Renal vasodilating capacity and endothelial function are impaired in patients with obstructive sleep apnea syndrome and no traditional cardiovascular risk factors

Objective:Patients with obstructive sleep apnea syndrome exhibit accelerated vascular aging and renal damage. Aim of the study was to investigate whether vascular dysfunction is a feature of obstructive sleep apnea syndrome per se or instead related to the presence of traditional cardiovascular risk factors.Methods:Forty patients with moderate-severe obstructive sleep apnea syndrome (20 with, 20 without traditional risk factors) and 20 matched healthy controls were enrolled. Renal vasodilating capacity, endothelium-dependent vasodilation in the brachial artery, carotid-femoral pulse wave velocity and carotid stiffness were measured. Oxidative stress, endothelial biomarkers and leukocyte adhesion molecule levels were also evaluated.Results:Apneic patients without traditional cardiovascular risk factors presented reduced endothelium-dependent vasodilation (3.72.1 versus 6.1 +/- 3.0%, P<0.05), increased serum E-selectin (49.8 +/- 11.5 versus 38.9 +/- 17.9ng/ml, P<0.05), and impaired renal vasodilating capacity (6.0 +/- 4.3 versus 10.4 +/- 6.1%, P<0.05), as compared to healthy controls. Endothelial NO synthase expression was reduced (0.0133 versus 0.0221x10(6)copies/g RNA, P<0.05), whereas oxidative stress parameters and leukocyte adhesion molecules were similar to controls. Patients with obstructive sleep apnea syndrome and traditional risk factors also exhibit increased aortic and carotid stiffness, increased renal resistive index and intima-media thickness, and reduced expression of the endothelial progenitor cell marker CD34: however, these parameters were similar to those of healthy controls in patients with isolated obstructive sleep apnea syndrome.Conclusion:Obstructive sleep apnea syndrome is characterized by endothelial dysfunction and activation and impaired renal vasodilating capacity even in the absence of traditional cardiovascular risk factors, possibly due to reduced endothelial NO synthase expression.