Effect of Class I (a, b, + c) drugs on Pacemaker cells?
In FA, and other books I've used, an effect of these drugs has been described (decreasing the slope of phase 4 depolarization)
But the Kaplan Lecturer for Pharmacology made an interesting point: the RMP in Pacemaker cells was less negative, in comparison to the more negative RMP in ventricular and atrial muscle cells.
And that Na channels tend to be in the 'ready' state, and more ready to depolarize when at the more negative potential (ventricular/atrial muscle cells).
And because the RMP is partly depolarized in SA and AV nodes (relative to ventricular/atrial muscle cells), any Na channels present there, would be inactive to begin with. This was the Kaplan Guys reasoning, and it made sense, and it helped reinforce the concept that cells 'maintained' in a sort of deplarized state, will keep their fast Na channels 'inactive'.
Is this a good way to think of it?