Proposes an electric field model as an alternative mechanism for cell-to-cell propagation in cardiac and smooth muscle, challenging the necessity of gap junctions.
Challenges gap junction-centric models in cardiac propagation; leaves open electric field mechanism as hypothesis-generating for targeted studies.
Cardiac muscle and visceral smooth muscle are similar in some regards, in that both tissues are composed of relatively short individual cells that interact in some way to allow the spread of excitation over all or much of the tissue, bringing about a synchronized and nearly simultaneous contraction of the cells to subserve a specific physiologic function. A prevailing view is that these short muscle cells possess low‐resistance interconnections, which allows local‐circuit action current to flow readily from one cell to the next, thereby allowing the propagation of excitation over the entire tissue. The gap junctions, which are observed morphologically, are thought to contain numerous low‐resistance connections. However, gap junctions are not observed in hearts of lower vertebrates or in some visceral smooth muscles. Therefore, the questions arise of what their role is in propagation and whether an alternative mechanism for transfer of excitation from cell to cell might apply in some normal physiologic circumstances and in some pathophysiologic conditions. The case for such an alternative mechanism that is electrical in nature, but does not require low‐resistance connections, is presented here. The arguments in support of low‐resistance coupling in smooth muscle are provided by Alex Bortoff in his accompanying article.
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Nicholas Sperelakis (1991) studied this question.
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