{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T09:53:29Z","timestamp":1648979609151},"reference-count":45,"publisher":"Canadian Science Publishing","issue":"10","license":[{"start":{"date-parts":[[2013,10,1]],"date-time":"2013-10-01T00:00:00Z","timestamp":1380585600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2013,10]]},"abstract":"<jats:p>This study focuses on the impact of aliskiren and (or) glucagon-like peptide-1 analogue on the binding affinity\/regulation of endothelin-1 (ET-1) to its receptor subtypes A (ET<jats:sub>A<\/jats:sub>R) and B (ET<jats:sub>B<\/jats:sub>R) at the level of the coronary endothelium and the cardiomyocytes in a type-1 diabetic rat model. Seven groups were used: (i) normal rats, (ii) rats with induced diabetes, (iii) rats with induced diabetes that were treated with insulin, (iv) rats with induced diabetes that were treated with exendin-4, (v) rats with induced diabetes that were treated with aliskiren, (vi) rats with induced diabetes that were co-treated with insulin plus aliskiren, and (vii) rats with induced diabetes that were co-treated with exendin-4 plus aliskiren. Heart perfusion with [<jats:sup>125<\/jats:sup>I]-ET-1 was employed to estimate ET-1 binding affinity (\u03c4 = 1\/K<jats:sub>\u2013n<\/jats:sub>) to ET<jats:sub>A<\/jats:sub>R and ET<jats:sub>B<\/jats:sub>R at the level of the coronary endothelium and the cardiomyocytes. Plasma ET-1 levels were measured using enzyme immunoassay, whereas densities of ET<jats:sub>A<\/jats:sub>R and ET<jats:sub>B<\/jats:sub>R were detected using Western blot. No significance differences were detected in the \u03c4 of ET<jats:sub>A<\/jats:sub>R and ET<jats:sub>B<\/jats:sub>R between normal and diabetic in cardiomyocytes and the coronary endothelium. Exendin-4 normalized the \u03c4 value for ET<jats:sub>A<\/jats:sub>R and ET<jats:sub>B<\/jats:sub>R on coronary endothelium, while aliskiren normalized it on cardiomyocytes. Furthermore, ET<jats:sub>A<\/jats:sub>R and ET<jats:sub>B<\/jats:sub>R densities were normalized with monotreatments of aliskiren and exendin-4, compared with up-regulated ET<jats:sub>A<\/jats:sub>R and down-regulated ET<jats:sub>B<\/jats:sub>R band densities in the diabetic animals. Our data indicate that aliskiren alleviates diabetes-associated hypertrophy in type 1 diabetes mellitus.<\/jats:p>","DOI":"10.1139\/cjpp-2013-0095","type":"journal-article","created":{"date-parts":[[2013,6,3]],"date-time":"2013-06-03T11:48:09Z","timestamp":1370260089000},"page":"830-838","source":"Crossref","is-referenced-by-count":2,"title":["Aliskiren, exendin-4, and insulin: their impact on endothelin receptor subtype(s) regulation\/binding in type 1 diabetic rat hearts"],"prefix":"10.1139","volume":"91","author":[{"given":"Sawsan M.","family":"Al Lafi","sequence":"first","affiliation":[{"name":"Department of Anatomy, Cell Biology and Physiology, Faculty of Medicine, American University of Beirut, Beirut 11-0236, Lebanon."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shushan B.","family":"Artinian","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Cell Biology and Physiology, Faculty of Medicine, American University of Beirut, Beirut 11-0236, Lebanon."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Suzan S.","family":"Boutary","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Cell Biology and Physiology, Faculty of Medicine, American University of Beirut, Beirut 11-0236, Lebanon."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nadine S.","family":"Zwainy","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Cell Biology and Physiology, Faculty of Medicine, American University of Beirut, Beirut 11-0236, Lebanon."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Khalil M.","family":"Bitar","sequence":"additional","affiliation":[{"name":"Department of Physics, Faculty of Arts and Sciences, American University of Beirut, Beirut 11-0236, Lebanon."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anwar B.","family":"Bikhazi","sequence":"additional","affiliation":[{"name":"Department of Anatomy, Cell Biology and Physiology, Faculty of Medicine, American University of Beirut, Beirut 11-0236, Lebanon."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"155","reference":[{"key":"refg1\/ref1","doi-asserted-by":"publisher","DOI":"10.3317\/jraas.2002.001"},{"key":"refg2\/ref2","doi-asserted-by":"crossref","unstructured":"Artinian, S.B., Al Lafi, S.M., Boutary, S.S., Bitar, K.M., Zwainy, N.S., and Bikhazi, A.B. 2011. 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