中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/21076
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 29490/55136 (53%)
Visitors : 1511951      Online Users : 414
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    CMUR > College of Medicine > School of Medicine > Proceedings >  Item 310903500/21076
    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/21076


    Title: NITRIC OXIDE AND GLUTAMATE IN THE DORSAL FACIAL AREA REGULATE THE COMMON CAROTID BLOOD FLOW OF CATS
    Authors: 龔志力;(Hsing-Tan Li);(Jon-Son Kuo)*
    Contributors: 醫學院醫學系學士班生理學科
    Date: 2007-03-17
    Issue Date: 2009-09-07 10:42:46 (UTC+8)
    Abstract: L-arginine (an NO precursor) or glutamate stimulation of the dorsal facial area (DFA) in the medulla increases ipsilateral common carotid arterial (CCA) blood flow. Nitrergic and glutamatergic fibers as well as nitrergic neurons are demonstrated in the DFA. Whether nitrergic and glutamatergic interactions in the DFA might regulate CCA blood flow was un-known. In microdialysis-HPLC study, perfusion in the DFA of S-nitroso-N-acetylpenicillamine (SNAP), an NO donor, increased glutamate concentration in the DFA; Co-perfusion of methylene blue (guanylate cyclase inhibitor) with SNAP abolished SNAP-induced glutamate increase. Intra-DFA microinjection of L-arginine or L-glutamate dose-dependently increased CCA blood flow. The L-arginine-induced increase in CCA blood flow was dose-dependently blocked by pretreatment of NG-nitro-arginine methyl ester (L-NAME, a non-specific NO synthase inhibitor), 7-nitroindazole (7-NI, a relatively selective neuronal NO synthase inhibitor), D-2-amino-5-phosphonopentanoate (D-AP5, a competitive NMDA receptor antagonist), and glutamate diethylester (GDEE, a competitive AMPA receptor antagonist). The L-glutamate-induced increase in CCA blood flow was dose-dependently attenuated by pretreatment of L-NAME, 7NI, and methylene blue. Findings suggest that in the DFA glutamatergic fibers may contain neuronal NO synthase for producing NO that activate cGMP to cause release of glutamate. The glutamate then activates NMDA and AMPA receptors on the nitrergic neurons in the DFA to increase CCA blood flow. In conclusion, nitrergic-glutamatergic fibers and nitrergic neurons containing NMDA and AMPA receptors are present in the DFA for regulation of the CCA blood flow.
    Relation: 第二十二屆生物醫學聯合學術年會
    Appears in Collections:[School of Medicine] Proceedings

    Files in This Item:

    There are no files associated with this item.



    All items in CMUR are protected by copyright, with all rights reserved.

     


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback