Relation Between Endothelial Function and Leptin Level in Essential Hypertensive Patients

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.