Effect of acute hypoxia on the pulmonary conversion of angiotensin I to angiotensin II in dogs.
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 less than 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 less than 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.
D000208:Acute Disease; D000803:Angiotensin I / Q000008:administration & dosage / Q000276:immunology / Q000378:metabolism*; D000804:Angiotensin II / Q000276:immunology / Q000378:metabolism*; D000809:Angiotensins / Q000378:metabolism*; D000818:Animals; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D004285:Dogs; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000503:physiopathology*; D007275:Injections, Intravenous; D008168:Lung / Q000503:physiopathology*; D010100:Oxygen / Q000097:blood; D013997:Time Factors; D014661:Vasoconstriction
D000809:Angiotensins; D000804:Angiotensin II; D002245:Carbon Dioxide; D000803:Angiotensin I; D010100:Oxygen