Abstract

That obstructive sleep apnea syndrome is an independent risk factor for the development of hypertension was established in the 1970s, and recent works on large samples have confirmed this fact. Investigations of the mechanisms that may lead to the development of hypertension with sleep-disordered breathing will allow not only confirmation of the relationship but also creation of better treatment. There is a multigenic basis of blood pressure regulation, and genetic factors play a role in the development of sleep-disordered breathing. Genes that may have little role in the physiologic variation of blood pressure may be more important in the manifestation of pathology. And one hypothesis is that genes involved in the development of a morphotype may also have a role in the development of hypertension. Furthermore, sleep-disordered breathing may be associated with abnormal sympathetic discharge during sleep, as shown by microneurography. This mechanism may explain how a sleep disorder leads to hypertension, but impairment of vascular endothelial controls may also be involved. Investigation of vascular endothelial vasodilation as demonstrated by forearm plethysmography or the dorsal hand vein technique indicates that impairment of endothelium-dependent vasodilation during wake is associated with sleep-disordered breathing. This endothelium-dependent vasodilation appears to be more frequently impaired than the endothelium-independent vasodilation, and the former impairment can be reversed by nasal continuous positive airway pressure. These findings are supportive fo the role of sleep-disordered breathing in the development of hypertension in man.

View details for Web of Science ID A1997YH47100015

View details for PubMedID 9406332