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Cardiovascular Research 2003 57(4):942-952; doi:10.1016/S0008-6363(02)00782-4
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Regulatory effects of G protein-coupled receptors on cardiac sarcolemmal Na+/H+ exchanger activity: signalling and significance

Metin Avkiran* and Robert S Haworth

Centre for Cardiovascular Biology and Medicine, King's College London, The Rayne Institute, St Thomas’ Hospital, Lambeth Palace Road, London SE1 7EH, UK

* Corresponding author. Tel.: +44-20-7928-9292x3375; fax: +44-20-7928-0658. metin.avkiran{at}kcl.ac.uk

In cardiac myocytes, sarcolemmal Na+/H+ exchanger (NHE) activity is subject to regulation by a variety of G protein-coupled receptor (GPCR) systems. This regulation usually manifests as an increase in NHE activity (e.g. in response to the stimulation of {alpha}1-adrenergic, angiotensin AT1, endothelin and thrombin receptors), although some GPCR systems have been shown to inhibit sarcolemmal NHE activity (e.g. β1-adrenergic receptors) or to attenuate its stimulation by other ligands (e.g. adenosine A1 and angiotensin AT2 receptors). The pertinent molecular signalling mechanisms are only now beginning to be unravelled, with the extracellular signal regulated kinase/ribosomal S6 kinase pathway and the protein kinase C pathway both appearing to play critical roles in the stimulation of sarcolemmal NHE activity. GPCR-mediated regulation of sarcolemmal NHE activity is likely to play significant roles in modulating myocardial function in both physiological and pathophysiological conditions. These roles include the regulation of (1) myocardial pHi and contractility, (2) myocardial susceptibility to injury and dysfunction during ischaemia and reperfusion, and (3) myocardial hypertrophy in response to neurohormonal and mechanical stimuli. Greater understanding of the pertinent molecular signalling mechanisms distal to GPCR stimulation may reveal novel targets for therapeutic manipulation.

KEYWORDS Contractile function; G-proteins; Hypertrophy; Ischemia; Myocytes; Na/H-exchanger; Receptors; Signal transduction


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