Journal Article10.1016/S0272-6386(96)90045-1
Endothelin in Organ Transplantation
TL;DR: Observations provide the rational to use ET receptor antagonists to formally address the potential role of ET in the initiation and propagation of posttransplantation complications; including systemic hypertension, acute allograft dysfunction, and perhaps most importantly, chronic allografted dysfunction.
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About: This article is published in American Journal of Kidney Diseases. The article was published on 01 Jan 1996. The article focuses on the topics: Transplantation & Organ transplantation.
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Citations
Outcomes in pediatric solid‐organ transplantation
TL;DR: LaRosa C, Jorge Baluarte H, Meyers KEC.
148
Prevention of cold ischaemia-reperfusion injury by an endothelin receptor antagonist in experimental renal transplantation.
I. Herrero,Joan Torras,Marta Riera,Enric Condom,Olga Coll,Josep M. Cruzado,Miguel Hueso,Jordi Bover,Nuria Lloberas,Jeroni Alsina,Josep M. Grinyó +10 more
TL;DR: It is concluded that cold ischaemia and preservation damage induces an increase in renal ET mRNA and irET expression in the reperfusion phase, contributing both to the deterioration of renal function and to tubular necrosis.
Assessment of oxidative stress in the early posttransplant period: comparison of cyclosporine A and tacrolimus-based regimens.
Abdulgaffar Vural,Mahmut Ilker Yilmaz,Kayser Caglar,Ahmet Aydin,Alper Sonmez,Tayfun Eyileten,Cengizhan Acikel,Bülent Güleç,Orhan Kozak,Köksal Öner +9 more
TL;DR: The study data suggest that the improvement in oxidative state parameters begins at the first day of renal transplantation and continues at the 28th posttransplant day in living donor transplantations.
52
Elevated neointimal endothelin-1 in transplantation-associated arteriosclerosis of renal allograft recipients
TL;DR: It is demonstrated that elevated ET-1 in the neointima is associated with Tx-AA and chronic rejection, and this results point to an important role for endothelial dysfunction in chronic renal allograft rejection.
46
Inhibition of endothelin-converting enzyme attenuates transplant vasculopathy and rejection in rat cardiac allografts.
TL;DR: It is concluded that, even in the absence of concomitant immunosuppression, inhibition of ET-1 biosynthesis significantly attenuates transplant vasculopathy and improves survival of LEW to F344 cardiac allografts.
39
References
Integrated cardiac, renal, and endocrine actions of endothelin.
TL;DR: It is indicated that endothelin is a potent vasoconstrictor that elevates systemic blood pressure in association with marked decreases in cardiovascular and renal function and may function as a counterregulatory hormone to the effects of endothelial-derived vasodilator agent(s).
Endothelin stimulates c-fos and c-myc expression and proliferation of vascular smooth muscle cells.
TL;DR: This work has shown that a potent vasoconstrictor peptide, endothelin (EDT), was isolated from vascular endothelial cells and stimulated the DNA synthesis of VSMCs in a dose‐dependent manner, which might be related to the development of atherosclerosis.
Chronic rejection in experimental cardiac transplantation: studies in the Lewis-F344 model.
David H. Adams,Mary E. Russell,Wayne W. Hancock,Mohamed H. Sayegh,Lauri R. Wyner,Morris J. Karnovsky +5 more
TL;DR: It is found that long-term surviving Lewis grafts in untreated F344 recipients are subjected to a chronic rejection process which results in the development of diffuse graft arteriosclerotic lesions, indistinguishable in appearance from those seen in human cardiac grafts.
Endothelins in the Kidney: Physiology and Pathophysiology
TL;DR: In summary, ET may be important in the pathogenesis of multiple diseases of the kidney and intense investigations are under way in an effort to develop specific inhibitors of ET action, including ECE inhibitors and ET receptor blockers.
The selective endothelin ETA receptor antagonist BQ123 antagonizes endothelin-1-mediated mitogenesis
TL;DR: Evaluated mitogenic effects of endothelin isopeptides and the selective ETA receptor antagonist BQ123 demonstrate that ET-1-mediated mitogenesis in vascular smooth muscle is mediated by ETA receptors.