Chromogranin A (CgA) is the major soluble protein co-stored and co-released with catecholamines (CAs) fromsecretory vesicles in the adrenal medulla chromaffin cells. Present in the diffuse neuroendocrine system, it hasalso been detected in rat and human cardiac secretory granules where it co-stores with natriuretic peptidehormones (NPs).Mounting evidence shows that CgA is a marker of cardiovascular dysfunctions (essential hypertension,hypertrophic and dilatative cardiomyopathy, heart failure) and precursor of the cardioactive peptides vasostatin-1 (VS-1) and catestatin (Cts). This review focuses on recent knowledge regarding the myocardial, coronary andanti-adrenergic actions of VS-1. In particular, the negative inotropism, lusitropismand coronary dilation effects ofrat CgA1–64 (rCgA) and human recombinant STACgA1–78 (hrSTACgA1–78) are summarized with attention ontheir counteracting isoproterenol- and endothelin-1-induced positive inotropism, as well as ET-1-dependentcoronary constriction. The interactions between vasostatins (VSs), NPs and CA receptors are proposed as aparadigm of the heart capacity to organize complex connection–integration processes for maintaininghomeostasis under intense cardio-excitatory stimuli (myocardial stress).© 2010 Elsevier
The interplay between chromogranin A-derived peptides and cardiac natriuretic peptides in cardioprotection against catecholamines-evoked stress
MAZZA, ROSA;IMBROGNO, Sandra;
2010-01-01
Abstract
Chromogranin A (CgA) is the major soluble protein co-stored and co-released with catecholamines (CAs) fromsecretory vesicles in the adrenal medulla chromaffin cells. Present in the diffuse neuroendocrine system, it hasalso been detected in rat and human cardiac secretory granules where it co-stores with natriuretic peptidehormones (NPs).Mounting evidence shows that CgA is a marker of cardiovascular dysfunctions (essential hypertension,hypertrophic and dilatative cardiomyopathy, heart failure) and precursor of the cardioactive peptides vasostatin-1 (VS-1) and catestatin (Cts). This review focuses on recent knowledge regarding the myocardial, coronary andanti-adrenergic actions of VS-1. In particular, the negative inotropism, lusitropismand coronary dilation effects ofrat CgA1–64 (rCgA) and human recombinant STACgA1–78 (hrSTACgA1–78) are summarized with attention ontheir counteracting isoproterenol- and endothelin-1-induced positive inotropism, as well as ET-1-dependentcoronary constriction. The interactions between vasostatins (VSs), NPs and CA receptors are proposed as aparadigm of the heart capacity to organize complex connection–integration processes for maintaininghomeostasis under intense cardio-excitatory stimuli (myocardial stress).© 2010 ElsevierI documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
