Key result
Endogenous ligands such as adrenergic agonists, thrombin, and endothelin modulate cardiac sarcolemmal Na+/H+ exchanger activity, which is an important determinant of myocardial injury during ischemia.
Endogenous ligands associated with ischemia modulate cardiac sarcolemmal Na+/H+ exchanger activity, potentially influencing the extent of myocardial injury during ischemia and reperfusion.
Does not yet alter ischemia management; leaves open ligand-specific NHE targeting for future trials.
The cardiac sarcolemmal Na+/H+ exchanger (NHE) extrudes one H+ in exchange for one Na+ entering the myocyte, utilizing for its driving force the inwardly directed Na+ gradient that is maintained by the Na+/K+ ATPase. The exchanger is quiescent at physiological values of intracellular pH but becomes activated in response to intracellular acidosis. Recent evidence suggests that a variety of extracellular signals (e.g., adrenergic agonists, thrombin, and endothelin) also modulate sarcolemmal NHE activity by altering its sensitivity to intracellular H+. Since sarcolemmal NHE activity is believed to be an important determinant of the extent of myocardial injury during ischemia and reperfusion, regulation of exchanger activity by endogenous ligands associated with ischemia is likely to be of pathophysiological importance.
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Avkiran et al. (1999) conducted a review in Myocardial ischemia. Endogenous ligands (e.g., adrenergic agonists, thrombin, endothelin) was evaluated. Endogenous ligands such as adrenergic agonists, thrombin, and endothelin modulate cardiac sarcolemmal Na+/H+ exchanger activity, which is an important determinant of myocardial injury during ischemia.
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