It is debated whether obstructive sleep apnoea (OSA) is a significant independent risk factor for sustained hypertension or cardiovascular morbidity and mortality. In an attempt to avoid the problem of confounding variables we have investigated whether withdrawing nasal continuous positive airway pressure (NCPAP) from patients with OSA for different proportions of the night leads to a subsequent rise in their morning blood pressures. Six patients with treated OSA had their NCPAP automatically varied between 3 cms H2O and a therapeutic pressure over 5 successive nights. The proportion of therapeutic NCPAP given was kept constant over the 5 nights and blood pressure measured the morning after the 5th night. Each patient had 5 different levels of sleep disruption, from no therapeutic NCPAP at all, through to 100% NCPAP. The nocturnal consequences of these different proportions of NCPAP were quantified both by oximetry and by a new EEG analysis that provides an objective estimate of the periodicity (fluctuations in the EEG depth) of the time course seen in patients with OSA. Increasing degrees of nocturnal hypoxic dipping and EEG periodicity were positively correlated with the subsequent morning systolic and diastolic blood pressures (p < 0.02). About 20% of the variance in systolic and diastolic blood pressure could be accounted for by the amount of either hypoxic dipping or EEG periodicity. The results of this study suggest that acute changes in awake blood pressure can be caused by sleep apnoea. It agrees with other data suggesting that OSA can have an independent influence on morning BP, but that this effect may have worn off by the afternoon and evening. Some of the discrepancies between the numerous studies in this area may be due to the timing of blood pressure measurements.