Isometric tension was recorded in uterine arterial ring preparation contracted by potassium (60 mM) and norepinephrine(1.8 X 10(-7) M). With pretreatment of various concentrations of nifedipine(2.9 x 10(-9) ~2.9 X10(-7) M) and verapamil(2.2 X 10(-7) -2.2 X 10(-5) M), the relaxation was dose-dependent and inhibitory effects of both agents were more marked on the potassium than norepinephrine-evoked contraction. After immersion of the arterial preparation in calcium-free solution, the potassium-evoked contraction was decreased to 21±4.1%(mean±SEM) of the response in normal Krebs solution and norepinephrine-evoked contraction to 26±3.8%. The responses to both agents were completely restored when the calcium concentration was increased to 4.0 mM. Pretreated nifedipine(2.9 x 10(-7) M) in calcium-free solution depressed the potassium-evoked contraction to 7.3±1.6% and norepinephrine-evoked contraction to 12±3.7%. In addition of calcium(0-4.0mM), the potassium-evoked contraction increased to 30±4.6% and that by norepinephrine to 45±5.4%. Pretreated verapamil(2.2 X 10(-5) M) in calcium-free solution depressed the potassium-evoked contraction to 14±3.6% and norepinephrine-evoked contraction to 18±3.3%. In addition of calcium(0-4.0mM), the potassium-evoked contraction increased to 41±4.2% and that by norepinephrine to 57±4.7%. It was concluded that nifedipine and verapamil relaxed KC1 contracted ring in the presence of external calcium and relaxed norepinephrine contracted ring in both the presence and absence of external calcium. These findings suggest that calcium antagonists interfere with the release of calcium from intracellular sites as well as with the slow inward current of calcium.