Daytime waking autonomic function and vascular control in OSA.

This paper deals with the potential role of two blood pressure regulatory systems in the development of hypertension in obstructive sleep apnoea (OSA). Beside the acute and long-term sympathoexcitation documented in this disease, there seems to be an impaired endothelium-dependent vascular relaxation. In particular, nitric oxide (NO)-mediated vasodilatation was impaired in patients with OSA. Both these changes act to increase blood pressure during physiological conditions. However, they may not be determinants for hypertension development in OSA as no differences between normo- and hypertensive patients with OSA were detected. Nevertheless, an altered balance between the vasoconstrictive influence of the sympathoadrenergic system and the vasodilatory action of NO-dependent vascular relaxation may be of importance in the development of sustained hypertension in OSA.