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. Author manuscript; available in PMC: 2008 Jan 15.
Published in final edited form as: Circ Res. 2006 Mar 23;98(8):1081–1088. doi: 10.1161/01.RES.0000218493.09370.8e

Figure 4.

Figure 4

PDE regulation of cAMP signals from β1-AR and β2-AR. A and C, Time course of ICNG in ARVMs expressing C460W/E583M CNGA2. The cells were first superfused with control external Ringer and then challenged with the drugs during the periods indicated by the solid lines. B and D, Summary of the results obtained in a series of experiments as in A and C, respectively. Specific activation of β1-AR and β2-AR as in Fig. 1. Selective PDE3 inhibition by cilostamide (Cil, 1 μmol/L) or selective PDE4 inhibition by Ro 20-1724 (Ro, 10 μmol/L) strongly potentiated cAMP triggered by β1-AR. Upon activation of β2-AR, robust cAMP accumulation necessitated concomitant PDE3 and PDE4 blockade. Experiment was ended with application of 100 μmol/L L-85. .Statistically significant differences as in figure 3.