Neural and humoral mechanisms mediating cardiovascular responses to obstructive sleep apnea

Patients with obstructive sleep apnea are at increased risk for hypertension. The mechanisms underlying this increased risk are not known. During sleep, repetitive apneic episodes result in hypoxemia and carbon dioxide retention, which cause increases in sympathetic nerve activity and elicit humoral vasoconstrictor responses. While these mechanisms explain nocturnal elevations in blood pressure, it is unclear why hypertension and elevated sympathetic nerve activity prevail even during the daytime. This review will examine briefly some of the neural and humoral mechanisms that are activated by nocturnal apneas and which may contribute to persistent increases in blood pressure even during daytime normoxia. Disruption of the autonomic and hemodynamic profile of normal sleep by apneic events manifests as raised blood pressure and heightened sympathetic nerve traffic during sleep. During awake daytime normoxia, baroreflex and chemoreflex dysfunction may contribute to maintenance of higher blood pressure and sympathetic activity. Sustained vasoconstrictor effects of nocturnal endothelin release may also be implicated in the elevated daytime blood pressures.