{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T13:01:25Z","timestamp":1791896485672,"version":"4.3.4"},"reference-count":34,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2001,2]]},"abstract":"<jats:p>\n            The  pathophysiological mechanisms responsible for  maintenance of chronic renovascular hypertension remain  undefined. Excess angiotensin II generation may lead to  release of reactive oxygen species and increased vasoconstrictor  activity. To examine the potential involvement of oxidation-sensitive  mechanisms in the pathophysiology of renovascular hypertension, blood  samples were collected and renal blood flow measured with electron-beam  computed tomography in pigs 5 and 10 weeks after induction of  unilateral renal artery stenosis (n=7) or sham operation (n=7).  Five weeks after procedure, plasma renin activity and mean  arterial pressure were elevated in hypertensive pigs.  Levels of prostaglandin F2\u03b1  (PGF\n            <jats:sub>2\u03b1<\/jats:sub>\n            )\u2013isoprostanes, vasoconstrictors and  markers of oxidative stress, also were significantly increased (157\u00b121  versus 99\u00b116 pg\/mL;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05)  and correlated with both plasma renin activity  (\n            <jats:italic>r<\/jats:italic>\n            =0.83) and  arterial pressure  (\n            <jats:italic>r<\/jats:italic>\n            =0.82). By 10 weeks, plasma  renin activity returned to baseline but arterial pressure  remained elevated (144\u00b110 versus 115\u00b15 mm Hg;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). Isoprostane levels  remained high and still correlated directly with the increase in  arterial pressure  (\n            <jats:italic>r<\/jats:italic>\n            =0.7) but not with plasma  renin activity. Stenotic kidney blood flow was decreased at  both studies. In shock-frozen cortical tissue, ex vivo  endogenous intracellular radical scavengers were  significantly decreased in both kidneys. The present study  demonstrates, for the first time, that in early renovascular  hypertension, an increase in plasma renin activity and  arterial pressure is associated with increased systemic  oxidative stress. When plasma renin activity later declines,  PGF\n            <jats:sub>2\u03b1<\/jats:sub>\n            -isoprostanes remain elevated, possibly  due to local activation or slow responses to angiotensin  II, and may participate in sustenance of arterial pressure.  Moreover, oxidation-sensitive mechanisms may influence ischemic  and hypertensive parenchymal renal injury.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.37.2.541","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"541-546","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":199,"title":["Increased Oxidative Stress in Experimental Renovascular Hypertension"],"prefix":"10.1161","volume":"37","author":[{"given":"Lilach O.","family":"Lerman","sequence":"first","affiliation":[{"name":"From the Department of Internal Medicine, Divisions of Hypertension  (L.O.L., J.D.K.), Nephrology (K.A.N.) and Cardiovascular Diseases (R.S.S.),  and the Department of Physiology and Biophysics (J.C.R.), Mayo Clinic,  Rochester, Minn; the Department of Medicine, University of Naples, Italy  (C.N.); and the Department of Medicine-0682, University of California, San  Diego, Calif (C.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl A.","family":"Nath","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Divisions of Hypertension  (L.O.L., J.D.K.), Nephrology (K.A.N.) and Cardiovascular Diseases (R.S.S.),  and the Department of Physiology and Biophysics (J.C.R.), Mayo Clinic,  Rochester, Minn; the Department of Medicine, University of Naples, Italy  (C.N.); and the Department of Medicine-0682, University of California, San  Diego, Calif (C.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Rodriguez-Porcel","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Divisions of Hypertension  (L.O.L., J.D.K.), Nephrology (K.A.N.) and Cardiovascular Diseases (R.S.S.),  and the Department of Physiology and Biophysics (J.C.R.), Mayo Clinic,  Rochester, Minn; the Department of Medicine, University of Naples, Italy  (C.N.); and the Department of Medicine-0682, University of California, San  Diego, Calif (C.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James D.","family":"Krier","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Divisions of Hypertension  (L.O.L., J.D.K.), Nephrology (K.A.N.) and Cardiovascular Diseases (R.S.S.),  and the Department of Physiology and Biophysics (J.C.R.), Mayo Clinic,  Rochester, Minn; the Department of Medicine, University of Naples, Italy  (C.N.); and the Department of Medicine-0682, University of California, San  Diego, Calif (C.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert S.","family":"Schwartz","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Divisions of Hypertension  (L.O.L., J.D.K.), Nephrology (K.A.N.) and Cardiovascular Diseases (R.S.S.),  and the Department of Physiology and Biophysics (J.C.R.), Mayo Clinic,  Rochester, Minn; the Department of Medicine, University of Naples, Italy  (C.N.); and the Department of Medicine-0682, University of California, San  Diego, Calif (C.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudio","family":"Napoli","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Divisions of Hypertension  (L.O.L., J.D.K.), Nephrology (K.A.N.) and Cardiovascular Diseases (R.S.S.),  and the Department of Physiology and Biophysics (J.C.R.), Mayo Clinic,  Rochester, Minn; the Department of Medicine, University of Naples, Italy  (C.N.); and the Department of Medicine-0682, University of California, San  Diego, Calif (C.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. Carlos","family":"Romero","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Divisions of Hypertension  (L.O.L., J.D.K.), Nephrology (K.A.N.) and Cardiovascular Diseases (R.S.S.),  and the Department of Physiology and Biophysics (J.C.R.), Mayo Clinic,  Rochester, Minn; the Department of Medicine, University of Naples, Italy  (C.N.); and the Department of Medicine-0682, University of California, San  Diego, Calif (C.N.)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.59.3.347"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.34.4.943"},{"key":"e_1_3_2_3_2","first-page":"394","volume":"20","year":"2000","unstructured":"Welch WJ. The pathophysiology of renin release in renovascular hypertension. 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