Abstract
Prostacyclin (PGI2) synthesis seems to be one of the major physiological mechanisms involved in regulating platelet and vessel wall interactions1. PGI2 is produced in large amounts by vascular endothelial cells, and vascular smooth muscle cells (SMC) also produce significant quantities2. The capacity of SMC to produce PGI2, especially after endothelial injury, seems to be of importance. It is probably this type of situation that is involved in the atherosclerotic process3: experimental atherosclerosis in rabbits has been associated with a severe decrease in PGI2 synthesis by arteries4. Lipid peroxide accumulation within the arterial wall or in the plasma may also be involved in this process5. Using arterial SMC in culture, we demonstrate here that, in comparison with healthy cultured cells, cells originating from atherosclerotic aorta have a decreased capacity to produce PGI2. The results were obtained using biological and radiochemical techniques and were confirmed by GC-MS. They suggest a potential role for PGI2 in inhibiting the atherosclerotic process.
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Larrue, J., Rigaud, M., Daret, D. et al. Prostacyclin production by cultured smooth muscle cells from atherosclerotic rabbit aorta. Nature 285, 480–482 (1980). https://doi.org/10.1038/285480a0
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DOI: https://doi.org/10.1038/285480a0
