Modeling electrical communication in large resistance arteries: Implications to the EDHF phenomenon

Large resistance arteries consist of one layer of endothelial cells and several layers of smooth muscle cells. In these arteries, the single endothelial layer can hyperpolarize, in a near parallel manner, the multiple smooth muscle layers. To ascertain whether charge movement through myoendothelial gap junctions is sufficient to enable smooth muscle hyperpolarization, electrical communication was examined in a series of computational arteries comprised of one layer of endothelium and 1–7 layers of smooth muscle. In our model, each vascular cell was treated as the electrical equivalent of a capacitor, (i.e. the cell membrane), coupled in parallel with a non‐linear resistor, (i.e. the cell's net ionic conductance); intercellular gap junctions were represented by ohmic resistors. Simulations revealed that the endothelium could hyperpolarize, in a sufficiently parallel manner, arteries comprised of 1–3 layers of smooth muscle. As the number of smooth muscle layers increased from 4 to 7, a substantive voltage differential arose between the endothelium and the multiple layers of smooth muscle. The inclusion of a smooth muscle inward rectifying K + current into our model eliminated this voltage disparity. Likewise, a subtle reduction in smooth muscle inward current also restored the endothelium's ability to effectively hyperpolarize multiple layers of smooth muscle. These observations highlight that with little myoendothelial coupling, the endothelium can hyperpolarize, in a near parallel manner, several layers of smooth muscle. In large arteries, there is no biophysical requirement for the endothelium to produce paracrine factors to electrically activate smooth muscle. Funded by AHFMR and HSFC.