The Sodium Calcium Exchanger and its Role in Cardiac Function: Effects of Digitalis

The structure and function of sodium-calcium exchanger

Introduction:
The sodium calcium exchanger comprises of electrogenic membranes that are attached to secondary transporters that facilitate the transport of calcium across the organelles or cell membranes to regulate the levels of calcium in the cytosol. The sodium calcium exchanger uses ATP as the energy molecule stored in the electrochemical gradient of sodium to allow sodium to flow across the plasma membrane in exchange for calcium ions in where one calcium ion is exported in exchange for three sodium ions (Sibarov et al., 2018). The antiporter membrane proteins play’s a significant role of intracellular calcium regulation. Digitalis has significant effects on the heart through its action on active cell transport. The substance enhances the actions of sodium calcium exchanger as well as sodium-potassium ATPase of the heart muscle cells. This inhibits ATPase irreversibly resulting in high levels of intracellular sodium. The build-up of sodium in the myocytes shifts sodium from the extracellular compartments through the sodium calcium exchanger in exchange for calcium ions.

The structure and function of sodium-calcium exchanger:

The sodium-calcium exchanger is a major mechanism which facilitates calcium efflux in cardiac myocytes. It is responsible for the regulation of cellular calcium content, and therefore affects the heart's contractility. During heart failure, there is an increase calcium efflux by the sodium-calcium exchanger, causing a decreased calcium load and dysfunction to the sarcoplasmic reticulum, resulting to a reduced contractility. On the other hand, in states of reduced calcium efflux due to elevated intracellular sodium, such as in glycosides like digitalis, the calcium load in the sarcoplasmic reticulum increases, increasing the cardiac contractility (Ottolia et al., 2014).

Effect of Digitalis on Heart:
Digitalis is a cardiac glycoside which primarily inhibits the sodium-potassium-ATPase. This causes higher intracellular sodium concentration, and therefore a reduced efficacy of the sodium-calcium exchanger. This ultimately leads to higher intracellular calcium concentration, which causes increased contractility, reduced velocity of electric conduction via atrioventricular node depression, and reduction of heart rate via the sinoatrial node depression in the cardiac muscles (Katzung and Trevor, 2014).

How digitalis affects the heart through its action on active cell transport including all related transport:
It is currently commonly concurred that sodium-potassium-ATPase a vehicle compound got from the sarcolemma sodium siphon, is the essential site at which digitalis applies its consequences for the myocardial cell. Hindrance of the capacity of this particle transport chemical to catalyse sodium ions efflux from the cell in return for potassium ions leads to both the helpful and harmful impacts of the heart glycosides. The instrument by which digitalis restrains the sodium pump has been set up in investigations of sodium-potassium-ATPase which show that the capacity of heart glycosides to hinder adenosine triphosphate (ATP)- upheld transport of sodium ions is diminished within the sight of raised degrees of potassium ions. These investigations clarify the capacity of hypokalaemia to potentiate the impacts of cardiovascular glycosides on the heart, and of high potassium ions concentrations to conquer the hindrance of sodium pump action by the heart glycosides. Late exhibits that the positive inotropic impact of the cardiovascular glycosides has corresponded with expanded intracellular sodium ions provide solid proof that these impacts of digitalis to disable sodium efflux are liable for the expanded myocardial contractility brought about by digitalis.
Digitalis' ability to increase cardiac contraction is closely associated with the disruption of active transport mechanisms involved in the movement of sodium and potassium across cell membranes. It is also a mechanism that explains the common toxicity problems with the use of cardiac glycosides: myocardial inflammation and heart obstruction.

Conclusion:
In conclusion, the sodium calcium exchanger is an antiporter membrane which relies on ATP to facilitate the exchange of sodium with calcium to regulate intracellular calcium levels.