腺苷对心房肌细胞钾钙通道的影响及受体机制

EFFECTS AND RECEPTOR MECHANISM OF ADENOSINE ON K^+, Ca^(2+) CHANNELS IN ATRIAL CELLS

运用膜片钳全细胞记录方式，研究腺着（Ado）及选择性腺着A;受体阻滞剂8-环戊基-1，3-二丙基黄嘌呤（DPCPX）对豚鼠心房肌细胞延迟整流性怀通道电流（IK）和L-型钙通道电流（L－ICA）的影响及受体机制。结果表明：3μmol／LAdo可加强IK，其峰值电流增大（P＜0.01），LK尾电流Ik．tail亦增大，Ik.tail的快、慢失活时间常数均减少。同时Ado可抑制L－ICa，峰值电流减少36.9％．其激活和失活时间常数均增大。Ado对两者的峰值电压、激活电位、反转电位及时间和电压依赖性均无影响。DPCPX可基本消除Ado对IK、L-ICa的作用，表明Ado对心房肌细胞钾、钙通道的影响由A1受体介导实现的。

Using patch clamp whole cell recording, we investigated the effects of Ado and DPCPXon IK, Ik.(rail)and L-ICh of enzymatic atrial myocytes from guinea pig heart- The resu1ts indicated: 3 mol/L Ado could increase IK and lk.(rail) and reduced both the fast and slow time constants of Ik(tail) (P <0. 0l )Meanwhile, Ado decreased L-Ica and prolonged its activation and inactivation time constants. But Adohad no effects on threshold, reversal potentials, maximal peak v0ltage, time-dependent and voltage-dependent of IK and L-(Ica) These acti0ns could be eliminated by DPCPX. The results suggested the effectsof Ado on IK t L-ICa in atrial cells were mediated by A, receptor.