Pharmacological inhibition of PKC attenuates βAR enhancement of
CICR. A, IP3R inhibition with 2-APB (20
μm, 5 min pre-treatment) does not inhibit βAR-dependent
increases in Ca2+ transient amplitude
(Δ405/485). Ca2+ transients were measured
in the absence and presence of 1 μm isoproterenol. Data are
pooled from 10 to 15 cells per treatment condition. Results are average
(±S.E.). B and C, PKC inhibition (1 μm
BIM, 5 min pre-treatment) significantly blunts (B) isoproterenol- and
(C) cpTOME-induced increases in Ca2+-transient amplitude
in PLCε+/+, but not PLCε–/–
cardiac myocytes. BIM did not affect naïve Ca2+ transient
amplitude. Data were pooled from 20–40 cells for each treatment
condition from n = 3 PLCε+/+ and n = 2
PLCε–/– mice. Results are average (±S.E.);
***, p < 0.001; #, p < 0.001 for
PLCε–/– response compared with
PLCε+/+; ns is not significant; one-way ANOVA,
Bonferroni post test.