Rhythmic contractions generating transit in the digestive tract are paced by a network of cells called interstitial cells of cajal (ICC-MP) found in the myenteric plexus. ICC generate cyclic depolarizations termed slow waves that are passively transmitted to the smooth muscle to initiate contractions. The opening of L-Ca²⁺ channels are believed to be primarily responsible for the influx of calcium generating a contraction in smooth muscle. However, L-Ca²⁺ channels are not thought to be important in generating the pacing current found in ICC. Using intact segments of circular (CM) and longitudinal (LM) muscle from wild-type and W/W^V mice, we found that L-Ca²⁺ channel currents are required for pacing at normal frequencies to occur. Application of 1 µM nicardipine caused a significant decrease in contraction amplitude and frequency in LM and CM that was successfully blocked with Bay K 8644. Nicardipine also abolished the pacing gradient found throughout the intestines, resulting in a uniform contraction frequency of 30-40 per min. Stimulating L-Ca²⁺ channels with Bay K 8644 neither removed nor recovered the pacing gradient. W/W^V mice, which lack ICC-MP, also exhibited a pacing gradient in longitudinal muscle. Application of nicardipine to LM segments of W/W^V mouse intestine did not reduce pacing frequency, and in jejunum resulted in a slight increase. Bay K 8644 did not affect pacing frequency in W/W^V tissue. In conclusion we found that L-Ca²⁺ channel activity was required for normal pacing frequencies and to maintain the pacing frequency gradient found throughout the intestines in wild type but not in W/W^V mouse intestine.