The safety role of gap junctions: a new perspective on atrio-ventricular nodal reentry.

In the normal heart, the atrio-ventricular node (AVN) is responsible for the appropriate atrio-ventricular delay. Most of the slow conduction in AVN is probably caused by the small number of gap junctions connecting the myocytes [1]. Experimental and theoretical studies show that although conduction velocity decreases by reducing gap junctions, in such conditions safety factor increases [2]. Disorderly arranged gap junctions in myocytes might contribute to alterations in conduction that are capable of precipitating reentry arrhythmias. Some evidences approve the dissimilar distribution of gap junction in different parts of AVN during AVN reentry. For example, some reports indicate the presence of few gap junctions between cells within the region of slow conduction through the AVN [3]. Previously we proposed that gap junctions are dynamic structures, which open and close in the diverse moments of each normal heart cycle, rather than being continuously open [4]. According to the aforementioned evidences, we suggest that besides the disordered distribution of gap junctions in AVN as a root of reentry, abnormal opening or closing of these gap junctions helps to generate a very low resistance pathway as a fast source for abnormal action potential propagation. According to previous results, we think that disordered distribution of gap junction in AVN provides a background for preparing two different pathways with different resistances. In this background, opening and closing of gap junctions may seriously affect the resistance of the two pathways. We assume that opening of gap junctions in the compact region, which is assumed to be the low resistance pathway, may be the main cause of AVN reentry. We assume that this view on gap junctions and their relation to reentry can be useful to design new drugs. Using substances that close AVN gap junctions during reentry, such as cardiac glycosides (with adequate concentrations) and nitric oxide, may be helpful for treating AVN reentry [5]. In such condition, closure of gap junctions in the AVN may not cause disorders because: