Angiotensin II stimulates respiration in awake dogs and antagonizes baroreceptor inhibition

The effects of intravenous infusions of physiologic doses of angiotensin II (AII) on expired ventilation (V̇E) and acid-base balance were examined in awake dogs. A control infusion of saline was followed by AII infusion, initially with mean arterial pressure (MAP) raised 15%, and then with MAP at control levels of concurrent infusion of sodium nitroprusside (SNP). To control for SNP, the protocol was repeated using arginine vasopressin (AVP). Ventilatory responses of CO₂ (VRC) were measured at the end of these protocols and separately with MAP elevated during infusion of AII. With AVP, increased MAP inhibited V̇E, heart rate (HR) and metabolism. However, with MAP elevated during AII infusion, stimulation by AII opposed baroreceptor reflexes and these variables, as well as plasma AVP, did not change. When MAP was lowered to control during AII infusion all variables increased. With AII, Pa_CO2 followed V̇E changes, decreasing 3 Torr with MAP at control levels; however, [H⁺] remained constant due to a decrease in arterial strong ion difference. The stimulatory effects of AII were not due to SNP; SNP did not stimulate V̇E during AVP infusion. The slope of the VRC was unaltered by AII infusion or MAP; however, AVP reduced the VRC slope. Physiological increases in AII stimulate V̇E and other systems at normal MAP and maintain several regulatory systems at control levels during baroreceptor inhibition.