It is unclear how the sinoatrial node (SAN) is electrically connected to atrial muscle so that it can drive the atrial muscle and not be electrotonically suppressed. The SAN connects to atrial muscle at the crista terminalis (CT), a bundle of atrial muscle. In the rabbit, the periphery of the SAN rises up one face of the CT before terminating (Fig. 1A) and there is potentially a large area of contact between the two tissues. However, it is possible that there is connective tissue separating the two, and the two are only electrically connected at the termination of the SAN. We have constructed an anatomical model of the SAN: a section through the rabbit SAN was discretised (resolution, 35 µm) to generate a two-dimensional discrete lattice model. Each node of the lattice is represented by a model of a SAN or atrial cell as appropriate (Zhang et al. 2000). In the SAN, C_m (cell capacitance) changes from 20 pF in the centre (distant from CT) to 65 pF in the periphery and ionic current densities are functions of C_m (Zhang et al. 2000). Each cell is electrically connected to its neighbours with a junctional conductance of 25 nS (SAN-SAN or SAN-atrial) or 175 nS (atrial-atrial). The length of electrical connection, L, between SAN and atrial muscle was varied between 0 and ~0.75 mm. When the SAN was separated from atrial muscle (L = 0), the action potential was initiated in the periphery of the SAN and it propagated to the centre. When the SAN was electrically coupled to atrial muscle (L > 0), the pacemaker activity of the periphery was electrotonically suppressed by the atrial muscle and the action potential was initiated in the centre (it then propagated to the periphery and atrial muscle). Depending on L, there were different behaviours (Fig. 1B).When L was small (L < 0.105 mm), the SAN showed pacemaking, but the current flowing from SAN to atrial muscle was too small to excite the atrial muscle. When L was greater (0.105 < L < 0.490 mm), the SAN showed pacemaking and the current flowing from SAN to atrial muscle was sufficient to excite the atrial muscle (however, over this range, an increase of L slowed the pacemaker activity of the SAN as a result of greater electrotonic suppression). Further increase of L (0.490 mm < L > 0.665 mm) resulted in exit block as a result of even greater electrotonic suppression, i.e. the SAN showed pacemaking, but failed to drive the atrial muscle. When L was even greater (L > 0.665 mm), the pacemaker activity of the SAN was abolished. We suggest that the connective tissue separating the SAN from atrial muscle ensures that there is an optimal amount of electrical connection between the two.

Figure 1. A, model of SAN. B, behaviour of SAN.

Zhang, H., Holden, A.V., Kodama, I., Honjo, H., Lei, M., Varghese, T. & Boyett, M.R. (2000). Am. J. Physiol. 279, H397-421.