Aim: The influence of niflumic acid (NFA), a C1- channel antagonist, on the mem-brane potentials in smooth muscle cells (SMC) of the cochlear spiral modiolar artery (SMA) in guinea pigs was examined. Methods: The intracellular recording and whole-cell recording technique were used to record the NFA-induced re-sponse on the acutely-isolated SMA preparation. Results: The SMC had 2 stable but mutually convertible levels of resting potentials (RP), that is, one was near-45 mV and the other was approximately -75 mV, termed as low and high RP, respectively. The bath application of NFA could cause a hyperpolarization in all the low RP cells, but had little effect on high RP cells. The induced responses were concentration-dependent. Large concentrations of NFA (≥100 μmol/L) often in-duced a shift of a low RP to high RP in cells with an initial RP at low level, and NFA (up to 100 μmol/L) had little effect on the membrane potentials of the high RP cells. However, when the high RP cells were depolarized to a level beyond -45 mV by barium and ouabain, NFA hyperpolarized these cells with the similar effect on those cells initially being the low RP. The NFA-induced response was almost completely blocked by charybdotoxin, iberiotoxin, tetraethylammonium, 1,2-bis(2-aminophenoxy) ethane-N,N,N,N,N,-tetraacetic acid tetrakis acetoxymethyl ester, but not by 4-aminopyridine, barium, glipizide, apamin, ouabain, and CdC12. Conclusion: NFA induces a concentration-dependent reversible hyperpolarization in SMC in the cochlear SMA via activation of the Ca2+-activated potassium channels.