The phenomenon of atrioventricular (AV) nodal "facilitation," described in traditional "black box"-functional studies, implies enhanced AV nodal dromotropic function. We investigated the role of atrial prematurities in the modulation of the nodal cellular responses in the mechanism of AV nodal facilitation. Atrial and His (H) bundle electrograms and microelectrode recordings from proximal AV nodal cells were analyzed in 15 superfused rabbit AV node preparations. The pacing protocol consisted of 30 basic beats (S₁; coupling interval S₁-S₁ = 300 ms) followed by a facilitating prematurity (S₂; coupling intervals S₁-S₂ of 300, 200, 150, and 130 ms) followed by the test beat (S₃; coupling interval S₂-S₃ scanned in 5-ms steps). Conduction curves (S₂-H₂ vs. S₁-S₂, S₃-H₃ vs. S₂-S₃, and S₃-H₃ vs. H₂-S₃) were constructed. Facilitation (i.e., shortening of S₃-H₃ when S₁-S₂ was shortened) was demonstrated in all preparations using the H₂-S₃ (P < 0.001) but not the S₂-S₃ format. Microelectrode recordings revealed a causal relationship between the improved proximal AV nodal cellular responses in facilitation and the prolonged S₂-S₃ interval. There was no evidence for enhanced nodal dromotropic function directly resulting from the introduction of the facilitating beats. Thus facilitation is based on inherent cycle-length-dependent properties of the AV node during application of a complex pacing protocol and primarily reflects the uncontrolled modulation of the proximal cellular response.