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Niflumic acid hyperpolarizes the smooth muscle cells by opening BKCa channels through ryanodine-sensitive Ca2+ release in spiral modiolar artery
Pages: 743-750
Year: Issue:  6
Journal: Acta Physiologica Sinica

Keyword:  spiral modiolar arterysmooth muscle cellniflumic acidhyperpolarizationCa2+stores;
Abstract: The mechanism by which niflumic acid(NFA),a C1-channel antagonist,hyperpolarizes the smooth muscle cells(SMCs)of cochlear spiral modiolar artery(SMA)was explored.Guinea pigs were used as subjects and perforated patch clamp and intracellular recording technique were used to observe NFA-induced response of SMC in the acutely isolated SMA preparation.The results showed that bath application of NFA.indanyloxyacetic acid 94(IAA-94)and disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate(DIDS)caused hyperpolarization and evoked outward currents in all cells at low resting potential(RP),but had no effects in cells at high RP.In the low RP SMCs,the average RP was about(-42.47±1.38)mV(n=24).Application of NFA(100μmol/L),IAA-94(10μmol/L)and DIDS (200 μmol/L)shifted the RP to(13.7±4.3)mV(n=9,P<0.01),(11.4±4.2)mV(n=.7,P<0.01)and(12.3±3.7)mV(n=8,P<0.01),respectively.These drug-induced responses were in a concentration-dependent manner.NFA-induced hyperpolarization and outward current were almost blocked by charybdotoxin(100 nmol/L),iberiotoxin(100 nmol/L),tetraethylammonium(10 retool/L),BAPTA-AM(50 μmol/L),ryanodine(10μmol/L)andcaffeine(0.1-10mmol/L),respectively,but not by nifedipine(100μmol/L),CdC12(100μmol/L)andCa2+-free medium.It is concluded that NFA induces a release of intracellular calcium from the Ca2+ stores and the released intracellular calcium in turn causes concentration-dependent and reversible hyperpolarization and evokes outward currents in the SMCs of the cochlear SMA via activation of the Ca2+-activated potassium channels.
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