endothelin-1 has been researched along with Uveitis--Anterior* in 3 studies
3 other study(ies) available for endothelin-1 and Uveitis--Anterior
Article | Year |
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Extra-Articular Symptoms in Constellation with Selected Serum Cytokines and Disease Activity in Spondyloarthritis.
Se recopilaron datos importantes y coherentes de 187 Estados Partes. Entre ellos, 43 (23,0%) prohibieron la entrada de extranjeros que habían visitado recientemente un país con un nivel generalizado de contagio del ebola y otros 15 (8,0%) impusieron otras restricciones importantes para dichos viajeros: el requisito de obtener un certificado médico que documentara que el individuo no estaba infectado con el virus ( Topics: Acquired Hyperostosis Syndrome; Adult; Arthritis, Psoriatic; Cytokines; Endothelin-1; Epidermal Growth Factor; Female; Humans; Interleukin-18; Interleukin-23; Interleukin-6; Male; Middle Aged; Risk; Spondylitis, Ankylosing; Uveitis, Anterior; Vascular Endothelial Growth Factor A | 2016 |
Effects of endothelin receptor antagonists on anterior chamber inflammation induced by intravitreal injection of endothelin-1.
To investigate the role of endothelin receptors (ET(A) and ET(B)) in the inflammatory reaction induced by endothelin-1 (ET-1), the time course of changes in aqueous protein concentration (APC) after the intravitreal injection of ET-1 (10(-4), 10(-5) M) was measured using a laser flare-cell meter in pigmented rabbit eyes. The effects of pre-treatment with specific ET(A) receptor antagonist (97-139) (10(-1), 10(-2), 10(-3), 10(-4) M), specific ET(B) receptor antagonist (BQ-788) (1.6 x 10(-3) M), and vehicle solution were assessed. The influence of ET(A)receptor antagonist pre-treatment on aqueous prostaglandin E(2) and leukotriene B(4) concentrations was also evaluated. As a result, pre-treatment with ET(A) receptor antagonist blocked the APC increase induced by 10(-4) M ET-1 in a dose dependent fashion, while BQ-788 did not suppress the inflammatory reaction. The injection of ET-1 increased aqueous prostaglandin E(2) concentration, which was inhibited by pre-treatment with ET(A) receptor antagonist. Aqueous leukotriene B(4) concentration was not affected by ET-1 nor ET(A) receptor antagonist. In conclusion, ET(A) receptor mediates the increases in aqueous protein and prostaglandin E(2) concentration induced by ET-1 injection, and this inflammatory reaction occurs via the cyclooxygenase pathway of arachidonic acid cascade. Topics: Animals; Caffeic Acids; Dinoprostone; Endothelin Receptor Antagonists; Endothelin-1; Eye Proteins; Female; Leukotriene B4; Male; Oleanolic Acid; Oligopeptides; Piperidines; Rabbits; Receptors, Endothelin; Uveitis, Anterior | 1999 |
Inflammatory reaction via arachidonic acid cascade after intravitreal injection of endothelin-1.
To investigate the characteristics of anterior chamber inflammatory reaction induced by intravitreal injection of endothelin-1 (ET-1).. The time course of changes in aqueous protein concentration (APC) after intravitreal injection of 10(-4), 10(-5), 10(-6) and 10(-7) M ET-1 into rabbit eyes was measured with a laser flare-cell meter. The influence of a topical diclofenac sodium (DFNa) pre- and post-treatment was assessed. Aqueous prostaglandin E2 and leukotriene B4 concentration was quantified using a radioimmunoassay technique.. Intravitreal injection of 10(-4) and 10(-5) M ET-1 significantly increased APC, while 10(-6) and 10(-7) M ET-1 did not induce anterior chamber inflammation. After 10(-5) M ET-1 injection, APC reached a maximum at 4 h post-treatment and returned to a normal level 48 h after injection. Eyes treated with 10(-4) M ET-1 displayed a bi-phasic time course, with peak values observed 4 to 8 h as well as 48 h after administration. Pre- and post-treatment with topical DFNa completely suppressed the APC increase in the 10(-5) M ET-1 preparation, and considerably inhibited it in the 10(-4) M ET-1 preparation. After ET-1 injection, aqueous prostaglandin E2 concentration increased significantly, followed by an increase in APC. There were no changes in leukotriene B4 concentration.. ET-1 induces anterior chamber inflammation via the cyclooxygenase pathway of the arachidonic acid cascade. The lipoxygenase pathway is not involved in this reaction. Topics: Administration, Topical; Animals; Anterior Chamber; Aqueous Humor; Cyclooxygenase Inhibitors; Diclofenac; Dinoprostone; Endothelin-1; Eye Proteins; Female; Inflammation; Injections; Leukotriene B4; Male; Rabbits; Radioimmunoassay; Uveitis, Anterior; Vitreous Body | 1998 |