{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T06:56:07Z","timestamp":1790924167047,"version":"4.1.0"},"reference-count":30,"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":[[1997,12]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            The incremental elastic modulus (Einc), which is the slope of the relationship between stress and strain of arteries, is a marker of vascular wall material stiffness. Isobaric Einc is reduced at the site of the radial artery in patients with essential hypertension and increased at the site of the common carotid artery in subjects with end-stage renal disease (ESRD). Whether the changes in Einc are influenced by the topography of the vessels, the composition of the arterial wall, and\/or by the presence of ESRD is largely ignored. Radial artery Einc was measured in 19 patients with ESRD and compared with the Einc of 89 subjects with essential hypertension and 20 normotensive control subjects. Transcutaneous measurements of radial artery internal diameter and wall thickness (echo-tracking device) and digital pulse pressure (Finapres) were allowed to calculate Einc under operational (ie, at the mean arterial pressure of each group) and isobaric (100 mm Hg) conditions, as well as for a given wall stress. Internal diameter and pulsatile changes in diameter were identical in the three groups. Wall thickness and mean blood pressure were significantly elevated in subjects with hypertension but not in ESRD patients. Circumferential wall stress was identical in the three groups. For the same operational wall stress, and therefore at the operational mean arterial pressure of each group, Einc (kPa \u00b7 10\n            <jats:sup>3<\/jats:sup>\n            ) was increased in patients with ESRD (5.53\u00b14.0 versus 3.3\u00b12.4 in control subjects;\n            <jats:italic>P<\/jats:italic>\n            &lt;.05) and normal in subjects with essential hypertension (3.87\u00b14.0). Under isobaric conditions, Einc was also significantly lower in subjects with hypertension and elevated in patients with ESRD. Thus, at the site of a medium-sized muscular artery constantly devoid of atherosclerosis, the stiffness of wall material is increased in patients with ESRD. The demonstrated alterations of the arterial wall are independent of the level of blood pressure and tensile stress and should be related to the status ESRD.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.30.6.1425","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:53:46Z","timestamp":1339462426000},"page":"1425-1430","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":84,"title":["Increased Stiffness of Radial Artery Wall Material in End-Stage Renal Disease"],"prefix":"10.1161","volume":"30","author":[{"given":"Jean-Jacques","family":"Mourad","sequence":"first","affiliation":[{"name":"From the Department of Internal Medicine (J.-J.M., X.G., M.S.) and Pharmacology (P.B., S.L.) and INSERM (U337), Broussais Hospital, Paris, and Manhe\u0300s Center (G.L.), 91700 Fleury Merogis, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xavier","family":"Girerd","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine (J.-J.M., X.G., M.S.) and Pharmacology (P.B., S.L.) and INSERM (U337), Broussais Hospital, Paris, and Manhe\u0300s Center (G.L.), 91700 Fleury Merogis, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pierre","family":"Boutouyrie","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine (J.-J.M., X.G., M.S.) and Pharmacology (P.B., S.L.) and INSERM (U337), Broussais Hospital, Paris, and Manhe\u0300s Center (G.L.), 91700 Fleury Merogis, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ste\u0301phane","family":"Laurent","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine (J.-J.M., X.G., M.S.) and Pharmacology (P.B., S.L.) and INSERM (U337), Broussais Hospital, Paris, and Manhe\u0300s Center (G.L.), 91700 Fleury Merogis, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michel","family":"Safar","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine (J.-J.M., X.G., M.S.) and Pharmacology (P.B., S.L.) and INSERM (U337), Broussais Hospital, Paris, and Manhe\u0300s Center (G.L.), 91700 Fleury Merogis, France."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ge\u0301rard","family":"London","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine (J.-J.M., X.G., M.S.) and Pharmacology (P.B., S.L.) and INSERM (U337), Broussais Hospital, Paris, and Manhe\u0300s Center (G.L.), 91700 Fleury Merogis, France."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"crossref","unstructured":"Yin FCP Ting C-T. 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