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    CMUR > China Medical University Hospital > Jurnal articles >  Item 310903500/29032
    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/29032


    Title: Successful inoue balloon mitral commissurotomy in double-orifice mitral stenosis
    Authors: Kim, MH;Cha, KS;Kim, JS;Hung, JS;Lau, KW
    Contributors: 附設醫院內科部心臟科;Dong A Med Coll, Cardiol Sect, Seo Gu, Pusan 602103, South Korea;China Med Coll Hosp, Cardiol Sect, Taichung, Taiwan
    Date: 2000
    Issue Date: 2010-09-24 14:19:16 (UTC+8)
    Publisher: WILEY-LISS
    Abstract: 1 The mechanisms underlying AVP-induced increase in [Ca2+](i) and glucagon release in clonal alpha-cells In-R1-G9 were investigated. 2 AVP increased [Ca2+](i) and glucagon release in a concentration-dependent manner. After the administration of AVP, glucagon was released within 30 s, quickly reached the maximum within 2 min, and maintained a steady-state concentration for at least 15 min. 3 In Ca2+-containing medium, AVP increased [Ca2+](i) in a biphasic pattern; a peak followed by a sustained plateau. In Ca2+-free medium, the Ca2+ response to AVP became monophasic with lower amplitude and no plateau. Both the basal and AVP-induced glucagon releases were lower in the absence than in the presence of extracellular Ca2+ When [Ca2+](i) was stringently deprived by BAPTA, a Ca2+ chelator, AVP still significantly increased glucagon release. 4 Pretreatment with thapsigargin, a microsomal Ca2+ ATPase inhibitor, abolished both the Ca2+ peak and sustained plateau. 5 AVP increased intracellular concentration of IP3. 6 U-73122 (8 mu M), a phospholipase C inhibitor, abolished AVP-induced increases in [Ca2+](i), but only reduced AVP-induced glucagon release by 39%. 7 Pretreatment with nimodipine, an L-type Ca2+ channel blocker failed to alter AVP-induced glucagon release or increase in [Ca2+](i). 8 The results suggest that AVP causes glucagon release through both Ca2+-dependent and -independent pathways. For the Ca2+-dependent pathway, the G(q) protein activates phospholipase C, which catalyzes the formation of IP3. IP3 induces Ca2+ release from the endoplasmic reticulum, which, in turn, triggers Ca2+ influx. Both Ca2+ release and Ca2+ influx may contribute to AVP-induced glucagon release.
    Relation: CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS 49(2):200-203
    Appears in Collections:[China Medical University Hospital] Jurnal articles

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