When the vagus nerves are stimulated with one burst of pulses per minute, but each burst is placed at a different time in the cardiac cycle, a "vagal effect curve" can be derived which displays the changes in cardiac cycle length (CCL) as a function of the elapsed time from the stimulus. This curve consists of a primary and a secondary phase of increased CCL. We performed experiments on open-chest anaesthetised dogs to test the hypothesis that the secondary phase of increased CCL is caused by an increase in the activity of the electrogenic Na+/K+ pump. In animals with a sinoatrial nodal rhythm (SANR), the mean peak values of the primary and secondary phases of increased CCL were 0.48 +/- 0.03 and 0.06 +/- 001 s, respectively, above the prestimulation level (0.52 +/- 0.01 s). Ouabain (40 micrograms X kg-1 iv) did not significantly alter this bimodal response. In animals with an atrioventricular junctional rhythm (AVJR), the peaks of the primary and secondary increases in CCL were 0.55 +/- 0.03 and 1.04 +/- 0.17 s, respectively, above the prestimulation level (0.72 +/- 0.02 s). In animals with AVJR, ouabain markedly attenuated the peak secondary increase in CCL to 19% of the corresponding control value. This attenuation supports the hypothesis that the prominent secondary increase in CCL evoked by a brief vagal stimulus during AVJR is ascribable to an increased activity of the electrogenic Na+/K+ pump.