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. 2001 Jun 1;533(Pt 2):329–340. doi: 10.1111/j.1469-7793.2001.0329a.x

Figure 6. Contribution of PKG, PDE3 and PDE2 to the inhibitory effect of cGMP on ICa in human atrial myocytes.

Figure 6

A, each symbol corresponds to a measure of ICa at 0 mV obtained every 8 s. The cell was first dialysed with intracellular GTP-free solution. Intracellular dialysis with 0.5 μm cGMP (first arrow) resulted in the usual stimulation of ICa, and switching to 5 μm cGMP (second arrow) partially reversed this stimulatory effect. Superfusion of the cell with KT 5823 (100 nm) or cilostamide (100 nm) had little or no effect on ICa, whereas EHNA (30 μm) restored the amplitude of the current observed in the presence of 0.5 μm cGMP. B, summary of several experiments similar to those shown in A. The effect of cGMP (0.5 μm, □; 5 μm, ▪) on ICa is shown in the absence or presence of KT 5823 (100 nm), cilostamide (100 nm) or EHNA (30 μm). The size of the bars indicates the mean effects expressed as percentage increase over basal ICa, and the lines the s.e.m., with the number of experiments indicated above. ** P < 0.01, *** P < 0.005, statistically significant differences using Student's t test.