Li Y L, He R R
Department of Physiology, Hebei Medical College, Shijiazhuang, China.
Zhongguo Yao Li Xue Bao. 1993 Sep;14(5):414-7.
The electrophysiological effects of N6-cyclopentyladenosine (CPA) and [-]-N6-[phenylisopropyl]adenosine (R-PIA) (both are selective adenosine A1 receptor agonists) on pacemaker cells in sinoatrial (SA) node of guinea pigs were investigated using intracellular microelectrodes. CPA and R-PIA increased the amplitude of action potential, amplitude of the maximal diastolic potential and maximal rate of depolarization (phase 0), but decreased the velocity of diastolic (phase 4) depolarization, the rate of pacemaker firing, and the duration of 90% repolarization in pacemaker cells of guinea pigs. 8-Phenyltheophylline (a nonselective antagonist of adenosine receptors) and glibenclamide (a potent blocker of ATP-sensitive K+ channels) inhibited the electrophysiological responses of pacemaker cells to CPA. These results suggest that the electrophysiological changes induced by CPA are adenosine receptor-dependent and mainly mediated by activation of ATP-sensitive K+ channels coupled to adenosine receptors.
采用细胞内微电极技术，研究了N6-环戊基腺苷（CPA）和[-]-N6-[苯异丙基]腺苷（R-PIA）（二者均为选择性腺苷A1受体激动剂）对豚鼠窦房结起搏细胞的电生理效应。CPA和R-PIA增加了动作电位幅度、最大舒张电位幅度以及最大去极化速率（0期），但降低了豚鼠起搏细胞舒张期（4期）去极化速度、起搏发放频率以及90%复极化持续时间。8-苯基茶碱（一种非选择性腺苷受体拮抗剂）和格列本脲（一种强效ATP敏感性钾通道阻滞剂）抑制了起搏细胞对CPA的电生理反应。这些结果表明，CPA诱导的电生理变化依赖于腺苷受体，主要由与腺苷受体偶联的ATP敏感性钾通道激活介导。
