Pulmonary angiotensin II production in respiratory failure.
Plasma angiotensin II concentration gradients across the pulmonary vascular bed, plasma renin concentration and serum converting enzyme activity were measured in 19 patients. The majority of the patients were critically ill. Nine patients had septicemia with acute respiratory failure, six patients had severe chronic lung disease and four patients had other serious disorders requiring haemodynamic monitoring. Pulmonary angiotensin II generation rates were calculated as the products of the pulmonary plasma flow and the angiotensin II concentration gradient across the lung. Several patients had a highly activated renin-angiotensin system. There was a strictly linear correlation between the plasma angiotensin II concentrations in mixed venous blood and in systemic arterial blood across a wide range, the concentration in arterial blood being 1.4-1.5 times that in mixed venous blood in each of the three groups of patients. Serum converting enzyme activity was not different from the level observed in a group of control patients above 50 years of age, but lower than in younger normal individuals. The maximal angiotensin II production rates in the pulmonary vascular bed of patients with life-endangering pulmonary disease were similar to the rates previously measured in hypertensive patients with renovascular or renal parenchymal disease. In conclusion, the process of angiotensin I conversion in the lung operates without impediment in spite of severe pulmonary injury.
D000293:Adolescent; D000328:Adult; D000368:Aged; D000804:Angiotensin II / Q000096:biosynthesis* / Q000097:blood; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008168:Lung / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000097:blood; D012131:Respiratory Insufficiency / Q000378:metabolism*
D000804:Angiotensin II; D012083:Renin