{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T01:19:07Z","timestamp":1788484747167,"version":"build-2803163510"},"reference-count":35,"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":"\n Abstract<\/jats:italic>\n \u2014We investigated whether a relationship exists between circulating transforming growth factor \u03b2 -1 (TGF-\u03b2\n 1<\/jats:sub>\n ), collagen type I metabolism, microalbuminuria, and left ventricular hypertrophy in essential hypertension and whether the ability of the angiotensin II type 1 receptor antagonist losartan to correct microalbuminuria and regress left ventricular hypertrophy in hypertensives is related to changes in TGF-\u03b2\n 1<\/jats:sub>\n and collagen type I metabolism. The study was performed in 30 normotensive healthy controls and 30 patients with never-treated essential hypertension classified into 2 groups: those with microalbuminuria (urinary albumin excretion >30 and <300 mg\/24 h) associated with left ventricular hypertrophy (left ventricular mass index >116 g\/m\n 2<\/jats:sup>\n for men and >104 g\/m\n 2<\/jats:sup>\n for women) (group B; n=17) and those without microalbuminuria or left ventricular hypertrophy (group A; n=13). The measurements were repeated in all patients after 6 months of treatment with losartan (50 mg once daily). The serum concentration of TGF-\u03b2\n 1<\/jats:sub>\n was measured by a 2-site ELISA method, and the serum concentrations of carboxy-terminal propeptide of procollagen type I (a marker of collagen type I synthesis) and carboxy-terminal telopeptide of collagen type I (a marker of collagen type I degradation) were measured by specific radioimmunoassays. The duration of hypertension and baseline values of blood pressure were similar in the 2 groups of patients. No differences in serum TGF-\u03b2\n 1<\/jats:sub>\n , carboxy-terminal propeptide of procollagen type I, and carboxy-terminal telopeptide of collagen type I were found between normotensives and group A of hypertensives. Serum TGF-\u03b2\n 1<\/jats:sub>\n , carboxy-terminal propeptide of procollagen type I, and the ratio of carboxy-terminal propeptide of procollagen type I to carboxy-terminal telopeptide of collagen type I were increased (\n P<\/jats:italic>\n <0.05) in group B of hypertensives compared with group A of hypertensives and normotensives. No differences in carboxy-terminal telopeptide of collagen type I were found among the 3 groups of subjects. After treatment with losartan, microalbuminuria and left ventricular hypertrophy persisted in 6 patients (then considered nonresponders) and disappeared in 11 patients (then considered responders) from group B. Compared with nonresponders, responders exhibited similar control of blood pressure and higher (\n P<\/jats:italic>\n <0.05) blockade of angiotensin II type 1 receptors (as assessed by a higher increase in plasma levels of angiotensin II). Whereas TGF-\u03b2\n 1<\/jats:sub>\n , carboxy-terminal propeptide of procollagen type I, and the ratio of carboxy-terminal propeptide of procollagen type I to carboxy-terminal telopeptide of collagen type I decreased (\n P<\/jats:italic>\n <0.05) in responders, no changes in these parameters were observed in nonresponders. These findings show that an association exists between an excess of TGF-\u03b2\n 1<\/jats:sub>\n , stimulation of collagen type I synthesis, inhibition of collagen type I degradation, and cardiorenal damage in a group of patients with essential hypertension. In addition, our results suggest that the ability of losartan to blunt the synthesis of TGF-\u03b2\n 1<\/jats:sub>\n and normalize collagen type I metabolism may contribute to protect the heart and the kidney in a fraction of patients with essential hypertension.\n <\/jats:p>","DOI":"10.1161\/01.hyp.36.4.517","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"517-522","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":97,"title":["Transforming Growth Factor \u03b2 in Hypertensives With Cardiorenal Damage"],"prefix":"10.1161","volume":"36","author":[{"given":"Concepcio\u0301n","family":"Laviades","sequence":"first","affiliation":[{"name":"From the Division of Nephrology, San Jorge General Hospital, Huesca (C.L.); Department of Clinical Chemistry, University Clinic, University of Navarra, Pamplona (N.V.); and Department of Cardiology, University Clinic and Vascular Pathophysiology Unit, School of Medicine, University of Navarra, Pamplona (J.D.), Spain."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nerea","family":"Varo","sequence":"additional","affiliation":[{"name":"From the Division of Nephrology, San Jorge General Hospital, Huesca (C.L.); Department of Clinical Chemistry, University Clinic, University of Navarra, Pamplona (N.V.); and Department of Cardiology, University Clinic and Vascular Pathophysiology Unit, School of Medicine, University of Navarra, Pamplona (J.D.), Spain."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Javier","family":"Di\u0301ez","sequence":"additional","affiliation":[{"name":"From the Division of Nephrology, San Jorge General Hospital, Huesca (C.L.); Department of Clinical Chemistry, University Clinic, University of Navarra, Pamplona (N.V.); and Department of Cardiology, University Clinic and Vascular Pathophysiology Unit, School of Medicine, University of Navarra, Pamplona (J.D.), Spain."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_1_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jhh.1000459"},{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199005313222203"},{"key":"e_1_3_1_3_2","doi-asserted-by":"crossref","unstructured":"Rodicio JL Campo C Ruilope LM. 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