期刊文献+

胍基丁胺在离体豚鼠乳头肌的电生理效应 被引量:6

ELECTROPHYSIOLOGICAL EFFECTS OF AGMATINE ON GUINEA PIG PAPILLARY MUSCLES IN VITRO
下载PDF
导出
摘要 应用细胞内微电极技术,观察了胍基丁胺(agmatine,AGM)对豚鼠乳头肌细胞的电生理效应。结果表明:(1)AGM浓度依赖地缩短正常乳头肌动作电位的时程;(2)对部分去极化的乳头肌,AGM(1mmol/L)除缩短动作电位时程外,还抑制动作电位零相最大上升速度,并降低其幅值和超射值;(3)预先应用一氧化氮合酶抑制剂LNAME(05mmol/L),不能影响AGM(1mmol/L)的电生理效应;(4)预先应用咪唑啉受体(imidazolinereceptor,IR)和α2肾上腺素能受体(alpha2adrenergicreceptor,α2AR)拮抗剂idazoxan(01mmol/L),则可完全阻断AGM(1mmol/L)的电生理效应。以上结果提示,AGM对乳头肌的电生理效应似由α2AR和IR介导,并与胞浆内Ca2+减少有关。 The cardiac electrophysiological effects of agmatine (AGM) were examined in guinea pig papillary muscle using intracellular microelectrode technique. The results obtained are as follows. (1) Duration of action potential(APD) in normal papillary muscles were decreased by AGM in a concentration dependent manner. (2) In partially depolarized papillary muscles, amplitute of action potential, overshoot, maximal velocity of phase 0 depolarization and APD were depressed by AGM. (3) Pretreatment with N G nitro L arginine methyl ester (L NAME, 0 5 mmol/L) did not affect the above effects of AGM (1 mmol/L) on papillary muscles. (4) The effects of AGM (1 mmol/L) could be blocked completely by pretreatment with idazoxan (0 1 mmol/L), an α 2 adrenoceptor (α 2 AR) and imidazoline receptor (IR) antagonist. All these results indicate that the effects of AGM on papillary muscles are likely due to a decrease of intracellular calcium mediated by α 2 AR and IR.
出处 《生理学报》 CAS CSCD 北大核心 1999年第3期321-326,共6页 Acta Physiologica Sinica
关键词 胍基丁胺 动作电位 乳头肌 电生理 心肌 agmatine action potential papillary muscle electrophysiology idazoxan
  • 相关文献

参考文献7

  • 1李晓滔,何瑞荣.胍基丁胺对大鼠血流动力学的影响及其细胞机制[J].生理学报,1999,51(2):229-233. 被引量:12
  • 2安瑞海,中国药理学报,1990年,11卷,310页
  • 3何瑞荣,Cardiovascular Physiology,1987年,75页
  • 4Gao Y,Life Sci,1995年,57卷,83页
  • 5Rasch W,Life Sci,1995年,56卷,2319页
  • 6Regunathan S,FASER J,1994年,8卷,A556页
  • 7Li G,Science,1994年,263卷,966页

二级参考文献3

  • 1Li G,Science,1994年,263卷,966页
  • 2Sun M K,Clin Exp Hyperten,1995年,17卷,115页
  • 3Gao Y,Life Sci,1995年,57卷,83页

共引文献11

同被引文献29

引证文献6

二级引证文献10

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部