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.