INTRODUCTION:Despite widespread use of the contact electrode for recording monophasic action potentials (MAPs) in both clinical and experimental research, the mechanism underlying the genesis of the contact MAP remains unproven. The "Franz hypothesis" assumes that the MAP is driven by a current source originating at the boundary between cells depolarized by the MAP electrode pressure and normal cells immediately adjacent to it. To date, no direct experimental data exist to support this hypothesis. METHODS AND RESULTS:In 10 Langendorff-perfused mouse hearts, a miniaturized MAP probe was inserted into the right ventricle (RV) and gently pressed against the endocardium of the upward-facing RV free wall. During stable contact and stable MAP recording, KCl-filled glass microelectrodes were lowered from above the RV to record transmembrane action potentials (TAPs) at the center of and 0.05 and 0.2 mm outside the perimeter of the MAP electrode contact site. TAPs at the center had normal resting potentials (RP) in epicardial layers (-78 +/- 4 mV) but showed gradual decrease toward deeper layers, reaching a minimum RP of -23 +/- 0.8 mV directly above the MAP electrode surface. RPs at 0.05 mm outside the MAP perimeter were normal at the epicardial surface and with increasing transmural depth showed significantly less decrease than central recordings (min RP -41 +/- 0.8 mV, n = 11, P < 0.00001). TAPs at 0.2 mm from the MAP electrode perimeter had normal RPs across the entire RV wall. CONCLUSION:These direct data are the first to support the hypothesis that the MAP is generated locally through pressure depolarization of a circumscript volume of cells that (1) has sharp voltage gradients toward normal cells, (2) provides a strong local current source, and (3) when simulated with a circuit model creates the field potential recorded by the contact MAP electrode.