In endothelium-intact preparations of rabbit coronary artery, acetylcholine (3 x 10(-8)-10(-6) M) caused a contraction in the presence of N omega-nitro-L-arginine methyl ester (10(-4) M). Removal of endothelium significantly attenuated the contraction. The present experiments were undertaken to elucidate whether the acetylcholine-induced contraction in endothelium-intact preparations was due to arachidonic acid metabolites, endothelin or superoxide. The acetylcholine-induced contraction in endothelium-intact preparations was attenuated by manoalide (10(-6) M and 3 x 10(-6) M) or oleyloxyethyl phosphorylcholine (10(-5) M) (phospholipase A2 inhibitors), BAY x 1005 (3 x 10(-6) and 10(-5) M) or L 663,536 (10(-6) and 10(-5) M) (leukotriene synthesis inhibitors) and ONO-1078 (10(-6) and 3 x 10(-6) M) or SK&F 104353 (10(-6) and 3 x 10(-6) M) (leukotriene antagonists). The contraction was not affected by aspirin (10(-4) M) or indomethacin (10(-6) M) (cyclooxygenase inhibitors), S-1452 (10(-8) M) or ONO-3708 (10(-7) M) (thromboxane A2 antagonists), FR139317 (10(-6) M) (endothelin receptor antagonist) or superoxide dismutase (150 u/ml) combined with catalase (1000 u/ml), or allopurinol (10(-5) M) (antioxidants). In contrast, the endothelium-independent contraction induced by acetylcholine was unaffected by any of these inhibitors and antagonists listed above. The present experiments demonstrate that in the presence of N omega-nitro-L-arginine methyl ester, acetylcholine partly causes an endothelium-dependent contraction in rabbit coronary artery which is probably due to leukotriene C4 and D4, but does not involve production of thromboxane A2, endothelin or superoxide.