The role of salt sensitivity in the development of heart failure with preserved ejection fraction and the relation of intrinsic steroids

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The production of CTS was enhanced in hypertensive HFPEF model. Ouabain activated p42/ 44 MAPKs and enhanced collagen production through the elevation of cytosolic Ca^<2+> concentration via NCX entry mode. SEA0400, the potent inhibitor of NCX entry mode, prevented the development of LV fibrosis and stiffening and the transition to HFPEF with the improvement of survival rate in the animal models. Thus, CTS and the subsequently activated Ca^<2+> entry mode of NCX may play an important role in the development of LV fibrosis and hypertensive HFPEF, and the blockade of the entry mode of NCX is likely a new therapeutic strategy for this phenotype of heart failure.