The Shape of the Electrical Action-Potential Upstroke

Abstract

See related article, pages 277–284 Since the first measurement of an action potential from cardiac tissue by Coraboeuf and Weidmann in 1948,1 the biological information contained in its shape has been the subject of many theoretical and experimental studies. In the context of the article published by Hyatt et al2 in the current issue of Circulation Research , describing the role of the shape of an optical action-potential upstroke, it seems important to define the action potential of a cardiac cell. An action potential, in the classical sense of the term, is caused by the change in transmembrane potential of a cardiac cell during excitation. It is usually measured from a very small site with a microelectrode (diameter <1 mm) or with a voltage-sensitive dye (smallest membrane area 6×6 mm).1,3 It is not disputed that the upstroke of the normal cardiac action potential is caused by the flow of ions through channels specific for Na+.4 In the sinoatrial node and the inner zone of the atrioventricular node, ionic current through the L-type Ca2+ channel may play an additional role (see Kleber et al5). In the setting of isopotentiality of the cell membrane (created artificially by voltage clamp) the ionic current during a subsequent action potential will change the charge distribution at the lipid membrane bilayer. Expressed in terms of a simple biophysical model, the change in membrane potential, dV/dt, is proportional to ion current flow and the steepest portion of the action-potential upstroke, dV/dtmax, occurs at maximal Na+ flow.4 In the case of a propagated action potential, the situation is more complex. Here, the net ionic charge flowing through channels and exchangers incorporates 2 components, a first component changing the membrane capacity and producing the action-potential upstroke …