To study the effects of airway obstruction (AWO) and arousal on coronary blood flow, mean arterial pressure (MAP) and heart rate (HR), pigs were chronically instrumented with arterial catheters, Doppler flow probes on the left circumflex coronary artery, and electrodes for determination of sleep stages. A modified balloon catheter was placed in the trachea to obstruct the upper airway during sleep. Following control studies, the role of beta adrenergic receptors in hemodynamic responses to AWO was assessed by administering propranolol, a beta adrenoreceptor blocking agent. In control studies, during nonrapid eye movement sleep (NREM), MAP was 85 +/- 2 mmHg before AWO and increased by 8 +/- 2 mmHg upon arousal. Mean arterial pressure was lower during rapid eye movement (REM) sleep (64 +/- 2 mmHg) and the increase upon arousal was threefold greater (22 +/- 2 mmHg). Heart rate was similar in both sleep stages (NREM 123 +/- 5 bpm; REM 125 +/- 6 bpm) and increased significantly upon arousal (NREM, 11 +/- 2 bpm; REM, 18 +/- 3 bpm increase). Coronary blood flow was similar during both stages (NREM 44 +/- 5 ml/min; REM 44 +/- 6 ml/min) and increased by 13% (NREM) and 22% (REM) during arousal. Coronary vascular resistance increased significantly by 17% during arousal from AWO during REM sleep. All changes were significant at p < 0.05. Following beta adrenergic receptor blockade studies using propranolol, baseline HR was reduced in NREM sleep and HR and coronary blood flow increases during arousal from apnea were eliminated. Adrenoreceptor blockade studies suggest that these effects were mediated by the beta adrenergic component of the sympathetic nervous system.