{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T09:39:30Z","timestamp":1780047570172,"version":"3.53.1"},"reference-count":48,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2001,3]]},"abstract":"<jats:p>\n            <jats:italic>We  previously reported that inhibition of  angiotensin-converting enzyme (ACE) prevented the  hypertension and left ventricular hypertrophy  induced by deoxycorticosterone acetate\u2013salt (DOCA-salt) in 129\/SvEvTac  mice, which have 2 renin genes (Ren-1 and  Ren-2<\/jats:italic>\n            ). In the present study, we induced hypertension by  uninephrectomy and DOCA-salt in mice having only the\n            <jats:italic>Ren-1<\/jats:italic>\n            gene (C57BL\/6J) and  investigated the effect of an ACE inhibitor (ramipril, 4  mg \u00b7 kg\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>1<\/jats:sup>\n            \u00b7 d\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>1<\/jats:sup>\n            )  and an angiotensin type 1 (AT\n            <jats:sub>1<\/jats:sub>\n            )  receptor antagonist (L-158809, 4  mg \u00b7 kg\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>1<\/jats:sup>\n            \u00b7 d\n            <jats:sup>\u2212<\/jats:sup>\n            <jats:sup>1<\/jats:sup>\n            )  on the development of hypertension, cardiac hypertrophy,  and renal injury. After 4 weeks of treatment, systolic blood  pressure in DOCA-salt mice was significantly increased (128\u00b12  mm Hg) compared with controls (109\u00b12 mm Hg)  (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.001), while plasma renin  concentration was decreased by 97%  (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.001). DOCA-salt also  induced left ventricular and renal hypertrophy  and renal damage as manifested by proteinuria. Collagen content in the  left ventricle and kidney was significantly higher in DOCA-salt mice  (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.001). Urinary  albumin (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05) and  proliferating cell nucleic antigen\u2013positive cells in the tubules and  interstitium of the renal cortex  (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.001) were significantly  increased in the DOCA-salt group. Neither the ACE inhibitor  nor the AT\n            <jats:sub>1<\/jats:sub>\n            antagonist had any  antihypertensive effect; however, they partially prevented cardiac  hypertrophy and completely inhibited left  ventricular collagen deposition. In the kidney, both the  ACE inhibitor and AT\n            <jats:sub>1<\/jats:sub>\n            antagonist partially reduced the increase in collagen but  had no effect on hypertrophy. They also significantly  prevented the effect of DOCA-salt on urinary albumin and  proliferating cell nucleic antigen expression in the kidney. Despite  the lack of an antihypertensive effect, both ACE inhibitor  and AT\n            <jats:sub>1<\/jats:sub>\n            antagonist prevented cardiac  remodeling and renal damage. Our results indicate that ACE  inhibitors and AT\n            <jats:sub>1<\/jats:sub>\n            antagonists exert beneficial effects on the heart and  kidney in DOCA-salt hypertensive mice independently of their effects on  blood pressure.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.37.3.974","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"974-980","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":35,"title":["Effects of Angiotensin-Converting Enzyme Inhibitor and Angiotensin Type 1 Receptor Antagonist in Deoxycorticosterone Acetate\u2013Salt Hypertensive Mice Lacking\n            <i>Ren-2 Gene<\/i>"],"prefix":"10.1161","volume":"37","author":[{"given":"Hongmei","family":"Peng","sequence":"first","affiliation":[{"name":"From the Hypertension and Vascular Research Division and Department of  Biostatistics and Research Epidemiology (J.A.M.), Henry Ford Hospital,  Detroit, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oscar A.","family":"Carretero","sequence":"additional","affiliation":[{"name":"From the Hypertension and Vascular Research Division and Department of  Biostatistics and Research Epidemiology (J.A.M.), Henry Ford Hospital,  Detroit, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcos E.","family":"Alfie","sequence":"additional","affiliation":[{"name":"From the Hypertension and Vascular Research Division and Department of  Biostatistics and Research Epidemiology (J.A.M.), Henry Ford Hospital,  Detroit, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie A.","family":"Masura","sequence":"additional","affiliation":[{"name":"From the Hypertension and Vascular Research Division and Department of  Biostatistics and Research Epidemiology (J.A.M.), Henry Ford Hospital,  Detroit, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nour-Eddine","family":"Rhaleb","sequence":"additional","affiliation":[{"name":"From the Hypertension and Vascular Research Division and Department of  Biostatistics and Research Epidemiology (J.A.M.), Henry Ford Hospital,  Detroit, Mich."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.24.2.195"},{"key":"e_1_3_2_2_2","first-page":"H739","volume":"257","year":"1989","unstructured":"Villarreal D, Freeman RH, Brands MW. 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