We studied the effect of acute hypoxia on pulmonary conversion of angiotensin I to II in anesthetized dogs. When arterial Po2 was decreased from 86 ± 14 (SD) to 33 ± 8 mm Hg without changing pH or Pco2, the single passage conversion of intravenous boluses of radiolabeled angiotensin I in tracer doses fell significantly (P < 0.005) from 72 ± 4 to 67 ± 6%. The effect of comparable levels of hypoxemia on the conversion of continuous intravenous infusions of pharmacological doses (1000 times physiological) of angiotensin I was greater: from 55 ± 14 to 33 ± 13% (P < 0.025). There was prompt return of percent conversion ratios to control levels when hypoxemia was reversed. We conclude that acute hypoxia is associated with a reversible decrease in pulmonary angiotensin converting enzyme availability.