Catestatin (CST), the Chromogranin A (CgA)-derived cationic and hydrophobic peptide, firstlyrecognized as an endogenous inhibitor of catecholamine secretion, functions as a physiological brake ofthe adreno-sympathetic-chromaffin system. Its wide spectrum of activities includes relevant multilevelcardiovascular and antihypertensive influences. At central systemic level, CST seems to modulate theautonomic cardiovascular control possibly acting on baroreceptor afferent fibers of the nucleus tractussolitarius. This, as well as clinical and experimental (CgA-KO mice) evidences point to an important role of CST in thedeterminism and prevention of essential hypertension. At organ level, CST exerts myocardial (negative inotropy and lusitropy)effects and potently vasodilates endothelin-1 (ET-1)–preconstricted coronaries through 2-adrenergic receptor(AR)-Gi/o protein-nitric oxide (NO)-cGMP signalling, while counterbalancing adrenergic (ISO) stimulation. The contractilemyocardial effects have been deeply analysed in fish and amphibian hearts, highlighting finely diversified mechanismsof action. CST also acts as cardioprotective agent in both pre- and post-conditioning through NO-dependentmechanisms implicating the Reperfusion Injury Salvage Kinase (RISK) signalling and the activation of mitoKATP channels.The CST-elicited cardiotropic and coronarotropic influences, along with the recently discovered proangiogenic andregulatory effects in glucose and lipid metabolism, contribute to delineate an integrated and updated picture of the peptidewhich emerges as a pleiotropic hormone with a wide range of cytokine-like characteristics. The aim of this review is to interlocksome older and more recent evidences which may help to better perceive the subtle links and differences amongthe puzzle pieces that still need to be deciphered.
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