{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T07:11:42Z","timestamp":1761894702853},"reference-count":29,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2008,4,10]],"date-time":"2008-04-10T00:00:00Z","timestamp":1207785600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Endocrinology"],"published-print":{"date-parts":[[2008,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold>Objective\u2002<\/jats:bold> Patients with primary aldosteronism (PA) experience more cardiovascular events than patients with essential hypertension matched for risk factor profile. Endothelial progenitor cells (EPC) represent a bone marrow\u2010derived cell population implicated in vascular healing whose number correlates to the cardiovascular risk factor profile. Aldosterone has been reported to decrease EPC proliferation in rats.<\/jats:p><jats:p><jats:bold>Design and patients\u2002<\/jats:bold> We assessed (i) the growth characteristics of EPC from six PA patients and six matched normotensive controls; (ii) the growth characteristics of EPC treated with increasing doses of aldosterone.<\/jats:p><jats:p><jats:bold>Measurements\u2002<\/jats:bold> Senescence and cell\u2010cycle analysis of EPC from PA patients and normotensive controls and of aldosterone\u2010treated EPC from healthy volunteers.<\/jats:p><jats:p><jats:bold>Results\u2002<\/jats:bold> No difference was found in the senescence rate between EPC from PA patients (72\u00b74% senescent cells) and controls (70\u00b77%, <jats:italic>P<\/jats:italic>\u00a0&gt;\u00a00\u00b705). No difference was also found in the cell\u2010cycle distribution determined by FACS (controls: 75\u00b72% cells in G0\/G1 phase; PA: 73\u00b75%, <jats:italic>P<\/jats:italic>\u00a0&gt;\u00a00\u00b705). Incubation of EPC with aldosterone did not modify their senescence rate (controls: 72\u00b74% senescent cells; aldosterone 10\u00a0nmol\/l: 70\u00b79%; aldosterone 100\u00a0nmol\/l 71\u00b76%, <jats:italic>P<\/jats:italic>\u00a0&gt;\u00a00\u00b705 for all comparisons) and cell\u2010cycle distribution (controls: 73\u00b73% cells in G0\/G1 phase; aldosterone 10\u00a0nmol\/l: 74\u00b79%; aldosterone 100\u00a0nmol\/l: 75\u00b74%, <jats:italic>P<\/jats:italic>\u00a0&gt;\u00a00\u00b705 for all comparisons). No expression of the mineralocorticoid receptor (MR) transcript was found in EPC by RT\u2010PCR analysis.<\/jats:p><jats:p><jats:bold>Conclusions\u2002<\/jats:bold> High aldosterone levels, both in PA patients and <jats:italic>in vitro<\/jats:italic>, exert no direct or indirect effect on EPC growth characteristics.<\/jats:p>","DOI":"10.1111\/j.1365-2265.2008.03271.x","type":"journal-article","created":{"date-parts":[[2008,4,10]],"date-time":"2008-04-10T13:54:31Z","timestamp":1207835671000},"page":"528-534","source":"Crossref","is-referenced-by-count":8,"title":["Primary aldosteronism (PA) and endothelial progenitor cell (EPC) bioavailability"],"prefix":"10.1111","volume":"69","author":[{"given":"Andrea","family":"Verhovez","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Annarita","family":"Zeoli","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tracy 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