Recently we have established that reflex vasoconstriction in response to pulmonary arterial baroreceptor stimulation can be demonstrated at the arterial pressures normally prevailing in the pulmonary circulation (Moore et al. 2004). The aim of this study was to examine whether there is interaction between reflex responses to stimulation of pulmonary arterial receptors and those from stimulation of carotid sinus baroeceptors. In ten chloralose-anaesthetized dogs (100 mg kg^-1 I.V.), a perfusion circuit allowed independent control of pressures distending the pulmonary, aortic arch, carotid sinus and coronary artery baroreceptors. The chest wall was sealed and a phasic intrathoracic pressure ranging from atmospheric to around − 10 mmHg (18 cycles min-1) applied. Vascular responses were determined from changes in perfusion pressure to the descending aorta (constant flow). Pulmonary baroreceptor stimulus-response curves were defined at two carotid sinus pressures (CSP) at around 65 and 125 mmHg. Sigmoid functions were fitted to the curves and indicators of baroreflex function i.e. maximal gain and set point determined. Blood samples were taken at regular intervals for determination of systemic arterial blood gases and pH. Animals were killed by exsanguination following a lethal dose of anaesthetic at the end of each experiment. Increasing pulmonary arterial pressure from 5 to 40 mmHg resulted in an increase in systemic perfusion pressure of 38 ± 8 mmHg at 60 mmHg CSP and 33 ± 8 mmHg at 120 mmHg CSP; the percentage increases in vascular resistance were not significantly different (P > 0.05 paired t test). When the carotid pressure was elevated, the pulmonary baroreceptor stimulus-response curve was displaced to the right, i.e. to a significantly higher pulmonary pressure (Table 1). Under the same conditions, the peak gain was reduced in 8 out of 10 experiments; however, the difference failed to achieve statistical significance. These results confirm that the set point of the pulmonary arterial baroreflex does occur within the range of normal physiological pressures. Furthermore, this set point is modified when the pressure stimulus to the carotid sinus baroreceptors is altered. We conclude, therefore, that the pulmonary arterial baroreflex is subject to modulation by input from carotid baroreceptors, and that this may play an important role in reflex cardiovascular control.