Figure 7.

Effect of β₁-adrenoceptor and β₃-adrenoceptor treatments on ERK1/2, p38 MAPK, stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) and Akt activation in neonatal rat cardiomyocytes. The cells were untreated or treated with 10 µM dobutamine in the presence of 1 µM ICI 118551 (β₁-AR treatment), or 2 µM CL-316243 (β₃-AR treatment) for 24 h. Following the treatments, cell lysates were analysed by Western blotting as described under Methods using phospho-specific antibodies. The same samples were also analysed on separate blot using an antibody that recognizes both unphosphorylated (total) and phosphorylated kinases to confirm equal loading on each lane. Data are expressed as percentage of the untreated control following the calculation of the phosphorylated/total ratio for each lane. The combined results (panel A for ERK1/2, panel B for p38 mitogen-activated protein kinase, panel C for SAPK/JNK and panel D for Akt) obtained from densitometric analysis of blots, represent the mean ± SEM of for to six independent experiments. *P < 0.05 and **P < 0.01, (a) versus untreated control, (b) versus β₁-adrenoceptor treated cells.