Abstract
Quinidine increases the refractory period and depresses both the rate and amplitude of beat of isolated rabbit atria. These effects can be enhanced by elevating the K content of the medium twofold and completely blocked by lowering the K to one-sixteenth the normal amount. Small amounts of acetylcholine act in a manner similar to low K. These observations suggest that quinidine produces its effects by depressing outward flux of K ions. Ion transport studies revealed this to be the case. The hypotheses that quinidine in final analysis acts by blocking the intracellularly released acetylcholine is presented and discussed.

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