Commentary on “Pathways of Microcirculatory Endothelial Dysfunction in OSA: A Comprehensive Ex Vivo Evaluation in Human Tissue”

Obstructive sleep apnea syndrome (OSA) is a clinical condition associated with unfavorable outcomes and may be considered a cardiovascular risk factor.1 Several mechanisms have been advocated in order to explain the increased cardiovascular risk associated with OSA, including increased adrenergic activity, cortisol release, clustering of other risk factors such as obesity, smoking and hypertension, oxidative stress, and systemic inflammation.1 However, an emerging role may be attributed to the onset of endothelial dysfunction at the level of the microcirculation, possibly or partly due to oxidative stress and low-grade inflammation. Endothelial dysfunction might also have a role in the development/maintenance of increased blood pressure levels. In this issue of the American Journal of Hypertension, a study by Gavrilin et al.2 has specifically addressed the possible role of microcirculatory endothelial dysfunction in OSA, as well as the pathways possibly involved. In this study,2 subcutaneous small resistance arteries were isolated from gluteal biopsies performed in patients with OSA, before and after intensive treatment with continuous positive airway pressure (CPAP), as well as in normal controls. The expression of angiotensin receptor type 1 (AGTR-1), NADPH oxidase (NOX 4), dimethylarginine dimethylaminohydrolase (DDAH 1), as well as of some other genes changed after intensive CPAP therapy, together with other disease markers of OSA such as endothelin-1, hypoxia inducible factor 1 alpha (HIF-1α), nuclear factor kappa B (NFκB), interleukin-8, and interleukin-6.2 The expression of endothelin-1, interleukin 1β, and DDAH 2 genes were significantly different between OSA patients and controls.2