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(Circulation Research. 2004;95:549.)
© 2004 American Heart Association, Inc.

Editorials

Sodium Calcium Exchange in the Heart

Necessity or Luxury?

David A. Eisner, Karin R. Sipido

From the Unit of Cardiac Physiology (D.A.E.), Oxford Rd, Manchester, UK; and the Laboratory of Experimental Cardiology (K.R.S.), KUL, Campus Gasthuisberg, Leuven, Belgium.

Correspondence to D.A. Eisner, Unit of Cardiac Physiology, 1.524 Stopford Bldg, Oxford Rd, Manchester M13 9PT, UK. E-mail Eisner@man.ac.uk

See related article, pages 604–611

Key Words: sodium calcium exchange • calcium • arrhythmia

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The sodium calcium exchange (NCX) was first discovered in cardiac muscle¹ and squid axon² and has since been found in most cell types (see reviews^3,4). It accounts for the previously observed effects of sodium on cardiac contractility.⁵ The exchanger transports 3 Na⁺ ions per Ca²⁺.^6–8 This stoichiometry has three important consequences.¹ Ca²⁺ fluxes and hence intracellular Ca²⁺ concentration ([Ca²⁺]_i) are very sensitive to intracellular Na⁺ concentration ([Na⁺]_i),⁹ and therefore, even small changes of [Na⁺]_i have large effects on contractility. In the case of vascular smooth muscle, the [Na⁺]_i-dependence of NCX has been suggested to account for aspects of hypertension.¹⁰² The activity of NCX is affected by membrane potential with depolarization hindering Ca²⁺ efflux and increasing Ca²⁺ influx. This voltage dependence may produce net Ca²⁺ entry into the cell at the start of the action potential and contribute to triggering Ca²⁺-induced Ca²⁺ release from the sarcoplasmic reticulum (SR)¹¹ (although the NCX is a much weaker trigger of Ca²⁺ release than is the L-type Ca²⁺ current¹²).³ Changes in the activity of NCX attributable to an increase in [Ca²⁺]_i activate inward current. Specifically, (1) inward current activated by the systolic Ca²⁺ transient will contribute to maintaining the action potential plateau,¹³ and (2) current activated by abnormal Ca²⁺ release in diastole generates^14,15 the delayed afterdepolarizations known to be a cause of triggered arrhythmias.^16–18

Effects of NCX on Systolic [Ca²⁺]_i

NCX does not only control the cytoplasmic Ca²⁺ concentration but, indirectly, also regulates the amount of Ca²⁺ stored in . . . [Full Text of this Article]

Related Article:

Functional Adult Myocardium in the Absence of Na⁺-Ca²⁺ Exchange: Cardiac-Specific Knockout of NCX1

Scott A. Henderson, Joshua I. Goldhaber, Jessica M. So, Tieyan Han, Christi Motter, An Ngo, Chana Chantawansri, Matthew R. Ritter, Martin Friedlander, Debora A. Nicoll, Joy S. Frank, Maria C. Jordan, Kenneth P. Roos, Robert S. Ross, and Kenneth D. Philipson
Circ. Res. 2004 95: 604-611. [Abstract] [Full Text] [PDF]

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