Introduction: An increase in atrial L-type Ca2+ current (ICaL) by noradrenaline (NA) may promote afterdepolarisations and atrial fibrillation (AF). However, the contribution of the individual adrenoceptor (AR) sub-types to such ICaL-increase is poorly understood; including in rabbit, a species commonly used to study AF mechanisms. Aim: To investigate effects, on NA-stimulated ICaL, of various broad-action and sub-type-specific α- and β-AR antagonists, alone or in combination, in rabbit atrial myocytes. Methods: ICaL was recorded by whole-cell-patch clamp at 35-37oC in left atrial myocytes isolated enzymatically from rabbit hearts (anaesthetic: Na+-pentobarbital, 100 mg/kg I.V.). Results: 1) Noradrenaline (310 nM) increased peak (at 0 mV) ICaL, from -14.38±2.18 to -19.70±2.94 pA/pF (i.e. by 39±10%); P=0.025 (1-way-ANOVA), n=6 cells, 3 rabbits. 2) Broad-action β-AR antagonism of this ICaL-response to NA was studied using propranolol (β1+β2-AR antagonist; 0.2 µM), which decreased ICaL in each of these 6 cells (reversible in each of 5 cells in which drug washout was studied), and on average by 55±5% (P<0.001 vs NA). 3) Broad-action α-AR antagonism of ICaL-responses to NA was studied using phentolamine (α1+α2-AR antagonist; 1 µM), either in the absence or presence of propranolol. Without propranolol (n=9 cells, 2 rabbits), phentolamine decreased ICaL in each of these 9 cells (reversible in 8), on average by 43±5% (P<0.001 vs NA). The degree of this ICaL-reduction (i.e. by phentolamine alone) was similar (P=0.143, un-paired t-test) to that from propranolol alone. When applied after propranolol (n=7 cells, 4 rabbits), phentolamine produced a mixed ICaL-response: decrease in 4 of these 7 cells (by 21, 29, 44 and 48%; reversible in 3 of those 4), and increase in the other 3 (by 16, 159 and 331%; reversible in each). There was no significant effect on average (P=0.535 vs NA+propranolol). 4) β-AR-subtype-specific antagonism of ICaL-responses to NA was investigated with CGP20712A (β1-antagonist; 0.3 µM: CGP) and ICI118551 (β2-antagonist; 0.1 μM: ICI). In each of 5 cells (4 rabbits) studied, CGP substantially decreased NA-stimulated ICaL, on average by 64±4% (P=0.002 vs NA). By contrast, ICI, in the continued presence of NA+CGP, increased ICaL in each of these cells, reversibly, and on average by 33±9% (P=0.028 vs NA+CGP). The degree of ICaL-increase by ICI was not significantly different (P=0.391) to the degree of ICaL-decrease by CGP. 5) α-AR-subtype-specific antagonism of NA-stimulated ICaL was studied with prazosin (α1-antagonist; 0.5 µM) and yohimbine (α2-antagonist; 10 µM). In each of 7 cells (3 rabbits) studied, prazosin decreased NA-stimulated ICaL, on average by 48±6% (P<0.001 vs NA). Yohimbine (still in the presence of NA+prazosin), decreased ICaL further, in 6 of these 7 cells (in the other, there was a moderate, reversible, increase), with no significant effect on average (P=0.237 vs NA+prazosin). The degree of ICaL-decrease by prazosin was not significantly different (P=0.073, Mann-Whitney) from that by CGP. Conclusion: Stimulation of ICaL by NA in rabbit atrial myocytes is mediated, based on adrenoceptor sub-type-antagonist responses, substantially by activation of β1- and α1-ARs, attenuated by β2-activation, with either a contributing or attenuating (and, on average, negligible) action of α2-activation.