Heart failure causes down regulation of the atrial L-type Ca2+ current (ICaL), which contributes to contractile and electrical dysfunction and increases susceptibility to atrial fibrillation. The reduction in atrial ICaL density has been suggested to involve reduction in both the expression and phosphorylation of the channel protein although the precise mechanisms remain unclear. The objective of this project was to examine the regulation of atrial ICaL in a surgical model of heart failure in rats. Procedures were approved by local ethics committee and performed in accordance with UK legislation. Adult male Wistar rats were subject to surgical ligation of the left anterior descending coronary artery (CAL, N=10) or equivalent sham operation (Sham, N=12) under general anaesthesia (ketamine 75 mg/kg, medetomidine 0.5 mg/kg, ip) with appropriate analgesia (buprenorphine 0.05 mg/kg, sc). Left atrial myocytes were isolated ~18 weeks after surgery. Single isolated cells were superfused with a Tyrode’s solution (37 °C) and whole-cell currents recorded from a holding potential of -80 mV using a ruptured patch-clamp technique. ICaL was activated by depolarisation to 0 mV (300 ms) following a pre-pulse to -40 mV to inactivate Na current, and measured as the difference between the peak inward current and the steady-state current at the end of the pulse. Data are presented as mean ± standard error of the mean and were compared by unpaired t-test. P<0.05 was used as the limit of statistical confidence. CAL rats had increased heart weight/tibia length (4.84±0.27 vs 3.02±0.07; P≤0.0001) and lung weight/tibia length (4.19±0.30 vs 3.72±0.08; P<0.01) ratios, indicating early stage heart failure. CAL cells were hypertrophied compared to Sham (94.7±5.2 pF; n=63 vs 56.6±2.1 pF; n=47; P≤0.0001). ICaL density at 0 mV was reduced in CAL compared to Sham (3.3±0.4 pA/pF; n=31 vs 7.3±0.7 pA/pF; n=33; P≤0.001). The response of ICaL at 0 mV to noradrenaline (NA; 1 μM) was increased from 3.2-fold in Sham to 6.8-fold in CAL so that there was no difference in ICaL density between the two groups (CAL -21.9±3.0 pA/pF, n=9 and Sham -23.7±4.5 pA/pF, n=5; ns). The PKA inhibitor H-89 (10 μM) had no effect on basal currents but abolished the effect of NA in both CAL and Sham. The absence of difference in ICaL density between CAL and sham myocytes in the presence of NA is consistent with a change in channel protein phosphorylation without a change in channel number. The regulation of L-type Ca2+ channel phosphorylation may be a potential therapeutic target for atrial arrhythmias in heart failure.