The role of Ca2+ in myogenic and neural activation in canine ileum circular muscle (CM) was studied during simultaneous recordings of contractile and electrical activity in cross-sectioned slabs of muscularis externa or of isolated CM with deep muscular plexus (DMP) intact. Ca(2+)-free Krebs solution abolished inhibitory junction potentials (IJP) and contractions before changes in CM membrane potentials and while slow waves (SW) persisted at lower amplitude and frequency. This medium abolished SW more rapidly in isolated CM than in intact muscle strips and affected triggered SW (TSW) by 100-ms pulses recorded near myenteric plexus or near DMP differentially in the full-thickness preparation; TSW did not occur in isolated CM. Ni2+, a nonselective Ca2+ channel antagonist, left IJP unchanged and reduced contractions, frequencies, and amplitudes of spontaneous SW and TSW, but increased their durations. Nifedipine abolished contractions but SW, TSW, and IJP were unaffected. Cyclopiazonic acid (CPA) increased SW frequency, produced spikes on SW plateaus, and increased CM tone, but did not affect IJP or resting membrane potentials. In nifedipine-pretreated strips, CPA decreased SW frequencies and amplitudes, evoked less tone, depolarized membrane potentials, and left IJP unaltered. The neuronal N-type Ca2+ channel blocker omega-conotoxin GVIA abolished IJP, without affecting SW or TSW. We conclude that Ca2+ influx, not through L- or N-type Ca2+ channels, helps initiate ileal SW; L-type Ca2+ channels provide Ca2+ for contraction and N-type Ca2+ channels provide Ca2+ for IJP mediator release. Frequencies of SW may be modulated by uptake of Ca2+ into pacemaker stores.