a–c Representative traces of EJPs in individual tissues stimulated with trains of five stimuli at 1 Hz. The zinc ionophore, pyrithione (Pyr, 3 µM) produced hyperpolarization and accelerated the decay time of EJPs (a), whereas the zinc chelator TPA (30 µM) induced the reverse response (b) and neutralized the effects of pyrithione (c). Insets are amplitude-normalized, expanded overlaid traces of the 5th EJP with/without treatment. d, e Changes in resting membrane potential (d) and membrane conductance (calculated from the 5th EJP; e) caused by pyrithione alone and with the following pretreatment: TPA (30 µM, zinc chelation), capsaicin (Caps; 10 µM; sensory nerve desensitization), BIBN4096 (BIBN; 1 µM; inhibition of CGRP receptors), glibenclamide (Glib; 3 µM; blockade of KATP channels), HC030031 (HC; 50 µM; inhibition of TRPA1) or ruthenium red (RuRed; 10 µM; inhibition of TRPA1), and capsazepine (Czpn; 10 µM; inhibition of TRPV1). Error bars are SEM. *Statistically significant, Brown–Forsythe–Welch ANOVA [F(7, 13.93) = 8.659, p = 0.0004 in (d) and F(7, 18.36) = 28.63, p < 0.0001 in (e)] with Dunnett T3 post-test vs. pyrithione. f–i Effects of pretreatment alone on EJP time course. d, e n = 6 arteries from separate rats.