NITRIC OXIDE-MEDIATED VASORELAXATION INDUCED BY SODIUM POLYOXYETHYLENE LAURYLETHER SULFATE

Ingestion of surfactants is known to cause hemodynamic changes with de creased total vascular resistance. Motivated by this clinical observat ion, we investigated the direct effects of a common anionic surfactant , sodium polyoxyethylene laurylether sulfate (LES), on isolated ring s egments of rat thoracic aorta, LES did not produce any vasocontractile responses, but relaxed ring segments precontracted with 10(-6) M phen ylephrine in a concentration-dependent manner. This LES-induced vasore laxation was significantly reduced by the removal of endothelium or pr etreatment with N-G-nitro-L-arginine methylester hydrochloride, methyl ene blue, or oxyhemoglobin to the same degree, but was not affected by pretreatment with indomethacin. A further study measuring NO2- plus N O3- (NOx, total metabolites of NO) in the medium of calf pulmonary art ery endothelial (CPAE) cells, a cultured cell line, revealed that LES caused a significant increase in NOx production. On the other hand, in a study measuring intracellular Ca2+ in fura-2-loaded CPAE cells, LES caused a significant increase in intracellular Ca2+, These results su ggest that LES causes endothelium-dependent vasorelaxation via a NO-me diated signaling pathway, which might be due to Ca2+ mobilization, (C) 1997 Academic Press.