Cellular basis for the negative dromotropic effect of adenosine on rabbit single atrioventricular nodal cells.
Cellular basis for the negative dromotropic effect of adenosine on rabbit single atrioventricular nodal cells.
复制标题
腺苷对兔单个房室结细胞负促促作用的细胞基础。
DOI：
10.1161/01.res.78.4.697
复制
发表时间：
1996
影响因子：
20.1
通讯作者：
Belardinelli,L
中科院分区：
文献类型：
--
作者：
Wang,D;Shryock,JC;Belardinelli,L
用全细胞膜片钳技术研究了腺苷对兔单个房室结细胞动作电位、率依赖性激活失败(房室二度传导阻滞的细胞基础)和兴奋性恢复的影响。腺苷(1μ/L)使房室结细胞动作电位时程缩短、波幅降低、上升速度减慢。腺苷(10μ/L)可引起房室结细胞明显超极化(7±1 mV)。腺苷增加房室结细胞激活失败(文氏周期)的发生率和频率依赖性；这种作用是浓度依赖的，并由A1腺苷受体介导。腺苷引起的速率依赖性激活失败与有效不应期延长18±2ms(P<0.05)、激活延迟时间延长以及激活房室结细胞所需的阈值电流幅度增加(从0.22±0.04增加到0.30±0.03 nA，P<；0.05)有关。结果提示，腺苷引起的房室结细胞兴奋性恢复缓慢是腺苷诱导的二度房室传导阻滞的细胞基础。腺苷降低房室结细胞的ICA、LAND激活的IK、ADO。腺苷对离子电流的这些作用可能有助于该核苷抑制房室结细胞的兴奋性。腺苷对房室结细胞率依赖性激活失败的增强作用提示，在室上性心动过速发作时，腺苷的负性变流作用应比在正常节律时更为明显。
The effects of adenosine on action potentials, rate-dependent activation failure (the cellular basis for second-degree atrioventricular [AV] block), and the recovery of excitability in rabbit isolated single AV nodal cells were studied using the whole-cell patch-clamp technique. Adenosine (1 μmol/L) shortened the duration, depressed the amplitude, and reduced the rate of rise of the AV nodal cell action potential. Adenosine (10 μmol/L) caused a significant hyperpolarization (7±1 mV) of AV nodal cells. Adenosine increased the occurrence and the rate dependence of activation failure (Wenckebach periodicity) of AV nodal cells; this effect was concentration dependent and mediated by A1adenosine receptors. The rate-dependent activation failure caused by adenosine was associated with a prolongation of the effective refractory period by 18±2 ms (P<.05), an increase in the duration of activation delay, and an elevation (from 0.22±0.04 to 0.30±0.03 nA,P<.05) of the threshold current amplitude required to activate AV nodal cells. The results suggest that the slowed recovery of excitability of AV nodal cells caused by adenosine forms the cellular basis for adenosine-induced second-degree AV block. Adenosine decreased ICa,Land activated IK,ADOof AV nodal cells. These actions of adenosine on ion currents may contribute to the effect of this nucleoside to depress excitability of AV nodal cells. The enhancement by adenosine of rate-dependent activation failure of AV nodal cells implies that the negative dromotropic effect of adenosine should be more pronounced during an episode of supraventricular tachycardia than during normal rhythm.