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. 2019 Nov 19;116(12):1958–1971. doi: 10.1093/cvr/cvz311

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© The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Model of cardiac NHE1 regulation by NO signalling. (A) The various experimental manoeuvres performed in this study are ranked by strength of NO signal. Higher NO stimulations will evoke greater cGMP production. At higher [cGMP], inhibition of PDE3 permits a steady rise in [cAMP]. The balance between cGMP and cAMP signals sets the level of NHE1 activity. Based on literature values for [NO] measured in vivo, NO-evoked NHE1 activation is expected to be within physiological signalling, whereas NO-evoked NHE1 inhibition would occur over the pathophysiological range of elevated [NO]. (B) Schematic of the signalling pathways, evoked by NO, that regulate NHE1 activity by means of a differential activation of PKG-and PKA-dependent cascades.