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

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Abstract
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.