Medizinische Universität Graz - Research portal

Logo MUG Resarch Portal

Selected Publication:

Pieske, B; Houser, SR.
Na+i handling in the failing human heart.
Cardiovasc Res. 2003; 57(4):874-886 Doi: 10.1016/S0008-6363(02)00841-6 [OPEN ACCESS]
Web of Science PubMed FullText FullText_MUG

 

Leading authors Med Uni Graz
Pieske Burkert Mathias
Altmetrics:

Dimensions Citations:

Plum Analytics:

Scite (citation analytics):

Abstract:
Proper contractile function of the heart depends on intact excitation-contraction processes and ion homeostasis of the myocytes. The Ca2+ ion activates contraction through its binding to troponin C. However, Ca2+ homeostasis is tightly linked to Na+ regulation because the primary mechanism for Ca2+ efflux in cardiac myocytes is via electrogenic Na+/Ca2+-exchange. While altered Ca2+-homeostasis has been demonstrated in animal models of heart failure and failing human cardiac tissue, the role of dysfunctional Na+ handling processes in altered excitation-contraction coupling remains obscure. Furthermore, altered Na+ handling has been implicated in a wide range of cellular processes, such as regulation of membrane potential, pH, and growth. This review will discuss (1) the evidence for altered [Na+]i homeostasis in the failing human heart, (2) how alterations in the Na+ electrochemical gradient can influence Ca2+ handling, contractile function, and a number of other cellular processes, and (3) the potential defects in Na+ channels and transporters that may underlie altered [Na+]i in the failing human heart.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Calcium - metabolism
Heart Failure, Congestive - metabolism
Humans - metabolism
Mammals - metabolism
Myocardial Contraction - physiology
Myocytes, Cardiac - metabolism
Sodium - metabolism

Find related publications in this database (Keywords)
calcium (cellular)
contractile function
heart failure
myocytes
Na/Ca-exchanger
© Med Uni GrazImprint