{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T20:25:54Z","timestamp":1792009554133,"version":"4.4.0"},"reference-count":57,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2006,12]]},"abstract":"<jats:p>\n                    This study tested the hypothesis that angiotensin promotes oxidative stress and inflammation in humans via aldosterone and the mineralocorticoid receptor. We measured the effect of intravenous aldosterone (0.7 \u03bcg\/kg per hour for 10 hours followed by 0.9 \u03bcg\/kg per hour for 4 hours) and vehicle in a randomized, double-blind crossover study in 11 sodium-restricted normotensive subjects. Aldosterone increased interleukin (IL)-6 (from 4.7\u00b14.9 to 9.4\u00b17.1 pg\/mL; F=4.94;\n                    <jats:italic>P<\/jats:italic>\n                    =0.04) but did not affect blood pressure, serum potassium, or high-sensitivity C-reactive protein. We next conducted a randomized, double-blind, placebo-controlled, crossover study to measure the effect of 3-hour infusion of angiotensin II (2 ng\/kg per minute) and norepinephrine (30 ng\/kg per minute) on separate days after 2 weeks of placebo or spironolactone (50 mg per day) in 14 salt-replete normotensive subjects. Angiotensin II increased blood pressure (increase in systolic pressure: 13.7\u00b17.5 and 15.2\u00b19.4 mm Hg during placebo and spironolactone, respectively;\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.001 for angiotensin II) and decreased renal plasma flow (\u2212202\u00b173 and \u2212167\u00b1112 mL\/min\/1.73 kg\/m\n                    <jats:sup>2<\/jats:sup>\n                    ;\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.001 for angiotensin II effect) similarly during placebo and spironolactone. Spironolactone enhanced the aldosterone response to angiotensin II (increase of 17.0\u00b110.6 versus 9.0\u00b15.7 ng\/dL;\n                    <jats:italic>P<\/jats:italic>\n                    =0.002). Angiotensin II transiently increased free plasma F\n                    <jats:sub>2<\/jats:sub>\n                    -isoprostanes similarly during placebo and spironolactone. Angiotensin II increased serum IL-6 concentrations during placebo (from 1.8\u00b11.1 to 2.4\u00b11.4 pg\/mL; F=4.5;\n                    <jats:italic>P<\/jats:italic>\n                    =0.04) but spironolactone prevented this effect (F=6.4;\n                    <jats:italic>P<\/jats:italic>\n                    =0.03 for spironolactone effect). Norepinephrine increased blood pressure and F\n                    <jats:sub>2<\/jats:sub>\n                    -isoprostanes but not aldosterone or IL-6. Aldosterone increases IL-6 in humans. These data suggest that angiotensin II induces IL-6 through a mineralocorticoid receptor\u2013dependent mechanism in humans. In contrast, angiotensin II\u2013induced oxidative stress, as measured by F\n                    <jats:sub>2<\/jats:sub>\n                    -isoprostanes, is mineralocorticoid receptor independent and may be pressor dependent.\n                  <\/jats:p>","DOI":"10.1161\/01.hyp.0000248135.97380.76","type":"journal-article","created":{"date-parts":[[2006,10,17]],"date-time":"2006-10-17T08:09:32Z","timestamp":1161072572000},"page":"1050-1057","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":145,"title":["Angiotensin II Induces Interleukin-6 in Humans Through a Mineralocorticoid Receptor\u2013Dependent Mechanism"],"prefix":"10.1161","volume":"48","author":[{"given":"James M.","family":"Luther","sequence":"first","affiliation":[{"name":"From the Divisions of Clinical Pharmacology (J.M.L., J.V.G., L.J.M., J.D.M., N.J.B.), Nephrology and Hypertension (J.M.L.), and Cardiovascular Medicine (D.E.V.), the Departments of Medicine and Pharmacology, and the Department of Biostatistics (C.Y.), Vanderbilt University Medical Center; Nashville, Tenn; and the Veterans Affairs Medical Center (D.E.V.), Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James V.","family":"Gainer","sequence":"additional","affiliation":[{"name":"From the Divisions of Clinical Pharmacology (J.M.L., J.V.G., L.J.M., J.D.M., N.J.B.), Nephrology and Hypertension (J.M.L.), and Cardiovascular Medicine (D.E.V.), the Departments of Medicine and Pharmacology, and the Department of Biostatistics (C.Y.), Vanderbilt University Medical Center; Nashville, Tenn; and the Veterans Affairs Medical Center (D.E.V.), Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laine J.","family":"Murphey","sequence":"additional","affiliation":[{"name":"From the Divisions of Clinical Pharmacology (J.M.L., J.V.G., L.J.M., J.D.M., N.J.B.), Nephrology and Hypertension (J.M.L.), and Cardiovascular Medicine (D.E.V.), the Departments of Medicine and Pharmacology, and the Department of Biostatistics (C.Y.), Vanderbilt University Medical Center; Nashville, Tenn; and the Veterans Affairs Medical Center (D.E.V.), Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chang","family":"Yu","sequence":"additional","affiliation":[{"name":"From the Divisions of Clinical Pharmacology (J.M.L., J.V.G., L.J.M., J.D.M., N.J.B.), Nephrology and Hypertension (J.M.L.), and Cardiovascular Medicine (D.E.V.), the Departments of Medicine and Pharmacology, and the Department of Biostatistics (C.Y.), Vanderbilt University Medical Center; Nashville, Tenn; and the Veterans Affairs Medical Center (D.E.V.), Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Douglas E.","family":"Vaughan","sequence":"additional","affiliation":[{"name":"From the Divisions of Clinical Pharmacology (J.M.L., J.V.G., L.J.M., J.D.M., N.J.B.), Nephrology and Hypertension (J.M.L.), and Cardiovascular Medicine (D.E.V.), the Departments of Medicine and Pharmacology, and the Department of Biostatistics (C.Y.), Vanderbilt University Medical Center; Nashville, Tenn; and the Veterans Affairs Medical Center (D.E.V.), Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jason D.","family":"Morrow","sequence":"additional","affiliation":[{"name":"From the Divisions of Clinical Pharmacology (J.M.L., J.V.G., L.J.M., J.D.M., N.J.B.), Nephrology and Hypertension (J.M.L.), and Cardiovascular Medicine (D.E.V.), the Departments of Medicine and Pharmacology, and the Department of Biostatistics (C.Y.), Vanderbilt University Medical Center; Nashville, Tenn; and the Veterans Affairs Medical Center (D.E.V.), Nashville, Tenn."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nancy J.","family":"Brown","sequence":"additional","affiliation":[{"name":"From the Divisions of Clinical Pharmacology (J.M.L., J.V.G., L.J.M., J.D.M., N.J.B.), Nephrology and Hypertension (J.M.L.), and Cardiovascular Medicine (D.E.V.), the Departments of Medicine and Pharmacology, and the Department of Biostatistics (C.Y.), Vanderbilt University Medical Center; 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