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The Sodium‐Calcium Ion Membrane Exchanger: Physiologic Significance and Pharmacologic Implications
Author(s) -
Yashar Payam R.,
Fransua Mesfin,
Frishman William H.
Publication year - 1998
Publication title -
the journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.92
H-Index - 116
eISSN - 1552-4604
pISSN - 0091-2700
DOI - 10.1002/j.1552-4604.1998.tb04442.x
Subject(s) - heart failure , inotrope , sodium calcium exchanger , extracellular , calcium , sodium , chemistry , intracellular , calcium in biology , sodium–hydrogen antiporter , pharmacology , medicine , cardiology , biochemistry , organic chemistry
The Na + ‐Ca 2+ exchanger is a non‐ATP—dependent protein that, under steady‐state conditions, extrudes Ca 2+ 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 Ca 2+ 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 + ‐Ca 2+ 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.