Fig 4.
Inhibition of the effect of theophylline on guinea pig vagus sensory nerve depolarization. A, Theophylline inhibition of capsaicin (1 μmol/L)–induced depolarization in the presence of various ion channel blockers: paxalline (BKCa channel, n = 5), apamin (SK channel, n = 5), clotrimazole (IK channel, n = 4), glibenclamide (KATP channel, n = 5), and vehicle (0.1% dimethyl sulfoxide, n = 7). Data are expressed as means ± SEs. *P < .05 and **P < .01 using 1-way ANOVA with the Bonferroni multiple comparison post hoc test. B, Inhibitory effect of NS309 (SK channel opener) on capsaicin-induced depolarization (n = 4-6). C, Point and line graphs showing the inhibition of capsaicin-induced depolarization by NS309 (30 μmol/L; left panel, n = 4) and the reversal induced by preincubation with the SK blocker UCL1684 (10 μmol/L; right panel, n = 3). D, Representative traces showing responses to capsaicin (1 μmol/L, solid triangles) recorded by using human vagus nerve before and after incubation with theophylline (10 μmol/L) in the presence of vehicle (0.1% dimethyl sulfoxide, top trace) or the SK channel blocker apamin (1 μmol/L, bottom trace, n = 4). E, Effect of vehicle, apamin, or clotrimazole on theophylline-induced inhibition of capsaicin-induced depolarization of human vagus nerve (n = 4). Data are expressed as means ± SEs. *P < .05 after analysis with the paired t test.