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A theoretical study of myoendothelial communication: K+‐mediated EDHF signaling and the role of myoendothelial projections

Experiments indicate that a small increase in the extracellular potassium concentration ([K+]o) may act as endothelium‐derived hyperpolarizing factor (EDHF). This hypothesis has been challenged by some studies and has received little theoretical analysis. Here we examine K+‐induced hyperpolarizations in mathematical models of isolated and integrated endothelial and smooth muscle cells. The effect of various components on the response is examined, including the role of channels, pumps, and the presence of distinct microdomains in myoendothelial projections. Activation of the sodium‐potassium pump by K+ generates only transient hyperpolarization and a rebound depolarization when [K+]o is restored. Activation of inward rectifying potassium channels by K+ could produce strong and sustained hyperpolarization, but the cell had to be initially depolarized. A large number of inward rectifying potassium channels introduces a bistable behavior and prevents return to resting state. K+‐mediated EDHF was small under most of the examined scenarios, including localization of important components in the myoendothelial projections. These results suggest a rather minor role for extracellular K+ as EDHF, but may also indicate limitations of the current electrophysiological models. [Supported by AHA grant NSDG043506N and NIH grant HL095101]