{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,7,15]],"date-time":"2024-07-15T13:10:27Z","timestamp":1721049027343},"reference-count":49,"publisher":"Institute of Physiology of the Czech Academy of Sciences","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Physiol Res"],"published-print":{"date-parts":[[2016,10,30]]},"abstract":"<jats:p>This study was designated to estimate protective role of ETA and ETB receptor antagonist against endothelin 1 (ET-1)-induced oxidative stress in lungs and determine whether these effects are mediated by nitric oxide (NO) synthase. Experiments were performed on Wistar rats divided into the following groups: I \u2013 saline (0.9 % NaCl); II \u2013 ET-1 (3 \u03bcg\/kg b.w.), III \u2013 BQ123 (1 mg\/kg b.w.) + ET-1 (3 \u03bcg\/kg b.w.), IV \u2013 BQ788 (3 mg\/kg b.w.) + ET-1 (3 \u03bcg\/kg b.w.), V \u2013 N-nitro-L-arginine methyl ester (L-NAME) (5 mg\/kg b.w.) + ET-1 (3 \u03bcg\/kg b.w.). ETA and ETB receptor antagonists or L-NAME were administered 30 min before ET-1 injection. The levels of the following substances were measured in the lungs homogenates: thiobarbituric acid reactive substances (TBARS), hydrogen peroxide (H2O2), reduced glutathione (GSH) and tumor necrosis factor-alpha (TNF-\u03b1). The results showed that ET-1 significantly increased TBARS, H2O2 (respectively: p&lt;0.001, p&lt;0.02) and TNF-\u03b1 levels (p&lt;0.02) and decreased the GSH level (p&lt;0.01) vs. control group. On the other hand, prior administration of ETA receptor blocker (BQ123) significantly attenuated TBARS (p&lt;0.01), H2O2 (p&lt;0.02), TNF-\u03b1 (p&lt;0.02) and increased GSH (p&lt;0.02) levels vs. ET-1. However, prior administration of ETB receptor blocker BQ788 did not cause significant changes in the: TBARS, H2O2 and TNF-\u03b1 (p&gt;0.05) levels, but significantly increased the GSH level and GSH\/GSSG ratio (p&lt;0.05). Administration of L-NAME significantly attenuated TBARS (p&lt;0.001), H2O2 (p&lt;0.05), TNF-\u03b1 (p&lt;0.01) and increased GSH (p&lt;0.05) levels vs. ET-1. In conclusion, we demonstrated that ET-1 induced oxidative stress in the lungs is mediated by ETA receptors. ETA receptor blockage inhibited generation of free radicals and TNF-\u03b1 and ameliorated antioxidant properties. Moreover, generation of reactive oxygen species is mediated by NOS in the lungs.<\/jats:p>","DOI":"10.33549\/physiolres.933263","type":"journal-article","created":{"date-parts":[[2020,2,28]],"date-time":"2020-02-28T08:49:26Z","timestamp":1582879766000},"page":"789-798","source":"Crossref","is-referenced-by-count":5,"title":["Influence of Endothelin 1 Receptor Blockers and a Nitric Oxide Synthase Inhibitor on Reactive Oxygen Species Formation in Rat Lungs"],"prefix":"10.33549","author":[{"given":"P.","family":"KLENIEWSKA","sequence":"first","affiliation":[{"name":"Experimental and Clinical Physiology, Department of Cardiovascular Physiology, Medical University of Lodz, Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.","family":"GOR\u0104CA","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"19169","published-online":{"date-parts":[[2016,10,15]]},"reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"BRIYAL S, GULATI K, GULATI A: Repeated administration of exendin-4 reduces focal cerebral ischemia-induced infarction in rats. 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