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- W2275015434 abstract "Intravascular pressure stimulates several smooth muscle cell TRP channels, including TRPM4, leading to membrane depolarization and vasoconstriction (the myogenic response). Previous studies using 9-phenanthrol (9-phen), a TRPM4 channel inhibitor, suggest that TRPM4 is essential for pressure-induced depolarization and constriction (Gonzales et al, AJP Cell 2010). We have recently shown that transmembrane protein 16A (TMEM16A), a Ca2+-activated chloride channel, contributes to pressure-induced depolarization and constriction (Bulley et al, Circ Res 2012). To investigate these apparently dissimilar results, we tested the hypothesis that 9-phen is also a TMEM16A channel blocker. Patch-clamp electrophysiology indicated that 9-phen inhibited whole-cell currents generated by recombinant TMEM16A channels expressed in HEK293 cells. Analysis of tail-currents indicated that 9-phen reduced TMEM16A currents in a concentration- and voltage-dependent manner. IC50s for 9-phen were 15 and 10 μM at −100 and +100 mV, respectively. Cell-attached patch recordings indicated that 9-phen (10 μM) reduced single TMEM16A channel open probability, amplitude, and mean open time, and increased mean closed time. Taken together, our data suggest that 9-phen inhibits TMEM16A channels, in part by acting as a pore-blocker. NHLBI/NIH" @default.
- W2275015434 created "2016-06-24" @default.
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- W2275015434 date "2013-04-01" @default.
- W2275015434 modified "2023-09-23" @default.
- W2275015434 title "9‐phenanthrol inhibits TMEM16A channels" @default.
- W2275015434 doi "https://doi.org/10.1096/fasebj.27.1_supplement.876.1" @default.
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