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Does not yet alter management of ischemia or HF; leaves open whether targeting the Na-Ca exchanger will prove beneficial.
The Na(+)-Ca2+ exchanger is a non-ATP-dependent protein that, under steady-state conditions, extrudes Ca2+ from the interior of the cell into the extracellular space via facilitated transport. The activity of the exchanger seems to be reduced in myocardial ischemia, leading to increased intracellular Ca2+ in the ischemic heart, which can result in arrhythmia, myocardial stunning, and necrosis. In contrast, congestive heart failure and myocardial hypertrophy are associated with increased exchanger activity and a decreased inotropic state. Pharmacologic agents are being developed to modulate sodium ion levels in the cell, which could enhance or reduce sodium-calcium exchange as needed in various pathophysiologic states. At this time there are no available drugs that act specifically on the Na(+)-Ca2+ exchanger itself. The exchanger has been cloned, and inhibitory peptides of the exchanger may soon be available for possible use in treatment of congestive heart failure.
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Yashar et al. (1998) studied this question.
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