Ventilation is stimulated by small reductions in arterial pressure in the awake dog

Changes in arterial pressure commonly accompany respiratory adaptations. The purpose of this study was to determine, in awake dogs (n = 6), the degree to which small acute decreases in arterial pressure affect ventilation and acid-base balance. Mean arterial pressure (MAP) was reduced by 6 ± 2, 10 ± 3, and 16 ± 2% by intravenous infusion of sodium nitroprusside for sequential 20-min periods. In another experiment, the ventilatory response to hypercapnia was determined during MAP reduction of 16 ± 3%. Step reductions in MAP were accompanied by increases in minute ventilation (maximum increase 152 ± 75%) and step reductions in arterial PCO₂ (Pa(CO₂); maximum reduction -4.8 ± 0.8 Torr). Although eupneic Pa(CO₂) threshold was lowered during MAP reduction, ventilatory sensitivity to CO₂ remained unchanged. Despite the lowered Pa(CO₂), arterial [H⁺] remained constant (acid-base balance was maintained) as a result of a concurrent decrease in strong ion difference. Plasma renin activity increased during MAP reduction (93 ± 39%) and may have contributed to the increase in minute ventilation, inasmuch as angiotensin II can stimulate respiration by a central mechanism. Evidence is provided that nitroprusside is unlikely to be a primary factor in these hypotensive responses. We conclude that relatively modest decreases in MAP have a consistent stimulatory effect on respiratory control. Therefore it is important to take into account effects of small changes in MAP when interpreting mechanisms for respiratory responses in awake animals.