In 10 tracheotomized anesthetized cats during steady-state inhalation of various concentrations of CO2 and O2, the acute respiratory response to baroreceptor stimulation produced by transient inflation of a balloon placed in the descending aorta was studied. The latter induced a sudden rise in mean arterial pressure, ranging from 62 to 95 mmHg. At all PACO2 levels above 30 mmHg, elevation in arterial pressure was accompanied by an immediate drop in tidal volume (VT) and prolongation of the durations of inspiration (Ti) and total breath (Ttot). Breaths obtained during baroreceptor stimulation fell along the same VT vs. Ti and VT vs. Ttot relationships obtained in the normotensive state, suggesting that the lung volume-related vagal control of Ti and Ttot is unaffected by changes in arterial pressure. Since, for a given change in arterial pressure, a constant reduction in VT was obtained at all PACO2 levels above 30 mmHg, it can be concluded that the interaction between PACO2 and arterial pressure is additive. In three cats, at PACO2 levels below 30 mmHg, aortic obstruction resulted in brief periods of apnea. Following apnea, the control of Ti and Ttot was transiently offset, describing hysteresis pathways on the VT vs. Ti and VT vs. Ttot relationships.