Fig. 6.
Activation of K-ATP K+ channels mediated the effect of isradipine on pacemaking. A. Representative cell-attached recordings of PPN CNs without or with chronic isradipine (500 nM, 1 h pre-incubation), before and after application of glibenclamide (100 nM) in the presence of the synaptic blockers picrotoxin and CNQX. Bar: 1 s. B–C. Firing frequency (B) and coefficient of variation (C) of PPN CNs with or without isradipine, before and after application of glibenclamide (B: Non-parametric one-way ANOVA, interaction *p = 0.0064; Dunn’s multiple comparison: control - + glibenclamide: NS; control - Isradipine: *p < 0.05; control - isradipine+glibenclamide: NS; Isradipine - + glibenclamide: *p < 0.05; isradipine+glibenclamide - + glibenclamide: NS; Isradipine - isradipine+glibenclamide: *p < 0.05. C: Non-parametric one-way ANOVA, interaction *p = 0.0087; Dunn’s multiple comparison: control - + glibenclamide: NS; control - isradipine: *p < 0.05; control - isradipine+glibenclamide: NS; isradipine - + glibenclamide: *p < 0.05; isradipine+glibenclamide - + glibenclamide: NS; Isradipine - isradipine+gliben-clamide: *p < 0.05; n = 7 in each group). Box plots indicate first and third quartiles, thick center lines represent medians, and whiskers indicate the range. D. Quantification of RNA abundance of Kir6.1, Kir6.2 and SUR subunits; n = 4 in each group. E. Cartoon illustrating the effect of Ca2+ entry through Cav1 channels and RYR Ca2+ release on Kir6/SUR1 channels.