Renin-angiotensin system stimulates respiration during acute hypotension but not during hypercapnia

We reported that intravenous infusion of angiotensin II (ANG II) stimulated ventilation (V̇E) in conscious dogs. Other studies in our laboratory have demonstrated that increases in respiration occurred in association with activation of the renin-angiotensin system during acute hypotension and during hypercapnia. Therefore, in conscious dogs (n = 5), we examined the effects of ANG II receptor blockade with intravenous saralasin (0.5 μg · kg^-1 · min^-1) on respiratory responses during progressive nitroprusside-induced hypotension and during the ventilatory response to increased inspired fraction of CO₂ (VRC). During hypotension (mean arterial pressure decreased ~20%) combined with ANG II receptor blockade, V̇E, heart rate, and arginine vasopressin increases were attenuated compared within unblocked studies. With ANG II receptor blockade during hypotension, alveolar ventilation and arterial PCO₂ (Pa(CO₂)) were unchanged, which contrasted with a doubling of alveolar ventilation and a decrease of 4.8 ± 1 Torr in Pa(CO₂) in unblocked studies. During hypercapnia, the slope of the VRC was not affected by ANG II receptor blockade, but with 6.5% inspired CO₂ fraction, V̇E and Pa(CO₂) were lower than in unblocked studies. These results indicated that ANG II contributed to the respiratory response to a modest hypotension but did not affect respiratory sensitivity to CO₂.