Presynaptic muscarinic facilitation of parasympathetic neurotransmission after sympathectomy in the rat choroid

作     者：Steinle, JJ Smith, PG 

作者机构：Univ Kansas Med Ctr Dept Mol & Intergrat Physiol Kansas City KS 66160 USA Univ Kansas Med Ctr RL Smith Mental Retardat Res Ctr Kansas City KS 66160 USA 

出 版 物：《JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS》 (药理学与实验治疗学杂志)

年 卷 期：2000年第294卷第2期

页      面：627-632页

核心收录：

学科分类：1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 100706[医学-药理学] 100602[医学-中西医结合临床] 10[医学] 

基　　金：NICHD NIH HHS [HD02528  HD33025] Funding Source: Medline 

主　　题：氯贝胆碱/药理学 脉络膜/血液供给 脉络膜/药物作用 脉络膜/神经支配 电刺激 酶抑制剂/药理学 神经节切除术 咪唑类/药理学 毒蕈碱激动剂/药理学 毒蕈碱拮抗剂/药理学 一氧化氮/生理学 一氧化氮合酶/拮抗剂和抑制剂 一氧化氮合酶Ⅰ型 副交感神经系统/药物作用 副交感神经系统/生理学 哌啶类/药理学 大鼠 Sprague-Dawley 受体 毒蕈碱/分类 受体 毒蕈碱/生理学 受体 突触前/生理学 局部血流/药物作用 局部血流/生理学 涎腺/神经支配 颈上神经节/生理学 颈上神经节/外科学 突触传递/药物作用 突触传递/生理学 时间因素 动物 女(雌)性 大鼠 

摘      要：The effect of sympathectomy on parasympathetic regulation of ocular perfusion was investigated. Uveal blood flow through the vortex veins was measured by laser Doppler flowmetry during electrical stimulation of the superior salivatory nucleus, which activates ocular parasympathetic nerves, in adult rats with intact innervation and 2 days or 6 weeks after excision of the ipsilateral superior cervical ganglion. In all groups, parasympathetic stimulation produced comparable increases in flux, which were abolished by the selective neuronal nitric-oxide synthetase inhibitor, 1-(2-trifluoromethylphenyl) imidazole. Atropine had no effect in control and acutely sympathectomized rats but abolished the flux increase in four of six chronically sympathectomized animals, and 1-(2-trifluoromethylphenyl) imidazole eliminated the residual response. The muscarinic receptor agonist bethanechol did not affect basal flow in control or sympathectomized rats. However, bethanechol enhanced parasympathetically mediated vasodilation, but only in rats studied at 6 weeks after sympathectomy, a finding consistent with the appearance of muscarinic prejunctional facilitation of nitrergic transmission. In chronically sympathectomized rats, the M-2 and M-4 receptor antagonists methoctramine and tropicamide did not affect choroidal flow during parasympathetic activation. However, pirenzepine increased flux, implying the presence of M-1 inhibitory autoreceptors on these nerves. Parasympathetically mediated increased flux was partially blocked by the M-3 antagonist 4-diphenylacetoxy-N-methylpiperdine, and the remaining vasodilation was blocked by atropine. We conclude that parasympathetic prejunctional facilitatory M-3 and probably M-5 receptors adopt a crucial role after chronic sympathectomy in maintaining nitrergic vasodilatory ocular neurotransmission in the face of down-regulated nitric oxide transmitter mechanisms.