权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Role of intracellular stored calcium on the generation of spontaneous activity in gastrointestinal smooth muscle

细胞内储存的钙对胃肠平滑肌自发活动产生的作用

基本信息

批准号：
14570044
负责人：
SUZUKI Hikaru
金额：
$ 2.43万
依托单位：
Nagoya City University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2003
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14570044/
关键词：
Gastric smooth muscle Spontaneous activity Stored calcium IP_3 Proteinkinase C Intracellular calcium Mitochondria Proton pump 消化管平滑筋歩調とり電位緩電位

项目摘要

Recording of electrical responses from the isolated stomach muscles of the guinea-pig produced periodical generation of slow potentials with about 30 mV in amplitude and 5-6 s in duration. Slow potentials were not inhibited by TTX or Ca antagonists. Slow potentials were abolished by DIDS or niflumic acid, suggested that the potentials were produced by activation of Ca-sensitive Cl channels. Measurement of intracellular Ca concentrations by using Ca-indicator fula-2 fluorescence indicated that slow potentials were associated with an increase in intracellular Ca concentrations. Ca-responses, together with slow potentials, were inhibited by BAPTA (an intracellular Ca chilator), 2-APB (an inhibitor of IP3 receptors) and CPA (an inhibitor of internal Ca-pump). Inhibitors of mitochondrial protonophore (CCCP) or mitochondrial ATP-sensitive K-channel (5-HDA) also abolished the generation of slow potentials and Ca-transients. These results suggested that mitochondrial activity produced as a results of proton production induces an activation of Ca-sensitive enzymes and finally produces IP3, which in tern elevates intracellular Ca concentrations by releasing from the internal stores and activates Ca-sensitive ion channels at the plasma membrane. These processes are considered involved in the generation of pacemaker potentials in gastric pacemaker cells.

记录豚鼠离体胃肌的电反应，可产生周期性的慢电位，幅值约30 mV，持续时间5-6 s。慢电位不受TTX或Ca拮抗剂的抑制。DIDS和尼氟灭酸可阻断慢电位，提示慢电位是由钙敏感性氯通道激活引起的。通过使用钙指示剂fula-2荧光测量细胞内钙浓度表明，慢电位与细胞内钙浓度的增加。细胞内钙通道阻滞剂BAPTA、IP 3受体抑制剂2-APB和内钙泵抑制剂CPA均能抑制慢电位和钙反应。线粒体质子载体（CCCP）或线粒体ATP敏感性K通道（5-HDA）的抑制剂也消除了慢电位和钙瞬变的产生。这些结果表明，作为质子产生的结果所产生的线粒体活性诱导Ca敏感酶的活化，并最终产生IP 3，IP 3通过从内部储存释放来升高细胞内Ca浓度，并激活质膜上的Ca敏感离子通道。这些过程被认为参与胃起搏细胞起搏电位的产生。