Molecular target
Cardiac Na+/K+ ATPase
Cardiac myocyte sodium-potassium pump; inhibition (digoxin) raises intracellular Na+ → reduces Na+/Ca2+ exchange → raises intracellular Ca2+ → positive inotropy. Hypokalemia (from licorice or diuretics) potentiates digoxin toxicity dramatically.
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Pharmaceutical agents
Drugs that act on Cardiac Na+/K+ ATPase
These medications have Cardiac Na+/K+ ATPase among their molecular targets. Sharing a target is a mechanistic relationship — it does not make any plant below an alternative to, or substitute for, these drugs.
Botanical connections
Plants whose compounds act on Cardiac Na+/K+ ATPase
Each plant below contains a named compound documented to act on Cardiac Na+/K+ ATPase. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.
- Cheiranthin / cardiac glycosidesCardenolide glycosides
Cheiranthin is a mixture of cardioactive steroidal glycosides (principally erysimoside and helveticoside) documented to inhibit cardiac Na⁺/K⁺-ATPase by a mechanism analogous to digitalis glycosides; preclinical pharmacological data suggest positive inotropic and potential antiarrhythmic activity, though robust clinical evidence is absent.
- Cardiac glycosides (genus-characteristic)Cardenolide glycosides
Digitalis genus members characteristically contain cardenolide glycosides that inhibit the cardiac Na⁺/K⁺-ATPase; the specific glycoside profile of D. lutea has not been well characterised in the verified literature provided. Any Digitalis species should be regarded as potentially cardiotoxic.