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Endothelium-dependent vasodilator responses of isolated rat aortic strips precontracted with norepinephrine to acetyl glyceryl ether phosphorylcholine (AGEPC) were compared in the presence and absence of bovine serum albumin (BSA). In the absence of BSA, AGEPC produced endothelium-dependent relaxation at concentrations higher than 10(-6) M, which was considered to be non-specific because similar relaxations were produced by other phospholipids (e.g., lysolecithin) at the same concentration range. This non-specific relaxation was suggested to be caused by changes in membrane fluidity of endothelial cells, since high concentrations of AGEPC and other phospholipids were found to produce structural changes in endothelial cells by phase contrast and electron microscopic studies; structural changes were never observed after the application of acetylcholine (ACh). In the presence of BSA (2.5 mg/ml), AGEPC caused endothelium-dependent relaxation at concentrations as low as 10(-9)M; however, relaxations by ACh and lysolecithin were not augmented by the presence of BSA. CV-3988 (10(-5)M), a specific antagonist of AGEPC, inhibited the relaxations by AGEPC in the presence of BSA. From these results, it is suggested that, in the presence of BSA, AGEPC may produce endothelium-dependent relaxation in a specific manner, which is different from the non-specific relaxations observed in the absence of BSA.

Potentiation by bovine serum albumin(BSA) of endothelium-dependent vasodilator response to acetyl glyceryl ether phosphorylcholine (AGEPC).