Nitric oxide-mediated vasorelaxation induced by sodium polyoxyethylene laurylether sulfate.

Ingestion of surfactants is known to cause hemodynamic changes with decreased total vascular resistance. Motivated by this clinical observation, we investigated the direct effects of a common anionic surfactant, sodium polyoxyethylene laurylether sulfate (LES), on isolated ring segments of rat thoracic aorta. LES did not produce any vasocontractile responses, but relaxed ring segments precontracted with 10(-6) M phenylephrine in a concentration-dependent manner. This LES-induced vasorelaxation was significantly reduced by the removal of endothelium or pretreatment with N(G)-nitro-L-arginine methylester hydrochloride, methylene blue, or oxyhemoglobin to the same degree, but was not affected by pretreatment with indomethacin. A further study measuring NO2- plus NO3- (NO(x), total metabolites of NO) in the medium of calf pulmonary artery endothelial (CPAE) cells, a cultured cell line, revealed that LES caused a significant increase in NO(x) 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 suggest that LES causes endothelium-dependent vasorelaxation via a NO-mediated signaling pathway, which might be due to Ca2+ mobilization.