The endothelin receptor antagonist decreases ischemia/reperfusion-induced tumor necrosis factor production in isolated rat hearts

Role of angiotensin and endothelin in testicular ischemia reperfusion injury

“…ET1, endothelial‐derived vasoconstricting peptide, is more potent than A‐II. It stimulates several activation mechanisms on neutrophils, and induces ROS and the pro‐inflammatory tumor necrosis factor‐α production 43–46 . A‐II‐ and ET1‐induced processes contribute to acute testicular ischemic events 2–4,27,47 .…”

“…It stimulates several activation mechanisms on neutrophils, and induces ROS and the pro-inflammatory tumor necrosis factor-a production. [43][44][45][46] A-II-and ET1-induced processes contribute to acute testicular ischemic events. [2][3][4]27,47 It has been postulated that the protective effects of ACE inhibitors, ARB and ETA/ETB receptor blockers on IR injury might be related to opposing the vasoconstrictor, pro-inflammatory and oxidant effects of A-II and ET1.…”

Endothelin-A Receptor Inhibition After Cardiopulmonary Bypass: Cytokines and Receptor Activation

“…Past in vitro and in vivo experimental models have established that ET-AR activation can induce the synthesis and release of TNF [22, 23]. Binding of ET to the ET-AR can result in the induction of an intracellular cascade which culminates in both pre-transcriptional and transcriptional events (Figure 3) [22, 33].…”

“…Thus measurements of relative changes in TNF/TNFRI and TNF/TNFRII within the systemic circulation provide an index of TNFR activation. Past in vitro and in vivo studies have demonstrated ET can induce the biosynthesis and release of TNF [22, 23]. Therefore, the hypothesis of this study is that administration of a selective ET-AR antagonist immediately following separation from CPB would alter the TNF receptor profile in a dose dependent manner.…”

Increased insulin‐stimulated endothelin‐1 release is a distinct vascular phenotype distinguishing Cushing's disease from metabolic syndrome

“…Furthermore, it has been shown that endothelin‐1 is locally produced in the atherosclerotic intima by macrophages and that chronic inflammatory processes may be involved in the generation of endothelin‐1 28,29 . Indeed, the presence of high TNF‐alpha levels in these patients may contribute to stimulate endothelin‐1 release 30 which, in turn, determine a further increase of TNF‐alpha levels 31 . Interestingly, CRP and IL‐6 levels were also higher in CD patients than in C patients.…”