What compounds enhance cardiac contractility by inhibiting the Na+/K+ ATPase pump?

Cardiac glycosides are a class of compounds that enhance cardiac contractility primarily by inhibiting the Na+/K+ ATPase pump. This pump is responsible for maintaining the gradient of sodium and potassium ions across the cell membrane of cardiac myocytes (heart muscle cells). By inhibiting this pump, cardiac glycosides increase intracellular sodium levels.

As a consequence of the elevated sodium levels, the sodium-calcium exchanger, which normally extrudes calcium from the cell in exchange for sodium, becomes less effective. This results in an increased concentration of intracellular calcium, which enhances the force of contraction of the heart muscle, thereby improving cardiac output. This mechanism is particularly relevant in treating conditions such as heart failure.

In contrast, beta blockers work by blocking the effects of adrenaline on beta-adrenergic receptors, reducing heart rate and cardiac output. Calcium channel blockers impede calcium entry into cells, which decreases myocardial contractility. ACE inhibitors primarily function by blocking the conversion of angiotensin I to angiotensin II, which leads to vasodilation and reduced blood pressure, but they do not directly enhance cardiac contractility.