Prostaglandins and neurotransmission at the guinea pig and rabbit urinary bladder.

High concentrations of prostaglandins (PGE1, PGE2, or PGE2 alpha) (2 x 10(-6) M) produced a slow contraction of longitudinal strips of detrusor muscle taken from the bladders of guinea pigs and rabbits. At a lower concentration (10(-6) M) prostaglandins enhanced contractions produced by field stimulation of nerves in guinea pig but not rabbit strips. The contractions were not affected by indomethacin. Contractions of guinea pig strips in response to acetylcholine at 10(-4) M were enhanced by prostaglandins and unaffected by indomethacin. Membrane potentials of smooth muscle cells recorded with micro electrodes, were unchanged up to 10(-6) M PGE2. Above this the cells were depolarized with an increase in frequency of spontaneous action potentials. Synchronous recording of electrical and mechanical activity with the double sucrose gap indicated a decrease in amplitude of the evoked excitatory junction potential and action potential even when the contraction was enhanced in the presence of PGE2. Responses to repeated stimulation at 10 Hz for 1 min were progressively depressed. This trend was slightly reduced by PGE2 but unaffected by indomethacin. It is concluded that prostaglandins are not normally released by the nerves to the urinary bladder but are able to facilitate contraction in the guinea pig. This effect is probably on the excitatory-contraction coupling, possibly by mobilizing Ca2+. Some modification of transmitter release by the nerves may also occur.