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PubMed1991

Effect of digitalis glycosides on norepinephrine release in the heart. Dual mechanism of action.

The effect of ouabain on exocytotic and nonexocytotic norepinephrine release was investigated in perfused rat and guinea pig hearts. The overflow of endogenous norepinephrine and its neuronal metabolite 3,4-dihydroxyphenylethyleneglycol (DOPEG) was determined by high-pressure liquid chromatography. DOPEG served as the indicator of free axoplasmic norepinephrine concentrations. The overflow of the norepinephrine cotransmitter neuropeptide Y (NPY) was determined by radioimmunoassay and NPY was used as marker for exocytotic release. Electrical stimulation of the left stellate ganglion resulted in exocytotic norepinephrine release in rat and guinea pig hearts. Ouabain caused an increase in stimulation-induced norepinephrine overflow from rat and guinea pig hearts by 40%. However, overflow of NPY was decreased by 40%, indicating a reduced exocytosis rate. Ouabain increased both norepinephrine and NPY overflow, suggesting enhancement of exocytosis, when neuronal catecholamine uptake (uptake1) was blocked by desipramine or when presynaptic alpha 2-adrenoceptors were inhibited by yohimbine. The results demonstrate an interaction of ouabain with both calcium-dependent exocytosis and uptake1 of norepinephrine. Under calcium-free conditions, ouabain or potassium-free perfusate resulted in norepinephrine release from hearts when the axoplasmic norepinephrine concentration was elevated by the reserpinelike agent Ro 4-1284. This release was independent from neural activity, not accompanied by NPY overflow, and suppressed by the uptake1 blocker desipramine. These findings are in keeping with carrier-mediated nonexocytotic norepinephrine release that is caused by reversal of the transport direction of the uptake1 carrier. During myocardial ischemia nonexocytotic norepinephrine release was accelerated and enhanced by inhibition of Na+,K(+)-ATPase before ischemia. This study demonstrates the potential of digitalis glycosides to interact both with transmitter exocytosis and with the neuronal catecholamine transport system by Na+,K(+)-ATPase inhibition. Interaction with the catecholamine transport system involves both inhibition of norepinephrine inward transport and induction of norepinephrine outward transport, resulting in nonexocytotic norepinephrine release.

Animals↗
PubMed1990

[What are the indications for digitalis glycosides in the current treatment of cardiac insufficiency?].

Digitalis was discovered over two centuries ago and has been in everyday use for 100 years: however nowadays it is not considered to be the almost exclusive treatment of heart failure as it used to be with diuretic therapy. In the last decade, our understanding of the physiopathology of heart failure and the body's mechanisms of adaptation have improved and this has lead to the use of new molecules and a different approach to the problem of left ventricular failure. The classical contra-indications and precautions of use of digitalis have been studied in detail. The use of digitalis is contested especially in patients in sinus rhythm or with ischemic heart disease and it is used less often in adult cardiac emergencies. The competition between digitalis and vasodilator therapy is now very apparent in some situations; however, the choice between these two groups of drugs (as treatment of first intention or in association) has to be carefully considered in each individual case. The future of digitalis therapy lies without doubt in pediatric cardiology where it remains irreplaceable.

Clinical Trials as Topic↗
PubMed1983

[Direct cardiac mechanism of action of digitalis glycosides].

The direct cardiac mechanism of action of digitalis remains obscure. The inhibition of membrane ATP-ase seems to correlate with the increase in free intracellular calcium at the contractile sites during membrane depolarization. Two mechanisms may explain this phenomenon: increase in the sodium-calcium exchange or labilisation of the calcium pool bound to the internal wall of the sarcoplasmic reticulum. Digitalis toxicity occurs when the sodium pump is inhibited to such an extent that cellular homeostasis cannot be maintained. The intracellular calcium overload is responsible for the increased automaticity of the automatic fibres by oscillations of the membrane potential, added to the spontaneous slope of diastolic depolarisation.

Animals↗