Figure 6.

Temporal and pharmacological profiles of CaMKII activation in response to β₁AR stimulation. (a) In Adv-β₁AR–infected β₁β₂ DKO myocytes, β₁AR stimulation (1 μM ISO for 6 hours) increased CaMKII autophosphorylation. This effect was blocked by KN93 (5 μM) but not by the PKA inhibitor PKI (5 μM). Similar results were obtained in three other experiments. (b) Time course of ISO-induced increase in CaMKII activity assayed by ³²P incorporation into a specific peptide substrate of the kinase (see Methods; n = 4 for each data point). (c) Pharmacological profile of CaMKII activation (n = 4–6). *P < 0.01 vs. cells in the absence of ISO or those in the presence of KN93, AIP, or nifedipine. P-CaMKII, autophosphorylated CaMKII.