Reduction in 42 K-efflux from rat atria by promazine and thioridazine.

Abstract

Rat left atria were suspended for one hour in Ringer solution containing approximately 6 μci/ml 42K. They were then transferred to a constant flow apparatus and the 42K‐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 of 42K 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 in 42K‐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 the 42K‐efflux. The per cent reduction in 42K‐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 in 42K‐efflux and the reduction in contractile force caused by promazine was found. It is concluded that the decrease in 42K‐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.