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Byline: N. Tamaru (1), K. Watanabe (1), M. Yoshida (1), D. M. Reitz-Vick (2), L. Townsend (2), J. Glover N. (2) Keywords: Key words: Angiotensin-converting enzyme (ACE)--Pulmonary artery endothelial cells--Hypoxia. Abstract: To compare the amount of angiotensin-converting enzyme (ACE) activity in pulmonary artery endothelial cells from different sites and to examine the effect of severe hypoxia (less than 1% of O.sub.2 in 5% CO.sub.2 and 95% N.sub.2) on the ACE activity expressed by these cells, endothelial cells were harvested and cultured from canine main pulmonary artery by scraping the luminal surface of the artery and from canine pulmonary artery microvessels by infusing chilled buffer with microcarrier beads and 0.02% ethylenediamine tetraacetic acid (EDTA). ACE activity in cell lysates and culture medium was evaluated by fluorometric assay with hippuryl-L-histidyl-L-leucine as a substrate. ACE activity in cell lysates and postculture medium of pulmonary microvascular endothelial cells (PMVEC) was higher than in cell lysates and culture medium of central pulmonary artery endothelial cells (PAEC). However, hypoxia suppressed cellular ACE activity in both PAEC and PMVEC. The degree of suppression of ACE activity by hypoxia, which was determined as (ACE activity in normoxia - ACE activity in hypoxia)/ACE activity in normoxia x 100(%), was larger in PMVEC than in PAEC. The pulmonary microvasculature may be a greater source of ACE than central pulmonary artery, and the ACE activity of pulmonary microvascular endothelial cells seem to be sensitive to hypoxia, although the small diameter of the vessels improves conditions for interaction of blood-borne substance with endothelial enzymes. Author Affiliation: (1) Division of Respiratory Medicine, Second Department of Medicine, Fukuoka University School of Medicine, Fukuoka 814-0180, Japan, JP (2) Tissue Culture Lab., Surgical Service, William Beaumont Hospital, Royal Oak, Michigan, US Article note: Accepted for publication 10 July 2000