Angiotensin-converting enzyme activity by canine pulmonary microvascular and central pulmonary artery endothelial cells exposed to hypoxia

To compare the amount of angiotensin-converting enzyme (ACE) activity in pu lmonary artery endothelial cells from different sites and to examine the ef fect of severe hypoxia (less than 1% of O-2 in 5% CO2 and 95% N-2) on the A CE 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 chi lled buffer with microcarrier beads and 0.02% ethylenediamine tetraacetic a cid (EDTA). ACE activity in cell lysates and culture medium was evaluated by fluorometr ic 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 centra l pulmonary artery endothelial cells (PAEC). However, hypoxia suppressed ce llular ACE activity in both PAEC and PMVEC. The degree of suppression of AC E activity by hypoxia, which was determined as (ACE activity in normoxia AC E activity in hypoxia)/ACE activity in normoxia x 100(%), was larger in PMV EC than in PAEC. The pulmonary microvasculature may be a greater sourer of ACE than central pulmonary artery, and the ACE activity of pulmonary microvascular endotheli al cells seem to be sensitive to hypoxia, although the small diameter of th e vessels improves conditions for interaction of blood-borne substance with endothelial enzymes.