In rat pulmonary vein (PV) cardiomyocytes (CM), norepinephrine (NE) induces an automatic activity consisting of bursts of slow action potentials which depend on Ca²⁺ (upstroke) and Na⁺ (inter-burst) channels. Our objective was to characterize low voltage-activated (LVA) currents in rat PVCM susceptible to trigger this activity. Whole-cell I_Ca (5 mM Ca²⁺) was recorded from − 100 mV with classical Na⁺- and K⁺-free solutions. A fast LVA I_Ca (FLVA-I_Ca), present in ≈ 56% of PVCM between ~ − 50 to − 20 mV, was blocked by 10 μM TTX and markedly increased by addition of NaCl (1 or 3 mM) or KCl (5 or 10 mM). Permeability ratios P′_Ca/P_Na and P′_Ca/P_K calculated for bi-ionic conditions were respectively 2.25 ± 0.51 and 1.88 ± 0.25, and not different from a value of 2. FLVA-I_Ca was increased by 10 μM NE and 300 nM BayK8644, decreased by 5 μM nifedipine but not blocked by ranolazine (10 μM). NiCl₂ (40 μM) and TTA-A2 (10 or 100 nM) increased FLVA-I_Ca. Similar results were obtained in left atrial (LA) CM. Neither Ba²⁺ nor Sr²⁺ alone could permeate the FLVA channel or block Ca²⁺ influx but revealed a large slower activating and inactivating LVA Ca²⁺ current (SLVA-I_Ca), present in 10 out of 80 PVCM, absent in LACM, and partially inhibited by 100 nM TTA-A2. Therefore, the ionic channel underlying FLVA-I_Ca is likely a fast voltage-gated non-selective channel with a dihydropyridine binding site. SLVA-I_Ca might correspond to Ca²⁺ influx through Ca_v3.x channels and contribute to triggering NE-induced automatic activity in the PV myocardial sleeve.

在大鼠肺静脉（PV）心肌细胞（CM）中，去甲肾上腺素（NE）诱导自动活动，该活动由取决于Ca ²⁺（上冲程）和Na ⁺（爆发间）通道的慢动作电位爆发组成。我们的目标是表征易触发该活动的大鼠PVCM中的低电压激活（LVA）电流。使用经典的不含Na ⁺和K ^+的溶液从− 100 mV记录全细胞I _Ca（5 mM Ca ²⁺）。快速的LVA I _Ca（FLVA-I _Ca）存在于〜-50至-20 mV之间的约56％的PVCM中，被10μMTTX阻断，并通过添加NaCl（1或3 mM）或KCl（ 5或10 mM）。渗透率P'在双离子条件下计算的_Ca / P _Na和_P'Ca / P _K分别为2.25±0.51和1.88±0.25，与2的值相同。FLVA-1 _Ca增加了10μMNE和300 nM BayK8644 ，硝苯地平减少5μM，但未被雷诺嗪（10μM）阻断。的NiCl ₂（40μM）和TTA-A2（10或100nM）增加FLVA-I_钙。在左心房（LA）CM中获得了相似的结果。Ba ²⁺和Sr ²⁺都不能单独渗透FLVA通道或阻断Ca ^2+的流入，但显示LVA Ca ²⁺电流激活和失活的速度较慢（SLVA-1 _Ca），在80个PVCM中有10个存在于LACM中，并且被100 nM TTA-A2部分抑制。因此，位于FLVA-1 _Ca下方的离子通道可能是具有二氢吡啶结合位点的快速电压门控非选择性通道。SLVA-1 _Ca可能对应于通过Ca _v 3.x通道的Ca ²⁺流入，并有助于触发NE诱导PV心肌套中的自动活动。