Journal
IUBMB LIFE
Volume 61, Issue 3, Pages 215-221Publisher
WILEY
DOI: 10.1002/iub.163
Keywords
Na+/K+ ATPase; Na+/Ca2+ exchanger; Na+ channels; phospholemman
Categories
Funding
- National Institutes of Health [HL-81526, RL-64724]
- American Heart Association [0735084N]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL064724, R01HL081562, R37HL030077] Funding Source: NIH RePORTER
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Intracellular Na+ concentration ([Na+](i)) is very important in modulating the contractile and electrical activity of the heart. Upon electrical excitation of the myocardium, voltage-dependent Na+ channels open, triggering, the upstroke of the action potential (AP). During the AP, Ca2+ enters the myocytes via L-type Ca2+ channels. This triggers Ca2+ release from the sarcoplasmic reticulum (SR) and thus activates contraction. Relaxation occurs when cytosolic Ca2+ declines, mainly due to reuptake into the SR via SR Ca2+-ATPase and extrusion from the cell via the Na+/Ca2+ exchanger (NCX). NCX extrudes one Ca2+ ion in exchange for three Na+ ions and its activity is critically regulated by [Na+](i). Thus, via NCX, [Na+](i) is centrally involved in the regulation of intracellular [Ca2+] and contractility. Na+ brought in by Na+ channels, NCX and other Na+ entry pathways is extruded by the Na+/K+ pump (NKA) to keep [Na+](i) low. NKA is regulated by phospholemman, a small sarcolemmal protein that associates with NKA. Unphosphorylated phospholemman inhibits NKA by decreasing the pump affinity for internal Na+ and this inhibition is relieved upon phosphorylation. Here we discuss the main characteristics of the Na+ transport pathways in cardiac myocytes and their pbysiological and pathophysiol ogical relevance. (C) 2009 IUBMB
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