{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T11:52:31Z","timestamp":1778759551634,"version":"3.51.4"},"reference-count":31,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2014,5,20]],"date-time":"2014-05-20T00:00:00Z","timestamp":1400544000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Clin Investigation"],"published-print":{"date-parts":[[2014,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Both increased and decreased levels of the adipokine retinol\u2010binding protein 4 (<jats:styled-content style=\"fixed-case\">RBP<\/jats:styled-content>4) have been reported in cardiovascular disease, and levels of <jats:styled-content style=\"fixed-case\">RBP<\/jats:styled-content>4 have been related to diabetes, metabolic syndrome and cardiovascular risk. Recently, clear <jats:italic>in vitro<\/jats:italic> and <jats:italic>ex vivo<\/jats:italic> vasodilatory and inhibitory of platelet activation effects of <jats:styled-content style=\"fixed-case\">RBP<\/jats:styled-content>4 has been shown and a reduced <jats:styled-content style=\"fixed-case\">RBP<\/jats:styled-content>4 level was found in high cardiovascular risk patients, suggesting a potential cardiovascular protective role for increased levels of <jats:styled-content style=\"fixed-case\">RBP<\/jats:styled-content>4.<\/jats:p><\/jats:sec><jats:sec><jats:title>Patients and methods<\/jats:title><jats:p>Plasma level of <jats:styled-content style=\"fixed-case\">RBP<\/jats:styled-content>4 (<jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content>) was determined in a cohort of <jats:styled-content style=\"fixed-case\">B<\/jats:styled-content>artter's and <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>itelman's syndrome (<jats:styled-content style=\"fixed-case\">BS<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">GS<\/jats:styled-content>) patients, a human model of endogenous <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>ng <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> signalling antagonism and activation of anti\u2010atherosclerotic and antiremodelling defenses, the opposite of cardiovascular risk patients, and in healthy normotensive subjects. Haem <jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>xygenase (<jats:styled-content style=\"fixed-case\">OH<\/jats:styled-content>)\u20101 protein level (sandwich immunoassay) as a potential mediator of <jats:styled-content style=\"fixed-case\">RBP<\/jats:styled-content>4 stimulation of <jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>3<jats:styled-content style=\"fixed-case\">K<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>kt pathway and flow\u2010mediated dilation (<jats:styled-content style=\"fixed-case\">FMD<\/jats:styled-content>) as a measure of endothelium (<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>)\u2010dependent response have also been measured.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">RBP<\/jats:styled-content>4 in <jats:styled-content style=\"fixed-case\">BS<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">GS<\/jats:styled-content> patients (40\u00b759\u00a0\u00b1\u00a015\u00b732\u00a0\u03bcg\/mL vs. 25\u00b705\u00a0\u00b1\u00a05\u00b756, <jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7011) along with <jats:styled-content style=\"fixed-case\">HO<\/jats:styled-content>\u20101 protein levels (9\u00b744\u00a0\u00b1\u00a03\u00b709\u00a0ng\/mL vs. 5\u00b749\u00a0\u00b1\u00a01\u00b704, <jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7003) and <jats:styled-content style=\"fixed-case\">FMD<\/jats:styled-content> (10\u00b752%\u00a0\u00b1\u00a02\u00b722 vs. 7\u00b799\u00a0\u00b1\u00a01\u00b713 <jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7006) were significantly increased compared with healthy normotensive subjects.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The increase of <jats:styled-content style=\"fixed-case\">RBP<\/jats:styled-content>4 in <jats:styled-content style=\"fixed-case\">BS<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">GS<\/jats:styled-content>, a human model of endogenous <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>ng <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> signalling antagonism and activation of anti\u2010atherosclerotic and antiremodelling defenses, the opposite of cardiovascular risk patient, found in concert with an increased <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>\u2010mediated vasodilation and <jats:styled-content style=\"fixed-case\">HO<\/jats:styled-content>\u20101 levels supports a protective role for this adipokine in vascular protection\/cardiovascular risk.<\/jats:p><\/jats:sec>","DOI":"10.1111\/eci.12270","type":"journal-article","created":{"date-parts":[[2014,4,16]],"date-time":"2014-04-16T18:09:07Z","timestamp":1397671747000},"page":"567-572","source":"Crossref","is-referenced-by-count":12,"title":["Increased 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