[Activity of apelin and APJ receptors on myocardial contractility and vasomotor tone].

Gianni Losano, Claudia Penna, Sandra Cappello, Pasquale Pagliaro
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Abstract

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.

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[apelin和APJ受体活性对心肌收缩力和血管舒缩张力的影响]。
APJ受体的配体是一种内源性肽Apelin。虽然最初是在胃肠道中发现的,但后来在几个器官和组织中发现了它的存在。在心血管系统中,apelin诱导心肌收缩力的增加和血管舒张性的降低。虽然收缩性的增加似乎依赖于Na+/H+和Na+/Ca2+交换器的激活,血管舒张归因于血管内皮细胞释放一氧化氮。apelin诱导的血管舒张导致平均充盈压力的降低,从而导致后负荷和预负荷的减少。当急性给予apelin时,尽管收缩力增加,但预负荷的减少有利于减少搏量和心输出量。相反,当肽给药2周时,心输出量显著增加,但未发生心肌肥厚。不排除在较长时间给药后可能发生肥厚。
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