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 (VE) and acid-base balance were determined 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 by concurrent infusion of sodium nitroprusside (SNP). To control for SNP, the protocol was repeated using arginine vasopressin (AVP). Ventilatory responses to CO2 (VRC) were measured at the end of these protocols and separately with MAP elevated during infusion of AII. With AVP, increased MAP inhibited VE, 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, PaCO2 followed VE 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 VE 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 VE and other systems at normal MAP and maintain several regulatory systems at control levels during baroreceptor inhibition.