{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T17:52:52Z","timestamp":1773424372966,"version":"3.50.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2000,2,1]]},"abstract":"<jats:p>Experiments were designed to elucidate the role of endothelin B receptors (ET<jats:sub>B<\/jats:sub>) on arterial pressure and renal function in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Male Sprague-Dawley rats underwent uninephrectomy and were treated with either DOCA and salt (0.9% NaCl to drink) or placebo. DOCA-salt rats given the ET<jats:sub>B<\/jats:sub>-selective antagonist, A-192621, for 1 wk (10 mg \u22c5 kg<jats:sup>\u2212<\/jats:sup><jats:sup>1<\/jats:sup>\u22c5 day<jats:sup>\u2212<\/jats:sup><jats:sup>1<\/jats:sup>in the food) had significantly greater systolic arterial pressure compared with untreated DOCA-salt rats (208 \u00b1 7 vs. 182 \u00b1 4 mmHg) whereas pressure in placebo rats was unchanged. In DOCA-salt, but not placebo rats, A-192621 significantly decreased sodium and water excretion along with parallel decreases in food and water intake. To determine whether the response in DOCA-salt rats was due to increased expression of ET<jats:sub>B<\/jats:sub>receptors, endothelin receptor binding was performed by using membranes from renal medulla. Maximum binding (B<jats:sub>max<\/jats:sub>) of [<jats:sup>125<\/jats:sup>I]ET-1, [<jats:sup>125<\/jats:sup>I]ET-3, and [<jats:sup>125<\/jats:sup>I]IRL-1620 increased from 227 \u00b1 42, 146 \u00b1 28, and 21 \u00b1 1 fmol\/mg protein, respectively, in placebo rats to 335 \u00b1 27, 300 \u00b1 38, and 61 \u00b1 6 fmol\/mg protein, respectively, in DOCA-salt hypertensive rats. The fraction of receptors that are the ET<jats:sub>B<\/jats:sub>subtype was significantly increased in DOCA-salt (0.88 \u00b1 0.07) compared with placebo (0.64 \u00b1 0.01). The difference between [<jats:sup>125<\/jats:sup>I]ET-3 and [<jats:sup>125<\/jats:sup>I]IRL-1620 binding is consistent with possible ET<jats:sub>B<\/jats:sub>receptor subtypes in the kidney. These results indicate that ET<jats:sub>B<\/jats:sub>receptors in the renal medulla are up-regulated in the DOCA-salt hypertensive rat and may serve to maintain a lower arterial pressure by promoting salt and water excretion.<\/jats:p>","DOI":"10.1152\/ajprenal.2000.278.2.f279","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T11:35:23Z","timestamp":1514028923000},"page":"F279-F286","source":"Crossref","is-referenced-by-count":48,"title":["Upregulation of endothelin B receptors in kidneys of DOCA-salt hypertensive rats"],"prefix":"10.1152","volume":"278","author":[{"given":"David M.","family":"Pollock","sequence":"first","affiliation":[{"name":"Vascular Biology Center, Departments of Surgery, Physiology and Endocrinology, and Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912-2500; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Graham H.","family":"Allcock","sequence":"additional","affiliation":[{"name":"Vascular Biology Center, Departments of Surgery, Physiology and Endocrinology, and Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912-2500; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arthi","family":"Krishnan","sequence":"additional","affiliation":[{"name":"Vascular Biology Center, Departments of Surgery, Physiology and Endocrinology, and Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912-2500; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brian D.","family":"Dayton","sequence":"additional","affiliation":[{"name":"Pharmaceutical Discovery, Abbott Laboratories, Abbott Park, Illinois 60064-3500"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jennifer S.","family":"Pollock","sequence":"additional","affiliation":[{"name":"Vascular Biology Center, Departments of Surgery, Physiology and Endocrinology, and Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912-2500; and"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1998.275.1.R245"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.6.1191"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1097\/00005344-199526003-00097"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(87)90021-2"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1016\/0014-5793(96)00212-8"},{"key":"B6","doi-asserted-by":"publisher","DOI":"10.1016\/0895-7061(95)96213-4"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.85.24.9797"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1996.tb02773.x"},{"key":"B9","doi-asserted-by":"crossref","first-page":"1028","DOI":"10.1016\/S0022-3565(25)39463-2","volume":"267","author":"Edwards R. 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