title: Selective association of endogenous ouabain with subclinical organ damage in treated hypertensive patients.
abstract: According to previous studies endogenous ouabain (EO) closely correlates with high blood pressure, congestive heart failure and kidney disease in humans. Our aims were to analyse associations between plasma, urinary EO level and various markers of cardiovascular damage in treated hypertensive patients. Forty-one adult patients with hypertension and/or diabetes mellitus (DM) and/or chronic kidney disease (CKD) were studied. We assessed plasma and urinary EO, pro-brain natriuretic peptide and catecholamines, profile of ambulatory blood pressure monitor and cardiovascular status by echocardiography and echo-tracking. The highest level of plasma EO (19.7±9.5 pmol l⁻¹) was measured in hypertensive patients with DM and CKD. The nighttime mean arterial blood pressure independently correlated with the level of plasma EO (P=0.004), while independent predictor of the β-stiffness of carotid artery was the urinary EO (P=0.011). Elevated level of EO was associated with nighttime blood pressure and subclinical organ damage in treated hypertensive patients, suggesting possible role of EO in the pathogenesis of impaired diurnal blood pressure rhythm and arterial stiffness.
authors.affiliation: 2nd Department of Medicine and Nephrological Center, Faculty of Medicine, University of Pécs, Pécs, Hungary.
authors.forename: G
authors.initials: G
authors.lastname: Nagy
authors.forename: B
authors.initials: B
authors.lastname: Gaszner
authors.forename: É
authors.initials: É
authors.lastname: Lányi
authors.forename: L
authors.initials: L
authors.lastname: Markó
authors.forename: E
authors.initials: E
authors.lastname: Fehér
authors.forename: J
authors.initials: J
authors.lastname: Cseh
authors.forename: T
authors.initials: T
authors.lastname: Kõszegi
authors.forename: J
authors.initials: J
authors.lastname: Betlehem
authors.forename: E
authors.initials: E
authors.lastname: Sulyok
authors.forename: A
authors.initials: A
authors.lastname: Cziráki
authors.forename: I
authors.initials: I
authors.lastname: Wittmann
mesh_terms: D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use; D015415:Biomarkers; D018660:Blood Pressure Monitoring, Ambulatory; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D002395:Catecholamines / Q000652:urine; D002908:Chronic Disease; D002940:Circadian Rhythm; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism; D004452:Echocardiography; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology*; D007674:Kidney Diseases / Q000150:complications / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010042:Ouabain / Q000097:blood / Q000652:urine; D010446:Peptide Fragments / Q000097:blood; D012307:Risk Factors
chemical_list: D000959:Antihypertensive Agents; D015415:Biomarkers; D002395:Catecholamines; D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain; D010042:Ouabain