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1. Circular muscle strips of the guinea-pig gastric muscle produced spontaneous electrical activity in the form of slow waves. The slow wave amplitude, maximum rate of rise, duration, and frequency were 31 mV, 60 mV sec-1, 4.3 sec, and 4.3 min-1 on average, respectively. These parameters were not appreciably affected by 3 microM nifedipine or nicardipine, even following membrane depolarization with 60 mM K+. 2. Ni2+ (1-100 microM) increased slow wave amplitude and frequency, but reduced the rate of rise, accompanied by membrane depolarization. The rate of rise and depolarization slowly recovered to the control values in the continuous presence of Ni2+, but slow wave frequency remained high. The recovery after wash-out was very poor particularly when a high concentration of Ni2+ was applied. 3. The effects of Co2+ were fundamentally the same as those of Ni2+. 4. Removal of external Ca2+ slowly reduced the rate of rise and amplitude of the slow waves in the absence and the presence of Ni2+ and Co2+, although the effects were reduced in the presence of these metal ions. 5. Concentrations of Ni2+ and Co2+ greater than 1 mM suppressed the slow waves. However, when the external Na+ was replaced with N-methyl-D-glucamine during the suppression, nearly normal electrical activity was resumed. 6. Since slow waves were not significantly affected by nifedipine (3 microM) and Ni2+ (100 microM), the inward currents generating slow waves do not seem to flow through L-type Ca2+ channels or typical T-type Ca2+ channels. Slow waves are probably potentiated by Ni2+ and Co2+ acting intracellularly. These ions at higher concentrations seem to inhibit the pacemaker activity more powerfully than they do the inward currents responsible for slow wave generation.

The Effects of Nickel and Cobalt Ions on the Spontaneous Electrical Activity, Slow Wave, in the Circular Muscle of the Guinea-pig Gastric Antrum.