Electrical slow waves determine the timing and force of peristaltic contractions in the stomach. Slow waves originate from a dominant pacemaker in the orad corpus and propagate actively to the pylorus. The mechanism of slow wave propagation is controversial. We tested whether Ca²⁺ entry via a voltage-dependent, dihydropyridine-resistant Ca²⁺ conductance is necessary for active propagation in canine gastric antral muscles. Muscle strips cut parallel to the circular muscle were studied with intracellular electrophysiological techniques using a partitioned- chamber apparatus. Slow wave upstroke velocity and plateau amplitude decreased from the greater to the lesser curvature and this corresponded to decreased density of interstitial cells of Cajal in the lesser curvature. Slow wave propagation velocity between electrodes impaling cells in 2 regions of muscle and slow wave upstroke and plateau were measured in response to experimental conditions that reduce the driving force for Ca²⁺ entry or block voltage-dependent Ca²⁺ currents. Nicardipine (0.1-1 µM) did not affect slow wave upstroke or propagation velocities. Upstroke velocity, amplitude and propagation velocity were reduced in a concentration-dependent manner by Ni²⁺ (1-100 µM), mibefradil (10-30 µM) and reduced extracellular Ca²⁺ (0.5 to 1.5 mM). Depolarization (by 10-15 mM K⁺) or hyperpolarization (10 µM pinacidil) reduced upstroke and propagation velocities. The higher concentrations (or lowest Ca²⁺) of these drugs and ionic conditions tested blocked slow wave propagation. Treatment with cyclopiazonic acid to empty Ca²⁺ stores did not affect propagation. These experiments show that voltage-dependent Ca²⁺ entry is obligatory for the upstroke phase of slow waves and active propagation.