Obstructive sleep apnoea (OSA), which is characterized by periodic inspiratory obstruction, is associated with hypertension and possibly with changes in the baroreceptor reflex. In this investigation we induced changes in inspiratory resistance and in inspiratory oxygen and carbon dioxide content, which simulate some of the changes in OSA, to determine whether this caused changes in the gain or setting of the carotid baroreflex. In eight healthy subjects (aged 21-62 years) we changed the stimulus to carotid baroreceptors, using neck chambers and graded pressures of -40 to +60 mmHg, and assessed vascular resistance responses in the brachial artery from changes in blood pressure (Finapres) divided by brachial artery blood flow velocity (Doppler ultrasound). Stimulus-response curves were defined during (a) sham (no additional stimulus), (b) addition of an inspiratory resistance (inspiratory pressure -10 mmHg), (c) breathing asphyxic gas (12% O(2), 5% CO(2)), and (d) combined resistance and asphyxia. Sigmoid or polynomial functions were applied to the curves and maximum differentials (equivalent to peak gain) and the corresponding carotid pressures (equivalent to 'set point') were determined. The sham test had no effect on either gain or 'set point'. Inspiratory resistance alone had no effect on blood pressure and did not displace the curve. However, it reduced gain from -3.0 +/- 0.6 to -2.1 +/- 0.4 units (P < 0.05). Asphyxia alone did increase 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). However, it did not affect gain. The combination of resistance and asphyxia both reduced gain and displaced the curve to higher pressures. These results suggest that inspiratory resistance and asphyxia cause changes in the baroreceptor reflex which could lead to an increase in blood pressure. These changes, if sustained, could provide a mechanism linking hypertension to obstructive sleep apnoea.