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Different Pathomechanisms of Essential and Obesity-associated Hypertension in Adolescents

Overview
Journal Pediatr Nephrol
Specialties Nephrology
Pediatrics
Date 2006 Aug 10
PMID 16896999
Citations 3
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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.

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References
1.
Terada L, Willingham I, Rosandich M, Leff J, Kindt G, Repine J . Generation of superoxide anion by brain endothelial cell xanthine oxidase. J Cell Physiol. 1991; 148(2):191-6. DOI: 10.1002/jcp.1041480202. View

2.
Shek E, Brands M, Hall J . Chronic leptin infusion increases arterial pressure. Hypertension. 1998; 31(1 Pt 2):409-14. DOI: 10.1161/01.hyp.31.1.409. View

3.
Marzinzig M, Nussler A, Stadler J, Marzinzig E, Barthlen W, Nussler N . Improved methods to measure end products of nitric oxide in biological fluids: nitrite, nitrate, and S-nitrosothiols. Nitric Oxide. 1997; 1(2):177-89. DOI: 10.1006/niox.1997.0116. View

4.
Rubanyi G, Vanhoutte P . Superoxide anions and hyperoxia inactivate endothelium-derived relaxing factor. Am J Physiol. 1986; 250(5 Pt 2):H822-7. DOI: 10.1152/ajpheart.1986.250.5.H822. View

5.
Nakagawa K, Higashi Y, Sasaki S, Oshima T, Matsuura H, Chayama K . Leptin causes vasodilation in humans. Hypertens Res. 2002; 25(2):161-5. DOI: 10.1291/hypres.25.161. View