Pharmacological actions of an antispasmodic agent, oxybutynin were investigated in the isolated procine coronary arteries. The coronary rings were contracted by acetylcholine (ACh) and KCl in a dose-dependent fashion. The ACh-induced contractions were signifcantly potentiated by removal of endothelium and EC₅₀=0.52μM of intact endothelial rings was about 2 times greater than EC₅₀=0.28μM of rings without the endothelium. These results suggest that the endothelium plays an inhibitory role in ACh-induced contraction. Oxybutynin and atropine inhibited dose-dependently 1.0μM ACh-induced contraction and atropine inhibited dose-dependently 1.0μM ACh-induced contraction and the IC_50s were 11.0 nM and 0.47 nM, respectively. Atropine did not affect 35 mM KCl-induced contraction but oxybutynin inhibited the contraction to the basal tension in a dose-dependent manner. The IC₅₀ of oxybutynin on the KCl-induced contraction was 49.7μM. The dose-response curve to ACh was parallelly shifted to the right by pretreating coronary rings with IC₅₀ of atropine (0.47 nM) or oxybutynin (11.0 nM) but the curve to KC1 was rightward shifted in a noncompetitive manner under pretreatment with IC₅₀ of oxybutynin (49.7μM). Oxybutynin inhibited 0.1μM Bay K 8644-induced contraction to the basal tension in a dose dependent manner, but 35μM histamine-induced contraction was inhibited to only 50e/e of the original level even in maximal concentration (5 × 10^-4M) of oxybutynin. These results suggest that oxybutynin causes antispasmodic action through sensitive blocking action on muscarinic receptors and inhibitory action on calcium influx in the procine coronary artery.