High density lipoproteins enhanced antiaggregating activity of nitric oxide derived from bovine aortal endothelial cells.
In the present study, the effect of high density lipoproteins (HDLs) on the antiaggregating activity of nitric oxide (NO) derived from endothelial cells was investigated with the use of cultured bovine aortal endothelial cells (BAECs). The BAECs were placed in an aggregometer in contact with rabbit platelets after blocking cyclo-oxygenase with acetylsalicylic acid. Under this circumstance, the antiaggregating effect of endothelial cells was exclusively dependent on the release of NO, which was further confirmed by prevention of antiaggregating activity of BAECs with 1 mmol/L N(G)-Nitro-L-arginine. When this system was used, thrombin (0.1 U/ml) evoked 67.33+/-7.52% aggregation of rabbit platelets (2  10(8)/ml). This effect was inhibited by NO derived from endothelial cells (1  10(5)  1  10(6)/ml) in a cell number dependent manner. HDLs (1 mg/ml), added into the system immediately before BAECs, enhanced this antiaggregating effect of NO. However, incubating BAECs with HDLs for an hour and removing the HDLs by centrifugation did not have the same effect, unless HDLs were present during aggregation. No direct effect of HDLs on platelet aggregation was observed. The above findings suggest that HDLs can enhance the antiaggregating effects of BAECs mediated by direct interaction with NO.
Chen
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Laboratory of Molecular Pharmacology, Hunan Medical University, Changsha 410078, China. chgzm@163.net
Yu
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QS
Guo
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ZG
D000818:Animals; D001011:Aorta / Q000166:cytology; D002417:Cattle; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D008075:Lipoproteins, HDL / Q000494:pharmacology*; D009569:Nitric Oxide / Q000502:physiology*; D010974:Platelet Aggregation; D011817:Rabbits
D008075:Lipoproteins, HDL; D009569:Nitric Oxide