期刊
CELL CALCIUM
卷 45, 期 1, 页码 1-10出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2008.05.005
关键词
Adrenoceptor; Cardiac; Endothelin-1 (ET-1); Isoprenaline; Isoproterenol; Na+-Ca2+ exchanger (NCX); Phosphorylation; Protein kinase A (PKA); Protein kinase C (PKC); Sodium-calcium exchanger; Ventricular myocyte
类别
资金
- British Heart Foundation
The cardiac Na+-Ca2+ exchanger (NCX) is an important regulator of intracellular ion homeostasis and cardiac function. Gaining insight into modulation of the NCX is therefore important in order to understand ion handling in the heart under physiological and pathological conditions. Typically, the functional contribution of the NCX is often regarded as secondary to the changes in luminal Na+ and Ca2+. Whilst it is welt accepted that the NCX can be regulated by various factors, including the concentrations of transported ions, direct receptor-mediated modulation of the cardiac NCX is more controversial. Evidence from several different laboratories supports the notion that the cardiac NCX is a direct target of neurotransmitters and hormones and their downstream signalling pathways; however, the issue remains unresolved due to conflicting data showing a lack of direct modulation. The present review summarizes overall findings regarding the modulation of the cardiac NCX, in particular on molecular mechanisms of direct phosphorytation of NCX by beta-adrenergic/adenylate cyclase/protein kinase A and (for comparative purposes) on endothelin-1/protein kinase C signalling pathways. It also aims to consider whether it is currently possible to reconcile discrepancies between studies in the interpretation of the regulation of the cardiac NCX by agents stimulating the beta-adrenoceptor/PKA pathway. (C) 2008 Published by Elsevier Ltd.
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