Mineralocorticoid receptor activation is crucial in the signalling pathway leading to the Anrep effect

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Published
2011-12-14
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  • http://onlinelibrary.wiley.com/termsAndConditions#vor
DOI
  • 10.1113/jphysiol.2011.218750
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Wiley

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<jats:p><jats:bold>Non‐technical summary </jats:bold> Myocardial stretch increases force in two phases. The first one is immediate and attributed to an increase in myofilament Ca<jats:sup>2+</jats:sup> responsiveness (Frank–Starling mechanism). The second phase gradually develops and is known as slow force response (SFR) or Anrep effect due to an increase in intracellular Ca<jats:sup>2+</jats:sup> transient. We previously showed that Ca<jats:sup>2+</jats:sup> entry through reverse Na<jats:sup>+</jats:sup>/Ca<jats:sup>2+</jats:sup> exchange underlies the SFR, as the final step of an autocrine/paracrine loop involving release of angiotensin II/endothelin, transactivation of the epidermal growth factor receptor, increased mitochondrial oxidative stress and a Na<jats:sup>+</jats:sup>/H<jats:sup>+</jats:sup> exchanger (NHE‐1) activation‐mediated rise in Na<jats:sup>+</jats:sup>. In the present study we show that mineralocorticoid receptor activation is a necessary step between endothelin and epidermal growth factor receptor activation in the stretch‐triggered reactive oxygen species‐mediated NHE‐1 activation leading to the SFR.</jats:p>

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