Digoxin inhibits which membrane protein on cardiac myocytes?

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Multiple Choice

Digoxin inhibits which membrane protein on cardiac myocytes?

Explanation:
Blockade of the Na+/K+ ATPase pump on cardiac myocytes explains how digoxin increases contractility. By inhibiting this pump, intracellular sodium rises, which reduces the driving force for the Na+/Ca2+ exchanger to expel calcium. With less Ca2+ being removed, intracellular calcium accumulates, enhancing calcium release during systole and producing a stronger, more forceful heartbeat (positive inotropy). Digoxin’s effect on calcium handling is indirect but central to its inotropic action. Other pumps aren’t targeted by digoxin in cardiac muscle for this effect: calcium ATPases (SERCA) resequester Ca2+ into the sarcoplasmic reticulum and are not inhibited by digoxin; the Na+/Ca2+ exchanger’s activity is modulated by the Na+ gradient rather than directly inhibited; and the H+/K+ ATPase is not present in cardiac myocytes (it’s primarily in gastric parietal cells).

Blockade of the Na+/K+ ATPase pump on cardiac myocytes explains how digoxin increases contractility. By inhibiting this pump, intracellular sodium rises, which reduces the driving force for the Na+/Ca2+ exchanger to expel calcium. With less Ca2+ being removed, intracellular calcium accumulates, enhancing calcium release during systole and producing a stronger, more forceful heartbeat (positive inotropy). Digoxin’s effect on calcium handling is indirect but central to its inotropic action.

Other pumps aren’t targeted by digoxin in cardiac muscle for this effect: calcium ATPases (SERCA) resequester Ca2+ into the sarcoplasmic reticulum and are not inhibited by digoxin; the Na+/Ca2+ exchanger’s activity is modulated by the Na+ gradient rather than directly inhibited; and the H+/K+ ATPase is not present in cardiac myocytes (it’s primarily in gastric parietal cells).

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