1. Respiratory related arterial pressure variability may reflect body fluid status and/or cardiac sympathetic function. The underlying mechanism is not clear. 2. In the present study, we used an electromagnetic blood flow meter to measure ascending aortic blood flow, from which stroke volume was integrated, to study respiration-stroke volume coupling and its underlying neural regulation. Experiments were performed on male Sprague-Dawley rats that were anaesthetized with pentobarbital sodium, paralysed with pancuronium and under mechanical ventilation. 3. Programmed irregular ventilation evoked significant variability in arterial pressure, aortic flow and stroke volume signals. Good coupling was noted between lung volume and aortic flow, as well as between lung volume and stroke volume; this coupling persisted under all experimental conditions. The aortic flow power and stroke volume variability and the transfer magnitude of the lung volume-aortic flow and lung volume-stroke volume couplings were suppressed by 1 mg/kg propranolol, but not by 0.3 mg/kg atropine or a combination of 0.3 mg/kg atropine and 2.5 mg/kg phentolamine. 4. These results suggest that respiratory related variability in aortic flow and stroke volume, which ultimately contributes to arterial pressure variability, is primarily under cardiac sympathetic control via beta-adrenoceptors in anaesthetized and mechanically ventilated rats.