Intracoronary Des-Acyl Ghrelin Acutely Increases Cardiac Perfusion Through a Nitric Oxide-Related Mechanism in Female Anesthetized Pigs

摘要: Des-acyl ghrelin (DAG), the most abundant form of in humans, has been found to reduce arterial blood pressure and prevent cardiac endothelial cell apoptosis. Despite this, data regarding its direct effect on function coronary flow, as well related involvement autonomic nervous system nitric oxide (NO), are scarce. We therefore examined these issues using both vivo vitro studies. In 20 anesthetized pigs, intracoronary 100 pmol/mL DAG infusion with a constant heart rate aortic pressure, increased flow NO release, whereas reducing vascular resistances (P < .05). Dose responses were evaluated five pigs. No effects contractility/relaxation or myocardial oxygen consumption observed. Moreover, blockade muscarinic cholinoceptors (n = 5) α- β-adrenoceptors 5 each) did not abolish observed responses, synthase inhibition prevented release. artery cells, dose dependently release through cAMP signaling ERK1/2, Akt, p38 MAPK phosphorylation synthase. conclusion, primarily perfusion ERK1/2 Akt appears play roles eliciting production cells.