Bladder contractility is mediated by different K+ channels in the urothelium and detrusor smooth muscle.

The roles played by K(+) channels in the urothelium (UE) and detrusor smooth muscle (DSM) in regulating agonist-induced bladder contraction is not known at present. Thus, the effects in carbachol (CCh)-induced contraction in UE-intact (+UE) and UE-denuded (-UE) rat detrusor strips pretreated with K(+)-channel blockers were investigated here. The K(+)-channel blockers used were 4-aminopyridine (4-AP), glibenclamide (Glib), iberiotoxin (IbTx), charybdotoxin (ChTx), and apamin. In the absence of K(+)-channel blockers, control CCh-induced contractions were more potent in -UE than +UE strips. Treatment with IbTx and apamin resulted in more potent CCh-induced contractions in +UE strips. In -UE strips, CCh potency was increased by ChTx and Glib, but decreased by 4-AP. Different K(+) channels in the UE and DSM were thus involved in regulating bladder contractions. Contractile mediatory function of these channels, specific to the UE or DSM, may be potential drug targets in the management of bladder disorders.