Cardiac glycosides such as ouabain inhibit Na+-dependent high-affinity noradrenaline uptake in sympathetic nerve terminals by interacting with (Na++K+)ATPase located in the neuronal membrane1–3. It has been suggested that the augmentation of noradrenaline concentration at the neuromuscular junctions following the inhibition of its uptake may contribute to the ouabain-induced cardiac arrhythmia seen with toxic doses of the drug4,5. Although it is generally accepted that the biochemical basis for the pharmacological response of cardiac glycosides must involve specific interaction of this class of drugs with the cardiac cell membrane Na+, K+-exchange pump, the precise molecular mechanism for the improvement of muscle performance by ouabain is controversial6,7. Many investigators claim that cardiac glycosides increase myocardial force of contraction by inhibiting (Na++K+)ATPase8–10. According to this hypothesis, such an inhibition might increase the intracellular concentration of Na+, which may augment the activity of the transmembrane Na+, Ca2+-exchange pump described by several workers11–14. We have found that ouabain stimulates Na+-dependent transport of noradrenaline by guinea pig heart sympathetic nerve terminals.
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Characterization of ouabain-induced noradrenaline and acetylcholine release from in situ cardiac autonomic nerve endings
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