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  • Title: [Does altered regulation of Na+ cause reduced myocardial contractility in heart failure?].
    Author: Swift F, Sjaastad I, Sejersted OM.
    Journal: Tidsskr Nor Laegeforen; 2003 Nov 06; 123(21):3036-40. PubMed ID: 14618171.
    Abstract:
    BACKGROUND: Cardiac contractility is largely regulated through transients in intracellular Ca2+ concentration [Ca2+]i. [Ca2+]i is under the influence of the sarcolemmal Na+/Ca2+ exchanger that exchanges Ca2+ for Na+ and which is mainly regulated by the intracellular Na+ concentration ([Na+]i). Consequently, [Na+]i influences cardiac contractility. [Na+]i is regulated by numerous proteins: Na+/K+ adenosine triphosphatases (ATPases), Na+-channels and Na+/H+ exchangers that control and are controlled by [Na+]i. In particular, the Na+/K+ ATPase and its crosstalk with the other proteins controls the intracellular level of Na+. MATERIAL AND METHODS: This review focuses on the significance of an efficient crosstalk between the topical proteins for control of [Na+]i. RESULTS: Co-localised proteins will sense the same [Na+]i; this is important as [Na+]i seems to vary in different parts of the cell. Evidence suggests that the regulation of [Na+]i is altered in heart failure. Several transport proteins have altered activity and expression patterns and this could partially explain the reduced contractility in heart failure. INTERPRETATION: A better understanding of the control of [Na+]i may lead to a new therapy for heart failure.
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