Endothelin-1 release from endothelial cells in culture is elevated both acutely and chronically by short periods of mechanical stretch

• Published in: Biochemical and biophysical research communications Vol. 200; no. 1; p. 395
• Main Authors: Macarthur, H, Warner, T D, Wood, E G, Corder, R, Vane, J R
• Format: Journal Article
• Language: English
• Published: United States 15-04-1994
• Subjects: 6-Ketoprostaglandin F1 alpha - metabolism; Animals; Aorta; Cattle; Cells, Cultured; Cycloheximide - pharmacology; Dactinomycin - pharmacology; Endothelin-1; Endothelins - biosynthesis; Endothelins - metabolism; Endothelium, Vascular - cytology; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiology; Epoprostenol - metabolism; Kinetics; Protein Precursors - biosynthesis; Stress, Mechanical; Time Factors
• ISSN: 0006-291X
• DOI: 10.1006/bbrc.1994.1462

The effects were examined of mechanical stretch on the release of endothelin-1 (ET-1) and prostacyclin (measured as 6-keto-prostaglandin (PG) F1 alpha) from cultured endothelial cells. Stretching (0.2 Hz) for 20, 60 or 360 min caused immediate (< or = 20 min) and secondary (up to 360 min) increases in ET-1 release. The secondary but not immediate release of ET-1 was prevented by actinomycin D (8 x 10(-7) M) or cycloheximide (3.6 x 10(-6) M). Neither compound affected the release of ET-1 from unstretched cells over 360 min. Stretching of the endothelial cells increased the accumulation of 6-keto-PGF1 alpha at 360 min but not at 20 min, suggesting that stretch does not produce a rapid, non-selective increase in autacoid production from endothelial cells. The intracellular amounts of ET-1 were approximately 20 times greater than those of big ET-1. Thus, endothelial cells contain stores of ET-1 that are released rapidly by stretch.