Apelin Antagonizes Myocardial Impairment in Sepsis

Effects of Acute Intravenous Infusion of Apelin on Left Ventricular Function in Dogs With Advanced Heart Failure

“…A comparison of our findings with those in the literature is difficult due to sparsity of published reports. In rats with sepsis induced by cecal ligation and puncture, mRNA and protein levels of APLN were decreased 38 . Pre-treatment with APLN in these rats partially prevented the decline in LV performance assessed based on peak LV +dp/dt 38 .…”

“…In rats with sepsis induced by cecal ligation and puncture, mRNA and protein levels of APLN were decreased 38 . Pre-treatment with APLN in these rats partially prevented the decline in LV performance assessed based on peak LV +dp/dt 38 . Contrary to our findings, studies in rats with HF produced by ligation of the left anterior descending coronary artery 5 showed that APLN levels as well as APJ concentration in LV tissue were increased and suggested that this increase represents a compensatory response to ischemia 5 .…”

The association between apelin-12 levels and paroxysmal supraventricular tachycardia

“…18 Apelin has been shown to exert potent positive inotropic effects on both normal and failing myocardium 20 by increasing intracellular calcium rather than enhancing the calcium sensitivity of the myofilaments. 13,21 The inotropic response to apelin may involve activation of phospholipase C, protein kinase C, and sarcolemmal sodium hydrogen exchange, and sodium calcium exchange. 21 In humans, apelin was reduced in patients with left ventricular dysfunction secondary to ischemic heart disease, congestive heart failure, and dyslipidemia.…”

Apelinergic system in endothelial cells and its role in angiogenesis in myocardial ischemia

“…Apelin has been found also to induce lower production of pro-inflammatory cytokines in macrophages (IL-6, IL-8 MIP-1α, M-CSF) and to reduce MCP-1 and TNF-α production [69]. Apelin-mediated inhibition of MCP-1 and IL-8 production has been reported also in peritoneal macrophages [113]. In view of the fact that there exist two monocyte/macrophage subpopulations, we might assume that the CD16 high subset, active later after MI, expresses a higher level of APJ receptor after hypoxia stimulation and hence responds to apelin more effectively.…”