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The effects of severe calcium deficiency and calcium excess on transmembrane potentials in isolated frog ventricular strips have been investigated. Resting potential rose about 5 mv above normal during perfusion with three times normal calcium and fell about 4 mv below normal during exposure to calcium-free Clark's solution. Mean overshoot rose about 3 mv during calcium lack, but was unaffected by excess calcium. Maximum depolarization rate increased about 20% during calcium deprivation and fell a similar amount during high calcium perfusion. However, the membrane potential at the moment of maximum depolarization rate was unchanged from normal by either experimental solution. High calcium augmented the "spike" and "plateau" during repolarization, while calcium deficiency abolished the spike, producing "hump-backed" action potentials with prolonged membrane reversal. These results are discussed, especially in relation to possible permeability changes during upstroke of the action potential.

Intracellular potentials from isolated normal frog hearts were measured in a series of 29 experiments, using microelectrodes of less than 1 micron tip diameter, a cathode follower input, direct coupled amplifier, and photographic registration of an oscilloscope trace. The perfusion fluid was Clark's solution, containing 1.08 mm calcium and 1.88 mm potassium. The average of 485 measurements of the normal resting potential was 84.5 mv. The average of 421 measurements of overshoot was 18.9 mv; and the average of 421 measurements of action potential was 102.5 mv. In eight experiments, including 141 values, the maximum depolarization rate was determined, using a graphical method of analysis. The average maximum upstroke velocity was 33.9 v/sec. The voltage-time curve of the action potential during the repolarization sequence showed considerable variation from fiber to fiber, but in most cases some evidence of a ‘spike’ component was seen.

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