者：李宏宝[1] 郭雅琼[1] 鲁彦[2] 伏晓琳[3] 刘颖璐[4] 郑天珍[1] 

机构地区：[1]兰州大学基础医学院生理学教研室 [2]甘肃省兰州市解放军第一医院检验科 [3]兰州大学第一医院急诊科,甘肃兰州730000 [4]山东大学医学院,济南250100

出　　处：《中国药理学通报》2011年第12期1672-1677,共6页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 30700266);陕西省卫生厅资助项目(No 06E05);兰州大学中央高校基本科研业务费专项资金(No lzujbky-2010-146)

摘　　要：目的探讨孤束核内salusinα的心血管效应及其机制。方法♂SD大鼠94只,其中50只大鼠单侧NTS或双侧NTS注射不同剂量salusinα(0.04～4 pmol)或人工脑脊液(artificial cerebrospinal fluid,aCSF),观察NTS内salusinα对大鼠血压和心率产生的影响。33只大鼠分别预先在NTS给予aCSF、非选择性谷氨酸受体拮抗剂犬尿希酸(KYN)、双侧颈部迷走神经切断(bilateral vagotomy)或在头端延髓腹外侧区(RVLM)给予aCSF/GABA受体激动剂muscimol,探讨NTS内salusinα的心血管效应机制。11只大鼠检测NTS水平salusinα对大鼠动脉压力反射(arterial baroreflex,ABR)功能的影响。结果在NTS双侧或单侧微量注射salusinα产生剂量依赖性的降低血压、减缓心率的作用。双侧微量注射salusinα不影响麻醉大鼠的ABR。NTS预先注射KYN(1nmol)或双侧迷走神经切除均不影响孤束核注salusinα产生的降低血压、减缓心率的效应(P>0.05)。RVLM预先注射muscimol(5 pmol)能有效阻断salusinα(4 pmol)在孤束核产生的降低血压、减缓心率的效应(P<0.05)。结论 NTS注射salusinα产生的降低血压、减缓心率的效应可能通过激动RVLM内GABA受体,抑制前交感神经元兴奋性发挥作用。Aim Salusin α and salusin β are newly identified bioactive peptides of 28 and 20 amino acid,respectively,which are reported to widely distribute in hematopoietic system,endocrine system and the central nervous system（CNS）.They are responsible for causing hypotension,bradycardia and mitogenic activities.The cardiovascular functions of salusin α in the nucleus tractus solitarii（NTS） are not fully defined.The present study is to comparatively determine the cardiovascular functions of salusin α into the NTS in anesthetized rats.Methods Ninety-four anesthetic male SD rats were employed in present study.The dose-dependant responses of blood pressure and heart rate of salusin α（0.04~4 pmol） in the NTS were determined by bilateral or unilateral microinjection salusin α or artificial cerebrospinal fluid（aCSF） into the NTS in 50 rats.In 33 rats,aCSF,KYN,bilateral vagotomy or aCSF/ muscimol in RVLM were prior applied before salusin α（4 pmol） was microinjected.The arterial baroreflex（ABR） functions of rats of pre-post injection of salusin α into the NTS were defined in 11 rats.Results Bilateral or unilateral microinjection of salusin α into the NTS produced dose-dependent hypotension and bradycardia.Bilateral microinjection of salusin α did not alter baroreflex sensitivity functions.Prior application of KYN（1 nmol）or bilateral vagotomy into the NTS did not alter the hypotension and bradycardia induced by intra-NTS salusin α（P0.05）.But pretreatment with muscimol（5 pmol）within the RVLM almost completely abolished the hypotension and bradycardia evoked by intra-NTS salusin α（P0.05）.Conclusion Microinjection of salusin α into the NTS produces significant hypotension and bradycardia,which probably originates from suppressing the activities of presympathetic neurons in the RVLM.

关 键 词：SALUSIN 大鼠 延髓 孤束核 头端延髓腹外侧区 动 脉压力反射 前交感神经元 

分 类 号：R-332[医药卫生] R322.81