It is well-known that electrical field stimulation (EFS)-induced contraction is mediated by a cholinergic mechanism and other neurotransmitters. NO, ATP, calcitonin gene-related peptide (CGRP), and substance P are released by EFS. To investigate the purinergic mechanism involved in the EFS-induced contraction, purinegic receptors antagonists were used. Suramine, a non-selective P2 receptor antagonist, reduced the contraction induced by EFS. NF023 (10−7∼10−4 M), a selective P2X antagonist, inhibited the contraction evoked by EFS. Reactive blue (10−6∼10−4 M), selective P2Y antagonist, also blocked the contraction in a dose-dependent manner. In addition, P2X agonist Ձ,Ղ-methylene 5'-adenosine triphosphate (ՁՂMeATP, 10−7∼10−5 M) potentiated EFS-induced contrac</SUP>tion in a dose-dependent manner. P2Y agonist adenosine 5'-[Ղ-thio]diphosphate trilithium salt (ADPՂS, 10−7∼10−5 M) also potentiated EFS-induced contractions in a dose-dependent manner. Ecto-ATPase activator apyrase (5 and 10 U/ml) reduced EFS-induced contractions. Inversely, 6-N,N-diethyl-D-Ղ,Ճ- dibromomethylene 5'-triphosphate triammonium (ARL 67156, 10−4 M) increased EFS-induced contraction. These data suggest that endogenous ATP plays a role in EFS-induced contractions which are mediated through both P2X-receptors and P2Y-receptors stimulation in cat esophageal smooth muscle.