Angiotensin I conversion and vascular reactivity in pathophysiological states in dogs

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Abstract
To determine if angiotension converting enzyme activity is altered by acute pathophysiological insults, angiotensin I [AI] conversion was assessed using a blood pressure response technique in anesthetized dogs studied during acute 100% O2 breathing and acute acid-base derangements. Systemic vascular reactivity to AII was determined by measuring the magnitude and duration of the arterial blood pressure response to intra-arterial injections of AII under these same conditions. AI conversion found in normoxia [91 .+-. 7 (SD)%] was unchanged by acute acidosis, alkalosis and hyperoxia. During acute hyperoxia the mean half time of the hypertensive response increased from 68 .+-. 25 (SD) s at a PaO2 [arterial blood O2 tension] of 112 .+-. 18 (SD) Torr to 100 .+-. 34 (SD) s at a PaO2 of 491 .+-. 47 (SD) Torr (P < 0.01). No other pathophysiological condition studied had any effect on reactivity of systemic vasculature to AII. Except during acute hypoxia as previously shown, converting enzyme activity is resistant to other pathophysiological insults, and vascular responsiveness to AII is enhanced by hyperoxia.