Abstract

The influence of cholinomimetic drugs on the release of previously accumulated 86Rb +-ions was studied in guinea pig isolated atria, incubated in a K +-free Tyrode solution, containing an equivalent concentration (2.7 mM) of Rb +. In this medium the atria showed entirely normal mechanical behaviour. Both acetylcholine and carbachol caused a pronounced, dose-dependent acceleration of 86Rb-release in electrically driven atria. The effect was blocked by atropine. High doses of acetylcholine and carbachol in the presence of atropine caused a positive inotropic effect, accompanied by an increased rate of 86Rb-release. Both effects were probably brought about by the mobilization of endogenous noradrenaline, since they were completely abolished in reserpinized animals. Diisopropylfluorophosphate (DFP) showed a negative chronotropic and inotropic action only in spontaneously beating atria. The effect was accompanied by an accelerated release of 86Rb. However, DFP in high doses neither affected the mechanical activity nor the rate of 86Rb-release in electrically driven atria (frequency 180/min). This observation might be explained by the depletion of acetylcholine of the atrial tissue as a result of electrical stimulation. It was concluded that cholinomimetic drugs increase the rate of 86Rb-release.

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