A study has been carried out on the actions of the prostaglandins E2 and F, , and their synthesis inhibitors, indomethacin and diclofenac sodium, upon isolated human ureteric smooth muscle, using the technique of microsuperfusion designed to ensure good tissue viability. lndomethacin 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 E, or F2a or by increasing the external potassium concentration, [K+],, of the superfusate.Prostaglandin E, or F , , alone 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 k 10 mV, n = 15). The depolarising action of raising [K+], was demonstrated and prostaglandin F2,(3 x 10-6M) was shown to produce a small depolarisation of the ureteric muscle cell membrane.