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LNAME(05mmol/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(alpha2adrenergicreceptor,α2AR)拮抗剂idazoxan(01mmol/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α2AR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