Introduction: Atrial fibrillation resulting from elevated adrenergic activity may involve an increase in atrial L-type Ca2+ current (ICaL) by noradrenaline (NA). However, the contribution of the individual adrenoceptor (AR) sub-types to such ICaL-increase is poorly understood, particularly in human atrium. 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 human atrial myocytes. Methods: ICaL was recorded by whole-cell-patch clamp at 35-37oC in myocytes isolated enzymatically from right atrial tissue samples obtained from consenting patients undergoing elective cardiac surgery. Results: 1) Noradrenaline substantially increased peak (at 0 mV) ICaL, in a concentration-dependent manner, to a maximally effective value (Emax) of 7.29 pA/pF (from Emin 2.82 pA/pF); and with a half maximally-effective concentration (EC50) of 156 nM; EC75 310 nM (n=8-31cells, 4-8 patients). 2) Broad-action β- and α-AR antagonism, of ICaL-responses to NA at EC75, were studied using propranolol (β1+β2-AR antagonist; 0.2 µM) and phentolamine (α1+α2-AR antagonist; 1 µM). In a group of 9 cells (3 patients), in which NA increased ICaL by 188±22% (mean±SE; P<0.001 vs control, 1-way-ANOVA), propranolol substantially decreased ICaL, by 60±4% (P<0.001 vs NA). Subsequently applied phentolamine decreased the remaining (i.e. α-stimulated) ICaL, by 37±4% (P<0.001 vs NA+propranolol). The degree of ICaL-reduction from phentolamine was significantly smaller (P=0.007) than that from propranolol. 3) β-AR-subtype-specific antagonism of ICaL-responses to NA (again at EC75) was investigated with CGP20712A (β1-antagonist; 0.3 µM: CGP) and ICI118551 (β2-antagonist; 0.1 μM: ICI). In each of 6 cells (2 patients) studied, CGP substantially decreased NA-stimulated ICaL, on average by 71±4% (P=0.032 vs NA). By contrast, ICI, in the continued presence of NA+CGP (studied in 5 of these cells), produced a mixed ICaL-response: a marked and reversible (upon washing out ICI) decrease in 2 cells (by 72 and 78%), and a reversible increase in the other 3 cells (by 12, 35 & 37%); with no significant effect on average (P=0.949 vs NA+CGP). 4) 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 6 cells (3 patients) studied, prazosin decreased NA (EC75)-stimulated ICaL, on average by 37±8% (P=0.017 vs NA). By contrast, yohimbine (still in the presence of NA+prazosin), produced a mixed ICaL-response: a moderate decrease in 4 cells (of 19, 36, 43 and 49%; reversible in 3 of these), a marked and reversible increase (by 78%) in one cell, and no effect in the other cell. There was no significant effect on average (P=0.940 vs NA+prazosin). The degree of reduction in NA-stimulated ICaL by prazosin was significantly smaller (P=0.002, un-paired t-test) than that by CGP. Conclusion: Stimulation of ICaL by NA in human atrial myocytes is mediated, based on adrenoceptor sub-type-antagonist responses, predominantly by β1-AR activation, with a smaller (though still substantial) contribution from α1-activation, and either a contributing or attenuating (and, on average, negligible) action of β2- or α2-activation.