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. 2021 Oct 9;2(6):zqab051. doi: 10.1093/function/zqab051

Figure 1.

Figure 1.

NO inhibits TRPM4 channel activity by activating the NO/cGMP/PKG signaling cascade. (A) Representative trace from a perforated patch-clamp experiment demonstrating that TICC activity, induced by applying negative pressure (−20 mmHg) through the patch pipette to stretch the plasma membrane, is blocked by the selective TRPM4 inhibitor 9-phenanthrol (30 µM). (B) Summary data demonstrating that TICC activity is inhibited by 9-phenanthrol (*P < .05; n = 6 cells from four animals). (C) Representative trace from a perforated patch-clamp experiment showing the effects of SNAP (100 µM) on TICCs induced by application of negative pressure (−20 mmHg) through the patch pipette. (D) Concentration–response curve for the inhibition of TICCs by SNAP (n = 5 cells from two animals per concentration). (E) Diagram depicting the NO/cGMP/PKG signaling cascade and pharmacological interventions. (F) Representative trace from a perforated patch-clamp experiment demonstrating that TICC activity induced by negative pressure (−20 mmHg) is significantly reduced by dibutyryl-cGMP (0.5 µM). (G) Summary data showing the significant reduction in TICC activity in response to dibutyryl-cGMP (*P < .05; n = 7 cells from four animals). (H) Representative trace showing that SNAP (30 µM) does not block TICC activity in the presence of the selective sGC inhibitor NS2028 (1 µM). (I) Summary data showing that NS2028 blocks the inhibitory effects of SNAP (n = 7 cells from five animals). (J) Representative trace showing that SNAP (30 µM) does not block TICC activity in the presence of the selective PKG inhibitor KT5823 (1 µM). (K) Summary data showing that KT5823 blocks the inhibitory effects of SNAP (n = 6 cells from four animals).