dc.contributor.author | Cantafio, Patrizia | |
dc.contributor.author | Canonaco, Marcello | |
dc.contributor.author | Angelone, Tommaso | |
dc.date.accessioned | 2019-09-19T12:20:27Z | |
dc.date.available | 2019-09-19T12:20:27Z | |
dc.date.issued | 16-12-2015 | |
dc.identifier.uri | http://hdl.handle.net/10955/1470 | |
dc.description | Scuola di Dottorato Life Sciences, Indirizzo: Biologia animale, Ciclo XXVIII, a.a. 2015-2016 | en_US |
dc.description.abstract | The myocardial response to mechanical stretch (Frank-Starling law) is an important physiological cardiac determinant. Modulated by many endogenous substances, it is impaired in the presence of cardiovascular pathologies and during senescence. Catestatin (CST: hCgA352-372), a 21-amino-acid derivate of Chromogranin A (CgA), displays hypotensive/vasodilatory properties and counteracts excessive systemic and/or intra-cardiac excitatory stimuli (e.g., catecholamines and endothelin-1). CST, produced also by the myocardium, affects the heart by modulating inotropy, lusitropy and the coronary tone through a Nitric Oxide (NO)-dependent mechanism. This study evaluated the putative influence elicited by CST on the Frank-Starling response of normotensive Wistar Kyoto (WKY) and hypertensive (SHR) hearts by using isolated and Langendorff perfused cardiac preparations. Functional changes were evaluated on aged (18-month-old) WKY rats and SHR which mimic human chronic heart failure (HF). Comparison to WKY rats, SHR showed a reduced Frank-Starling response. In both rat strains, CST administration improved myocardial mechanical response to increased end-diastolic pressures. This effect was mediated by EE/IP3K/NOS/NO/cGMP/PKG, as revealed by specific inhibitors. CST-dependent positive Frank-Starling response is paralleled by an increment in protein S-Nitrosylation, AKT/eNOS/nNOS and PLN phosphorylations. Our data suggested CST as a NO dependent physiological modulator of the stretch-induced intrinsic regulation of the heart. This may be of particular importance in the aged hypertrophic heart, whose function is impaired because of a reduced systolic performance accompanied by delayed relaxation and increased diastolic stiffness. | en_US |
dc.description.sponsorship | Università della Calabria | en_US |
dc.language.iso | it | en_US |
dc.relation.ispartofseries | BIO/09; | |
dc.subject | Fisiologia animale | en_US |
dc.subject | Peptidi | en_US |
dc.subject | Ratti | en_US |
dc.title | <<Ia>> catestatina migliora la risposta Frank-Starling in cuori di ratto normotesi e ipertesi agendo come attivatore fisiologico del pathway trasduzionale ossido nitrico-dipendente | en_US |
dc.type | Thesis | en_US |