Na+ transport in cardiac myocytes; Implications for excitation-contraction coupling

✍ Scribed by Donald M. Bers; Sanda Despa

• Publisher: John Wiley and Sons
• Year: 2009
• Tongue: English
• Weight: 187 KB
• Volume: 61
• Category: Article
• ISSN: 1521-6543
• DOI: 10.1002/iub.163

✦ Synopsis

Abstract

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, Ca^2+^ enters the myocytes via L‐type Ca^2+^ channels. This triggers Ca^2+^ release from the sarcoplasmic reticulum (SR) and thus activates contraction. Relaxation occurs when cytosolic Ca^2+^ declines, mainly due to re‐uptake into the SR via SR Ca^2+^‐ATPase and extrusion from the cell via the Na^+^/Ca^2+^ exchanger (NCX). NCX extrudes one Ca^2+^ 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 [Ca^2+^] 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 physiological and pathophysiological relevance. © 2009 IUBMB IUBMB Life, 61(3): 215–221, 2009