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Under stressful\/pathological conditions, CgA cleavage generates the CgA<jats:sub>1\u2010373<\/jats:sub> proangiogenic fragment. The present work investigated the possibility that human CgA<jats:sub>1\u2010373<\/jats:sub> influences the mammalian cardiac performance, evaluating the role of its C\u2010terminal sequence.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Haemodynamic assessment was performed on an ex vivo Langendorff rat heart model, while mechanistic studies were performed using perfused hearts, H9c2 cardiomyocytes and in silico.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>On the ex vivo heart, CgA<jats:sub>1\u2010373<\/jats:sub> elicited direct dose\u2010dependent negative inotropism and vasodilation, while CgA<jats:sub>1\u2010372<\/jats:sub>, a fragment lacking the C\u2010terminal R<jats:sub>373<\/jats:sub> residue, was ineffective. Antibodies against the PGPQLR<jats:sub>373<\/jats:sub> C\u2010terminal sequence abrogated the CgA<jats:sub>1\u2010373<\/jats:sub>\u2010dependent cardiac and coronary modulation. Ex vivo studies showed that CgA<jats:sub>1\u2010373<\/jats:sub>\u2010dependent effects were mediated by endothelium, neuropilin\u20101 (NRP1) receptor, Akt\/NO\/Erk1,2 pathways, nitric oxide (NO) production and S\u2010nitrosylation. In vitro experiments on H9c2 cardiomyocytes indicated that CgA<jats:sub>1\u2010373<\/jats:sub> also induced eNOS activation directly on the cardiomyocyte component by NRP1 targeting and NO involvement and provided beneficial action against isoproterenol\u2010induced hypertrophy, by reducing the increase in cell surface area and brain natriuretic peptide (BNP) release. Molecular docking and all\u2010atom molecular dynamics simulations strongly supported the hypothesis that the C\u2010terminal R<jats:sub>373<\/jats:sub> residue of CgA<jats:sub>1\u2010373<\/jats:sub> directly interacts with NRP1.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These results suggest that CgA<jats:sub>1\u2010373<\/jats:sub> is a new cardioregulatory hormone and that the removal of R<jats:sub>373<\/jats:sub> represents a critical switch for turning \u201coff\u201d its cardioregulatory activity.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.13570","type":"journal-article","created":{"date-parts":[[2020,10,19]],"date-time":"2020-10-19T06:14:27Z","timestamp":1603088067000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["The chromogranin A<sub>1\u2010373<\/sub> fragment reveals how a single change in the protein sequence exerts strong cardioregulatory effects by engaging neuropilin\u20101"],"prefix":"10.1111","volume":"231","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1743-4724","authenticated-orcid":false,"given":"Carmine","family":"Rocca","sequence":"first","affiliation":[{"name":"Laboratory of Cellular and Molecular Cardiovascular Patho\u2010Physiology Department of Biology, E. and E.S. 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