Sleep apnea and hypertension

To examine the central inspiratory drive response to hypoxia in patients with obstructive sleep apnea (OSA), according to their circadian BP profile, and in healthy control subjects. Another objective was to evaluate the relationships among sleep architecture, hypoxic sensitivity, urinary catecholamine excretion, and BP in OSA patients.

Polysomnography, 24-h ambulatory BP recording, and urinary excretion of catecholamines were simultaneously examined in 24 consecutive OSA patients and 11 healthy subjects. OSA patients were categorized as being normotensive (type 1), having BP elevation only during sleep (type 2), and as being hypertensive with elevated BP at all times (type 3). The response of mouth occlusion pressure at 0.1 s after onset (P(0.1)) to progressive isocapnic hypoxic stimulation was measured.

There was a significant difference in the P(0.1) response to hypoxia among control subjects ([mean +/- SD] 0.353 +/- 0.129 cm H(2)O/%) and type 1 (0.228 +/- 0.062 cm H(2)O/%), type 2 (0. 345 +/- 0.106 cm H(2)O/%), and type 3 (0.508 +/- 0.118 cm H(2)O/%) OSA patients. In OSA patients, chemosensitivity was related to the apnea-hypopnea index and to the nocturnal excretion of epinephrine. Significant relationships between the nocturnal excretion of epinephrine and BP were noted. On multiple linear regression analysis, the P(0.1) response to hypoxia was the only variable significantly related to diurnal (r(2) = 0.364; p = 0.005) and nocturnal mean BP (r(2) = 0.461; p = 0.002).

The findings of the present study suggest a possible mediating role of the peripheral chemosensitivity in the association between sleep apnea and hypertension.