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Mineralocorticoid receptor activation is crucial in the signalling pathway leading to the Anrep effect
Author(s) -
Caldiz Claudia I.,
Díaz Romina G.,
Nolly Mariela B.,
Chiappe de Cingolani Gladys E.,
Ennis Irene L.,
Cingolani Horacio E.,
Pérez Néstor G.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.218750
Subject(s) - angiotensin ii , mineralocorticoid receptor , endocrinology , transactivation , medicine , angiotensin ii receptor type 1 , chemistry , aldosterone , receptor , eplerenone , autocrine signalling , biology , biochemistry , gene , transcription factor
Non‐technical summary Myocardial stretch increases force in two phases. The first one is immediate and attributed to an increase in myofilament Ca 2+ 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 2+ transient. We previously showed that Ca 2+ entry through reverse Na + /Ca 2+ 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 + /H + exchanger (NHE‐1) activation‐mediated rise in Na + . 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.