Dexamethasone induced enhanced enkephalin degradation by angiotensin-converting enzyme (ACE) of endothelial cells.
The Leu-enkephalin breakdown by ectopeptidases of cultivated endothelial cells is increased in a concentration-dependent manner by dexamethasone treatment. This glucocorticoid induced selectively the angiotensin-converting enzyme (ACE) of the cells. The activity of the closely related enzyme neutral metalloenopeptidase (NEP) and the aminopeptidase N (APN) also present on the endothelial cell surface were not affected or slightly decreased by dexamethasone. The data indicate the significance of ACE for degradation of Leu-enkephalin during the stress reaction.
Melzig
M F
MF
Research Institute for Molecular Pharmacology, Department of Cellular and Biochemical Pharmacology, Berlin.
Heder
G
G
D000595:Amino Acid Sequence; D000626:Aminopeptidases / Q000378:metabolism; D000818:Animals; D001013:Aorta, Thoracic / Q000166:cytology / Q000201:enzymology; D002417:Cattle; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D003907:Dexamethasone / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000201:enzymology*; D004745:Enkephalins / Q000378:metabolism*; D008969:Molecular Sequence Data; D015260:Neprilysin / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism*
D004745:Enkephalins; D003907:Dexamethasone; D000626:Aminopeptidases; D007703:Peptidyl-Dipeptidase A; D015260:Neprilysin