We investigated the signaling pathway on sphingosinephosphorylcholine (SPC) -induced contraction in cat esophageal smooth muscle cells. SPC induced in a dose-dependent manner contractile effect. We have previously shown that lysophospholipid (LPL) receptor subtypes including the $S1P_1,;S1P_2,;S1P_3,;and;S1P_5$ receptor are present in esophageal smooth muscle. Only EDG-5 $(S1P_2)$ receptor antibody penetration into permeablilized cells inhibited the SPC-induced contraction. Pertussis toxin (PTX) and specific antibodies to $G_{i1},;G_{i2},;G_{i3};and;G_o$ inhibited the contraction, implying that SPC-induced contraction depends on PTX-sensitive $G_{i1},;G_{i2},;G_{i3};and;G_o$ protein. A phospholipase inhibitor U73122 and incubation of permeabilized cells with $PLC-{eta}3$ antibody inhibited SPC-induced contraction. The PKC-mediated contraction may be isozyme specific since only $PKC{varepsilon}$ antibody inhibited the contraction. Preincubation with MEK inhibitor PD98059 blocked the SPC-induced contraction, but p38 MAPK inhibitor SB202190 did not. Cotreatment with GF109203X and PD98059 did not show synergistic effects, suggesting that these two kinases are involved in the same signaling pathway in the SPC-induced contraction. The data suggest that S1P-induced contraction in feline esophageal smooth muscle cells depends on activation of the $G_{i1},;G_{i2},;G_{i3};and;G_o$ proteins and the $PLC{eta}3$ isozyme via the $S1P_2$ receptor, leading to stimulation of a $PKC{varepsilon}$ pathway, which subsequently activates a p44/p42 MAPK pathway.