{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T14:21:21Z","timestamp":1773325281155,"version":"3.50.1"},"reference-count":25,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2000,7]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014We have previously  reported that hyperglycemia in healthy human subjects increased the  renal vasodilator response to the angiotensin-converting  enzyme inhibitor captopril. This observation raised  intriguing possibilities relevant to the pathogenesis of  nephropathy in patients with diabetes mellitus. To  ascertain whether the effect of captopril was indeed mediated by a  reduction in angiotensin II (Ang II) formation, we  performed another study in which an Ang II antagonist,  eprosartan, was used in place of captopril. Nine healthy subjects were  studied in high sodium balance (ie, sodium intake 200 mmol\/d). On  the first day, the subjects received 600 mg eprosartan orally, and  renal plasma flow (RPF) and glomerular filtration rate  (GFR) were measured. Glucose was infused intravenously on  the second and third study days to increase plasma glucose to a level  below the threshold for glycosuria (\u22488.8 mmol\/L). Eprosartan at  a dose of 600 mg or placebo was administered randomly on the second or  third study day 1 hour after initiation of glucose infusion. RPF  increased (by 76\u00b17 mL \u00b7 min\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 1.73  m\n            <jats:sup>\u22122<\/jats:sup>\n            ,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01) in response to sustained  moderate hyperglycemia and then increased further (by 147\u00b115 mL  \u00b7 min\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 1.73 m\n            <jats:sup>\u22122<\/jats:sup>\n            ,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01) when eprosartan was administered during  hyperglycemia. Eprosartan, conversely, did not affect RPF and GFR in  normoglycemic subjects. GFR was not affected by either hyperglycemia or  eprosartan. Neither plasma renin activity nor plasma Ang II  concentration changed during hyperglycemia, suggesting that the  hormonal responses responsible for the enhanced renal vasodilator  response to eprosartan occurred within the kidney. The enhancement of  the renal vasodilator effect of eprosartan during hyperglycemia is  consistent with activation of the intrarenal  renin-angiotensin system.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.36.1.122","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"122-126","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":31,"title":["Effect of Angiotensin II Antagonist Eprosartan on Hyperglycemia-Induced Activation of Intrarenal Renin-Angiotensin System in Healthy Humans"],"prefix":"10.1161","volume":"36","author":[{"given":"Suzette Y.","family":"Osei","sequence":"first","affiliation":[{"name":"From the Departments of Medicine and Radiology, Brigham and Women\u2019s  Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Deborah A.","family":"Price","sequence":"additional","affiliation":[{"name":"From the Departments of Medicine and Radiology, Brigham and Women\u2019s  Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lori M. B.","family":"Laffel","sequence":"additional","affiliation":[{"name":"From the Departments of Medicine and Radiology, Brigham and Women\u2019s  Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maria C.","family":"Lansang","sequence":"additional","affiliation":[{"name":"From the Departments of Medicine and Radiology, Brigham and Women\u2019s  Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Norman K.","family":"Hollenberg","sequence":"additional","affiliation":[{"name":"From the Departments of Medicine and Radiology, Brigham and Women\u2019s  Hospital and Harvard Medical School, Boston, Mass."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1993.00410080037006"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1001\/archinte.1996.00440030080010"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.33.1.559"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.66.1.234"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1977.tb07537.x"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1210\/jcem-57-4-764"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.30.2.240"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.394"},{"key":"e_1_3_2_9_2","first-page":"26","volume":"13","year":"1980","unstructured":"Schnurr E, Lahme W, Kuppers H. 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