title: Different pathomechanisms of essential and obesity-associated hypertension in adolescents.
abstract: Obesity-induced hypertension and essential hypertension in lean patients are two different forms of hypertension. The main goal of this study was to test whether there are differences in biochemical parameters between subjects with obesity-associated hypertension and those with essential hypertension. We examined whether the biochemical responses to angiotensin-converting enzyme inhibitor (ACEI) ramipril therapy reveal properties of these two conditions that might explain the differences in clinical outcome. Before ramipril therapy, the hypertensive group exhibited increases in ACE activity (p<0.05), plasma malondialdehyde (MDA) concentration and the malondialdehyde/nitric oxide end-product ratio (MDA/NO(x)) (p<0.05), and decreases in xanthine oxidase (XO) activity (p<0.05) and plasma nitric oxide end-product (NO(x)) level (p<0.01). Before medication, plasma endothelin-1 (ET-1), plasma leptin, and leptin receptor levels were normal. Following ramipril treatment, ACE activity normalized. Before ACE inhibitor treatment, the obese-hypertensive group exhibited elevated levels of plasma ET-1 (p<0.05), plasma leptin (p<0.01), XO activity (p<0.05), plasma MDA and MDA/NO(x) (p<0.05), and reduced levels of plasma NO(x)(p<0.01) and leptin receptors (p<0.001). Following medication, the plasma NO(x) level, MDA/NO(x), and XO activity returned to normal while ACE activity decreased (p<0.001). In patients with essential hypertension, NO availability and ACE activity, and in those with obesity-associated hypertension, hyperleptinemic effects, NO level, endothelin-1 concentration and XO activity, may be important factors in the pathology.
authors.affiliation: Department of Pediatrics, Albert Szent-Györgyi Medical and Pharmaceutical Centre, University of Szeged, Korányi fasor 14-15, Szeged H-6721, Hungary. a.barath@gmail.com
authors.forename: Akos
authors.initials: A
authors.lastname: Baráth
authors.forename: Sándor
authors.initials: S
authors.lastname: Túri
authors.forename: Ilona
authors.initials: I
authors.lastname: Németh
authors.forename: Csaba
authors.initials: C
authors.lastname: Bereczki
authors.forename: Balázs
authors.initials: B
authors.lastname: Gellén
authors.forename: Ibolya
authors.initials: I
authors.lastname: Haszon
authors.forename: Péter
authors.initials: P
authors.lastname: Monostori
mesh_terms: D000293:Adolescent; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D015992:Body Mass Index; D019332:Endothelin-1 / Q000097:blood / Q000502:physiology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology*; D020738:Leptin / Q000097:blood / Q000502:physiology; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009569:Nitric Oxide / Q000097:blood / Q000502:physiology; D009765:Obesity / Q000097:blood / Q000150:complications* / Q000503:physiopathology*; D007703:Peptidyl-Dipeptidase A / Q000097:blood / Q000502:physiology; D017257:Ramipril / Q000627:therapeutic use; D014969:Xanthine Oxidase / Q000097:blood / Q000502:physiology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D019332:Endothelin-1; D020738:Leptin; D009569:Nitric Oxide; D008315:Malondialdehyde; D014969:Xanthine Oxidase; D007703:Peptidyl-Dipeptidase A; D017257:Ramipril