Electrical slow waves in colonic myocytes are due in part to inward Ca current, which may explain the relationship between slow waves and contractions.
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Supports Ca2+ current role in animal colonic slow waves; leaves open applicability to human GI motility.
Canine colonic myocytes were studied with the whole cell patch-clamp technique. In 1.8 mM Ca2+, inward currents were evoked by depolarization. Currents activated positive to -50 mV, peaked at approximately 0 mV, and reversed at approximately +50 mV. Inward current was potentiated by high external Ca2+ concentration and BAY K8644 and was decreased by low external Ca2+, nifedipine, and Mn2+, indicating that the current was carried by Ca2+. Overlap of the activation-inactivation properties indicated a "window current" range (-40 to -20 mV) in which inward current might be sustained for long durations at potentials achieved during electrical slow waves. Voltage-clamp protocols simulating physiological depolarizations elicited sustained inward currents. Maximum changes in intracellular Ca2+ resulting from sustained inward currents were calculated, which suggested that depolarizations at the level of slow waves may increase cell Ca2+ sufficiently to cause contraction. The data suggest that electrical slow waves in colonic myocytes are due in part to inward Ca current. This current appears to be sufficient to explain the relationship between slow waves and contractions and provides an explanation for the mechanical threshold in colonic muscles.
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Langton et al. (1989) studied this question.
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