The effects of flavoxate hydrochloride (Bladderon®, piperidinoethyl-3-methylflavone-8-carboxylate; hereafter referred as flavoxate) on voltage-dependent nifedipine-sensitive inward Ba 2+ currents in human detrusor myocytes were investigated using a conventional whole-cell patch-clamp. Tension measurement was also performed to study the effects of flavoxate on K +-induced contraction in human urinary bladder. Flavoxate caused a concentration-dependent reduction of the K +-induced contraction of human urinary bladder. In human detrusor myocytes, flavoxate inhibited the peak amplitude of voltage-dependent nifedipine-sensitive inward Ba 2+ currents in a voltage- and concentration-dependent manner (K i = 10 μM), and shifted the steady-state inactivation curve of Ba 2+ currents to the left at a holding potential of -90mV. Immunohistochemical studies indicated the presence of the α 1c subunit protein, which is a constituent of human L-type Ca 2+ channels (Ca v1-2), in the bundles of human detrusor smooth muscle. These results suggest that flavoxate caused muscle relaxation through the inhibition of L-type Ca 2+ channels in human detrusor.
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