Urinary bladder smooth muscle (UBSM) exhibits spontaneous contraction.  This spontaneous mechanical activity has been suggested to be closely related to the action potential generated in this smooth muscle cell to enhance Ca²⁺ influx through voltage-gated L-type Ca²⁺ channels.  In guinea-pig UBSM, both action potential and rhythmic mechanical contraction occur spontaneously in the presence of atropine, phentolamin, propranolol, suramin and tetrodotoxin, which suggests that both phenomena are myogenic in origin.  Although nisoldipine and diltiazem completely eliminate action potential generation, they inhibit only partly spontaneous mechanical activity.  On the other hand, iberiotoxin, a selective BK channel blocker, increases action potential frequency and UBSM contraction amplitude and its frequency.  Unexpectedly, but interestingly, 2-aminoethoxydiphenyl borate (2-APB) causes apparent dissociation between membrane electrical and mechanical activity in this guinea-pig smooth muscle.  Elevation of intracellular Ca²⁺ concentrations during a burst of action potentials can be significantly reflected as the changes in spontaneous mechanical activity in UBSM.  However, action potential does not seem to be the exclusive trigger mechanism to determine the generation of UBSM spontaneous mechanical activity.