Obstructive sleep apnoea (OSA) has been found to predispose to hypertension, independently of common risk factors. The mechanisms that link these two conditions, however, are not clear. We propose that either the asphyxia and/or changes in inspiratory resistance that occur in OSA may change the gain and/or setting of arterial baroreceptors, leading to blood pressure being maintained at a higher level.
We studied eight healthy subjects (aged 21-62 years, 4 males, 4 females). The stimulus to carotid baroreceptors was changed using a neck chamber and graded pressures of -40 to +60 mmHg. We assessed the forearm vascular resistance responses from changes in blood pressure (Finapres) divided by brachial flow velocity (Doppler ultrasound). Stimulus response curves were defined during: (i) sham (no additional stimulus), (ii) breathing an asphyxic gas (12 % O2, 5 % CO2), (iii) inspiratory resistance ~10 mmHg, (iv) asphyxia and resistance. Sigmoid functions were applied to the curves and the maximum differentials (equivalent to peak gain) and the corresponding carotid pressures (equivalent to ‘set point’) were determined. All data are presented as means ± S.E.M. Statistical analyses were performed using paired t tests.
The sham test had no effect on blood pressure, gain or ‘set point’. Asphyxia alone increased blood pressure (+7.0 ± 1.1 mmHg, P < 0.0005) and displaced the curve to higher pressures by +16.8 ± 2.1 mmHg (P < 0.0005), but had no effect on gain. Inspiratory resistance alone had no effect on blood pressure or ‘set point’. However, it reduced gain from -3.0 ± 0.6 to -2.1 ± 0.4 units (P < 0.05). The combination of both asphyxia and inspiratory resistance increased blood pressure (+7.5 ± 2.5 mmHg, P < 0.02) and ‘set point’ (+16.8 ± 4.9 mmHg, P < 0.02) and reduced gain (-1.8 ± 0.6, P < 0.02).
The results of the present study show that inspiratory resistance reduces the gain of the baroreflex, and in combination with asphyxia also shifts the curve to hypertensive levels. If these changes are sustained they would provide a mechanism linking hypertension and OSA.
All procedures accord with current local guidelines.