The catecholamine release-inhibitory peptide catestatin (chromogranin A344-364) modulates myocardial function in fish

摘要: SUMMARY Catestatin (CST), the 21-amino acid, cationic and hydrophobic peptide proteolytically derived from ubiquitous chromogranin A (CgA), is an endogenous inhibitor of catecholamine release, a potent vasodilator in vivo anti-hypertensive agent mammals, including humans. Recently, we discovered that CST also functions as important negative modulator heart performance frog rat. To gain evolutionary perspective on cardiotropism fish, analysed influence bovine (CgA 344-364 ) eel heart, well eventual species-specific mechanisms its myocardial action. Experiments were carried out fresh-water eels ( Anguilla anguilla L.) using electrically paced isolated working preparation. Stroke volume stroke work used measures ventricular performance. Under basal conditions, (from 11 nmol l –1 to 165 caused concentration-dependent inotropism, which was abolished by inhibitors either β 1 /β 2 (propranolol) or 3 (SR 59230 adrenergic receptors, G i/o protein (PTx) nitric oxide synthase (L-NMMA), guanylate cyclase (ODQ) blockers. This suggests β-adrenergic receptor-G protein-NO-cGMP-dependent mechanism. By contrast, CST-induced cardio-suppression not influenced atropine, unspecific muscarinic antagonist, thus excluding cholinergic receptor involvement. counteracted (isoproterenol)-mediated positive inotropism. increased preload (i.e. Frank–Starling response) induced significant increase response, blocked L-NMMA thapsigargin, but independent cyclase. In conclusion, this first report fish modulates under basal, preload, conditions counteracts adrenergic-mediated strikingly supports significance establishes cardioactive role peptide.