Aim: 

Chromogranin A (CGA), the ubiquitous glycoprotein secreted with catecholamines upon chromaffin cell stimulation, generates several regulatory peptides (vasostatins, pancreastatin, catestatin, parastatin) which are powerful inhibitors of endocrine secretion (Helle et al., 2007). The CGA peptidic fragment catestatin (Cts) acts as an inhibitor of catecholamine release, a vasodilator in vivo and an anti-hypertensive agent in mammals. We recently discovered that it functions as an important cardio-suppressive modulator of both frog (Mazza et al., 2008) and rat (Angelone et al., 2008) heart performance. In an evolutionary perspective, we aimed to explore Cts (bovine CGA344-364) influence on isolated and perfused eel (Anguilla anguilla L.) heart preparations and the eventual species-specific mechanisms underlying its myocardial action.

Methods: 

Stroke Volume (SV) and Stroke Work (SW) were used as measure of inotropism. Concentration-response curves were generated exposing the hearts to increasing doses of Cts; inhibitors of the nitric oxide (NO) signalling were used to study its involvement in the Cts-induced effects. The Cts influence was also investigated in chemically- and physically-stimulated preparations.

Results: 

Under basal (unstimulated) conditions, Cts caused a negative inotropic effect which, as in frog and rat hearts, was NO-dependent. An antiadrenergic effect and a positive modulation of the Frank-Starling response were also highlighted.

Conclusion: 

On the whole, these data, compared with those obtained in frog and rat, strongly support an early role of Cts as a cardio-suppressive peptide in vertebrates. Helle et al. Cell Mol Life Sci. 64: 2863-86, 2007. Mazza et al. Am J Physiol. 295: 113-122, 2008. Angelone et al. Endocrinol. 49: 4780-93, 2008.