Fig. 6. Sinus dysrhythmia and sinoatrial Ih in HCN2-deficient mice. (A) Telemetric ECG recordings (lead II) obtained simultaneously from wild-type and HCN2-deficient mice at rest. (B) RR intervals from wild-type and HCN2-deficient mice at rest (r) and during spontaneous physical activity (a) plotted against time. (C) Ih in sinoatrial node cells. Averaged current traces from wild-type (solid lines) and HCN2–/– mice (dashed lines) under control conditions and in the presence of 100 µM cAMP in the pipette solution. (D) Characterization of Ih. Currents were evoked by 3 s pulses to a range of test potentials from a holding potential of –40 mV. Current amplitudes at the end of the pulse are plotted against the test potential (58 wild-type cells, 60 HCN2 knockout cells, P < 0.05 at all potentials). (E) Maximum diastolic potentials (MDPs) determined from action potentials of isolated sinoatrial node cells. The inset shows an example of action potentials recorded from an HCN2-deficient cell. Scale bars: 200 ms, 20 mV. *P < 0.05 versus wild-type. (F) Beating of isolated heart atria. The standard deviation (SD) of atrial beat-to-beat intervals is a measure of dysrhythmia. *P < 0.05 versus wild-type. ISO, isoproterenol. Mean beating frequency was not significantly different between the three groups.