Reduction in42K‐Efflux from Rat Atria by Promazine and Thioridazine

Rat left atria were suspended for one hour in Ringer solution containing approximately 6 μci/ml42K. They were then transferred to a constant flow apparatus and the42K‐efflux was determined by measuring the radioactivity in the effluent. The mechanical activity was recorded simultaneously. The atria were driven by electrical stimulation at 180 beats per min. In normal Ringer solution a constant decrease in potassium efflux, assumed to reflect the transfer of42K through the cell membranes, was obtained after about 15 min. The addition of promazine 5 × 10‐6M to 5 × 10‐5M and thioridazine 10‐5M to 5 × 10‐5M to the Ringer solution caused a dose dependent reduction in42K‐efflux and in the amplitude of the atrial contractions. A reduction in the extracellular potassium concentration decreased, while an increase of the extracellular potassium concentration increased the42K‐efflux. The per cent reduction in42K‐efflux caused by promazine 5 × 10‐5M was almost the same under these experimental conditions, whereas the depressant action of the drug on the atrial contractile force increased with increasing concentrations of potassium. No direct proportionality between the reduction in42K‐efflux and the reduction in contractile force caused by promazine was found. It is concluded that the decrease in42K‐efflux caused by the drug is due to a reduced membrane permeability for this ion, and that the decrease in contractile force can be dissociated from this effect.