{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T17:40:02Z","timestamp":1715535602367},"reference-count":26,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2000,10]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014Kidney function and  structure were compared in control rats (group 1) and in 3 groups of  rats made hypertensive by administration of aldosterone and  saline for 8 weeks (groups 2, 3, and 4). Group 2 rats received only  aldosterone and saline, while group 3 also received  losartan and group 4 also received enalapril. Rats in all  groups were subjected to uninephrectomy before beginning the  experiment. Hypertension and proteinuria in rats given  aldosterone and saline were not affected by  losartan or enalapril (8-week values for blood pressure in  mm Hg: 135\u00b13 group 1, 193\u00b14 group 2, 189\u00b14 group 3, 189\u00b15 group 4;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05 groups 2, 3, and 4 versus 1; 8-week values for  proteinuria in mg\/d: 44\u00b18 group 1, 278\u00b134 group 2, 267\u00b137 group 3,  289\u00b136 group 4;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05 groups 2, 3, and 4 versus 1).  Vascular, glomerular, and  tubulointerstitial injury accompanied hypertension  and proteinuria at 8 weeks. Losartan and enalapril did not  prevent vascular injury, which was characterized by thickening of  arterial and arteriolar walls and by fibrinoid necrosis and  thrombotic microangiopathy. Likewise, losartan and enalapril  did not reduce the prevalence of glomerular segmental  sclerosis (1\u00b11% group 1, 10\u00b12% group 2, 11\u00b12% group 3, 13\u00b12%  group 4;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05 groups 2, 3, and 4 versus 1) or limit  tubulointerstitial injury as reflected by the  volume fraction of the cortical interstitium (15\u00b11% group 1, 20\u00b11%  group 2, 21\u00b11% group 3, 21\u00b11% group 4;\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05  groups 2, 3, and 4 versus 1). These findings suggest that local  angiotensin II activity does not contribute to the  development of renal injury in mineralocorticoid-salt  hypertension.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.36.4.569","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"569-574","update-policy":"http:\/\/dx.doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":8,"title":["Effect of Angiotensin II Blockade on Renal Injury in Mineralocorticoid-Salt Hypertension"],"prefix":"10.1161","volume":"36","author":[{"given":"Mitra","family":"Sorooshian","sequence":"first","affiliation":[{"name":"From the Division of Nephrology, VA Palo Alto Health Care System and  Stanford University, Palo Alto, Calif (M.S., T.W.M.), and Department of  Pathology, University of California, San Francisco (J.L.O.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jean L.","family":"Olson","sequence":"additional","affiliation":[{"name":"From the Division of Nephrology, VA Palo Alto Health Care System and  Stanford University, Palo Alto, Calif (M.S., T.W.M.), and Department of  Pathology, University of California, San Francisco (J.L.O.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Timothy W.","family":"Meyer","sequence":"additional","affiliation":[{"name":"From the Division of Nephrology, VA Palo Alto Health Care System and  Stanford University, Palo Alto, Calif (M.S., T.W.M.), and Department of  Pathology, University of California, San Francisco (J.L.O.)."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","unstructured":"Olson JL. 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