Dependence of electrical slow waves of canine colonic smooth muscle on calcium gradient

1. The ionic dependence of the upstroke and plateau components of slow waves of canine colonic circular muscles was studied. 2. Reduced extracellular Ca2+ caused a decrease in the amplitude of the upstroke and plateau components, a decrease in the depolarization velocity, and a decrease in frequency. The reduction in the upstroke phase per 10-fold reduction in external Ca2+ was close to the value predicted by the Nernst relationship, suggesting that the membrane permeability to Ca2+ increases steeply during this phase. 3. Nifedipine (10(-9)-10(-6)) reduced the plateau component, but concentrations of 10(-6) M did not abolish the upstroke component. The data suggest that a nifedipine-resistant component of Ca2+ current may be involved in the upstroke. 4. Inorganic Ca2+ channel blockers (Mn2+ and Ni2+) blocked spontaneous slow waves at concentrations of 1.0 mM or less. 5. The upstroke component was more sensitive to Ni2+ than to Mn2+; a concentration of 0.040 mM-Ni2+ caused more than a 50% reduction in upstroke velocity. Ni2+ also reduced the plateau phase of slow waves. 6. The results suggest that the upstroke and plateau components of slow waves are dependent upon activation of voltage-dependent Ca2+ currents. The current responsible for the upstroke is partially resistant to dihydropyridines (at least at 10(-6) M). The current responsible for the plateau component is nifedipine-sensitive.