Summary—A study has been carried out on the actions of the prostaglandins E2and F2αand their synthesis inhibitors, indomethacin and diclofenac sodium, upon isolated human ureteric smooth muscle, using the technique of microsuperfusion designed to ensure good tissue viability.Indomethacin and diclofenac sodium were shown to abolish almost completely the contractile response of ureteric muscle to electrical field stimulation. Contractile activity, in the presence of the inhibitors, could be restored by prostaglandin E2or F2αor by increasing the external potassium concentration, [K+]o, of the superfusate.Prostaglandin E2or F2αalone were shown to increase dramatically both the phasic and tonic component of the electrically stimulated contractions, on occasions inducing spontaneous activity.A possible mechanism of action was elucidated with an electrophysiological technique using intracellular microelectrodes. The mean membrane potential recorded was 54.7 mV (SD ± 10 mV, n=15). The depolarising action of raising [K+]owas demonstrated and prostaglandin F2α(3 times 10‐6M) was shown to produce a small depolarisation of the ureteric muscle cell