Mechanism of endothelium-dependent vasorelaxation evoked by lysophosphatidylcholine.

Vasorelaxation induced by lysophosphatidylcholine (LPC) and platelet activating factor (PAF) was examined in rings isolated from rat aorta and mesenteric artery. LPC caused dose-dependent vasodilatation, which was sensitive to CV-6209, a PAF antagonist, and NG-monomethyl-L-arginine, a nitric oxide synthase inhibitor, but insensitive to indomethacin. PAF (10(-7)M) caused a tachyphylactic effect in mesenteric artery, but no tachyphylactic effect was demonstrated with LPC. Vasorelaxation patterns with LPC differed from those with PAF in the rat mesenteric artery. These results suggest that LPC-induced vasorelaxation may involve increased nitric oxide production mediated by the PAF receptor pathway, another receptor pathway possibly blocked by CV-6209, or PAF itself produced in endothelial cells in response to LPC.