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. Author manuscript; available in PMC: 2010 Mar 11.
Published in final edited form as: Prog Biophys Mol Biol. 2009 Jan 30;98(2-3):161–170. doi: 10.1016/j.pbiomolbio.2009.01.010

Fig. 3.

Fig. 3

The effects of IK(ACh) on the human atrial action potential waveform. (A) Simulated action potentials (APs) corresponding to the control (no IK(ACh)) and to superfusion with 10 nM ACh (data shown in red). The stimulation protocol employed a 310 pA stimulus current lasting 6 ms at a basic cycle length of 1 s (1 Hz). As shown by the red trace, activation of IK(ACh) hyperpolarizes the resting membrane potential (RMP) and abbreviates the action potential duration (APD). (B) Note that 10 nM ACh results in delayed activation of the human atrial myocyte AP (indicated by arrow). However, there is no decrease in the amplitude of the delayed AP. (C) Concentration–response relationship for [ACh] vs. RMP in the human atrial myocyte. In this and all subsequent panels the control value is marked with an asterisk. (D) Concentration–response relationship of [ACh] vs. dV/dtmax of the human atrial myocyte. (E) Concentration–response relationship of [ACh] vs. action potential amplitude (APA) of the human atrial myocyte. (F) Concentration–response relationship of [ACh] vs. action potential duration at 90% repolarization (APD90) of the human atrial myocyte.