Studies on the inhibitory effect of ouabain on the release of [3H]-noradrenaline from the rat heart.

In the rat Langendorff heart perfused with Krebs solution and prelabeled with [3H]-noradrenaline, ouabain caused arrhythmia as well as significant inhibition of spontaneous and electrically stimulated release of tritium. However, there is no causal relationship between the inhibition of tritium release and the occurrence of arrhythmia. Chromatographic analysis of the labeled perfusate suggests that ouabain reduced intact [3H]-noradrenaline fraction obtained during electrical stimulation. The inhibitory effect of ouabain on electrically stimulated release was completely antagonized by atropine, but not by indomethacin and phenoxybenzamine. However, none of the above agents antagonized the inhibitory effect of ouabain on spontaneous tritium release. Infusion of acetylcholine also inhibited electrically stimulated tritium release, and this effect was largely abolished by atropine. Thus it appears that in high concentrations, ouabain may release acetylcholine, which in turn activates presynaptic muscarinic inhibitory receptors leading to inhibition of noradrenaline release from the rat heart.