The effects of hydrostatic pressure on cardiac conduction and excitability were studied in 39 rabbit right atrial preparations. Increases in pressure significantly increased atrial conduction time, i.e., 41% at 150 ATA. Excitability, determined from strength-duration (S-D) curves, was depressed by pressure. The slope constant of the S-D curve increased 64% at 150 ATA. Rheobase and the X-asymptote were not affected significantly. The depression of excitability partially accounted for the slowed conduction. Frequency stress and pressure had an additive effect to produce even greater decreases in excitability and increases in conduction time. Atrial refractoriness to premature stimuli also increased as a function of pressure. Nitrous oxide (2.5 ATA) partially reversed the effects of 150 ATA of pressure on conduction time and excitability. The results suggest that pressure acts by altering basic functional components of the myocardial cell membrane. Some of these changes, particularly when combined with frequency stress, i.e., rapid heart rate, may pose a serious threat to humans exposed to hyperbaric environments.