Relation Between Endothelial Function and Leptin Level in Essential Hypertensive Patients

Abstract

Insulin resistance and sympathetic activation are shown to

play a role in the pathogenesis of essential hypertension. The role of sympathetic activation in essential hypertension has been

documented by a variety of tecniques. It has been known that leptin, produced by mainly adipose tissue, play a role in the pathogenesis of hypertension by causing sympathetic activation. Besides that, leptin may cause oxidative stress in endothelial cells by

inducing free oxygen radicals. Both oxidative stress and sympathetic activation may be a cause of endothelial dysfunction, described as an impairment of endothelium-dependent vasodilatation,

seen also in essential hypertensive patients. In view of these data, in this study we aimed to investigate a relation between endothelium-dependent dilatation and leptin in patients with essential

hypertension.

Thirty-five patients with essential hypertension (age: 44.2±7.1,

male/female: 19/16) and age and gender matched 38 healty controls (age:44.8 ± 5.6, male/female:20/18) were included in this study.

The measurements of endothelial function were done by ultrasonography described by Celermajer et al. Serum leptin levels did not

differ significantly between the two groups (3.86±4.4, 3.01±3.2 p>0.

05). Flow and nitrate mediated dilatation were found to be reduced

in hypertensive group when compared to control group. Flow mediated dilatation: 5.2±3.2 vs 12.7±3.6, p<0.001; nitrate mediated dilatation: 17.2±5.8 vs 22.4±5.5, p<0.001. Although there were

positive relation of leptin with body mass index and adipose tissue mass (respectively; r=0.47 ve r=0.50, p<0.01), there were no relation

between leptin and flow and nitrate mediated dilatation (r=-0.042

r=-0.038, p>0.05). As a conclusions; essential hypertensive patients

were characterized by endothelial dysfunction. In additon, there

was no relation between leptin and endothelial function in essential hypertensive patients.