Activity of apelin and APJ receptors on myocardial contractility and vasomotor tone

Apelin, an endogenous peptide, is the ligand of APJ receptors. Although initially it was identified in the gastrointestinal tract, later its presence was found in several organs and tissues. On the cardiovascular system apelin induces an increase in myocardial contractility and a reduction of vasomotor tone. While the increase in contractility seems to depend on an activation of Na+/H+ and Na+/Ca2+ exchangers, vasodilation is attributed to a release of nitric oxide from the vascular endothelial cells. Apelin-induced vasodilation leads to a reduction of mean filling pressure which in turn causes a decrease of afterload and preload. When apelin is given acutely, the decrease in preload favors the reduction of stroke volume and cardiac output in spite of an increased contractility. On the contrary, when the peptide is administered for 2 weeks, cardiac output increases significantly without the occurrence of cardiac hypertrophy. It is not excluded that hypertrophy might occur after a longer administration.