Previously, we demonstrated M3-receptor-mediated tonic contrac- tion of porcine coronary smooth muscle (CSM) mainly triggered by Ca2+ entry via store-operated Ca2+ channels (SOCs), while contraction strongly depended on arachidonic acid (AA) produc- tion by PLA2 and the AA metabolites emerging from the COX- pathway. Here, the signal pathways involved in tonic contraction of CSM strips upon M3-receptor-mediated, L-VOCC-dependent Ca2+ influx were evaluated by means of specific inhibitors: 4- BPB, an inhibitor of PLA2, had no effect on the contractile response and indomethacin (COX inhibition) reduced it only by 51±3% (p<0.001). However, NDGA (LOX inhibition) almost suppressed the response (92±2% inhibition, p<0.001). As with SOC-dependent contraction, the PKC inhibitor, GF109203X, as well as the RhoK inhibitor, Y-27635, nearly abolished the contractile response (90±4% and 90±1% inhibition, p<0.001). Conclusion: 1) only SOC-dependent, but not L-VOCC-dependent Ca2+ entry seems to activate PLA2 indicating different subsarco- lemmal compartmentalization of the Ca2+ entering each pathway, 2) L-VOCC-dependent contraction rather depends on the AA metabolites emerging from the LOX pathway, 3) activation of PKC as well as of RhoK are essential signaling steps in M3- receptor-mediated tonic contraction of CSM, regardless wether activator Ca2+ is delivered by L-VOCCs or by SOCs.