Digoxin and other glycosides increase inotropy at the cellular level by inhibiting the Na+-K+ ATPase pump. The glycosides bind to the Na+-K+ ATPase pump, which is responsible for active transport of Na+ across the myocardial cell membrane. This blockage leads to an increase in intracellular Na+ which, in turn, enhances Na+-Ca2+ exchange. This leads to an increase in intracellular Ca2+ which, in turn, contributes to an increase in inotropy.
By what mechanism do the beta-adrenergic sympathomimetic drugs increase calcium that leads to increased inotropy?
The beta-adrenergic agents stimulate adenylate cyclase which results in an increase in cyclic AMP. CAMP phosphorylates a protein kinase which, in turn, increases the Ca2+ influx through the calcium channel.
Does the positive inotropic action of digoxin persist in the presence of full beta-adrenergic blockade?
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The inotropic functions of digoxin are not mediated by catecholamine release or through increased sensitivity to catecholamines. Adenylate cyclase activity which is responsible for the positive inotropic effects of beta-adrenoreceptor agents is not influenced by digoxin.
Does the same increase in oxygen consumption during the use of an inotropic agent like digoxin occur in the failing heart as well?
No. Digoxin decreases heart size when administed to a patient in congestive heart failure. There is a reduction in oxygen consumption, heart size, and wall tension, as explained by Laplace's law.