Heart failure causes down-regulation of the atrial L-type Ca2þ current (ICaL) that has consequences on contractile function and susceptibility to atrial fibrillation. The reduction in atrial ICaL density has been suggested to involve changes in both the expression and phosphorylation of channel protein. The objective of this project was to examine the mechanism of the decrease in atrial ICaL in a surgical model of heart failure. Heart failure was induced in adult male Wistar rats by surgical ligation of the left anterior descending coronary artery (CAL) under general anesthesia. Control animals were subject to equivalent sham operation (Sham). Left atrial myocytes were isolated~ 18 weeks after surgery and superfused with a Tyrode’s solution (37 C). Whole-cell L-type Ca currents (ICaL) were recorded during depolarisation to 0 mV from a holding potential of À80 mV and normalised to wholecell capacitance, which was also used as an index of cell size. CAL cells were hypertrophied (94.755. 2 pF, n= 63) compared to Sham (56.652. 1 pF, n= 47; P% 0.0001). ICaL density at 0 mV was reduced in CAL compared to Sham (3.350. 4 pA/pF; n= 31 vs 7.350. 7 pA/pF; n= 33; P% 0.001), but the response of ICaL to 1 μmol/L norepinephrine was greater in CAL (x6. 8) than in Sham (x3. 2) so that there was no difference in ICaL density between the two groups in the presence of norepinephrine. These data indicate a change in channel protein phosphorylation without a change in channel density. The regulation of L-type Ca2þ channel phosphorylation may be a potential therapeutic target for atrial arrhythmias in heart failure.