Abstract
In order to clarify the possible interactions between nitric oxide (NO) and arachidonic acid (AA) pathways, human amnion-like WISH cells were perifused to measure the effects of the following substances on [3H]arachidonic acid release: (1) sodium nitroprusside (SNP), a nitric oxide donor; (2) 1,1,1-trifluoromethyl-6,9,12,15-heicosatetraen-2-one, a cytosolic phospholipase A2 (cPLA2) inhibitor; (3)l -arginine, the substrate of nitric oxide synthase (NOS); (4) 3-(5′-Hydroxymethyl-2′-furyl)-1-benzylindazole and 1H-[1,2,4]oxadiazolo[4,3-α]quinoxalin-1-one, activator and inhibitor of soluble guanylyl cyclase, respectively; (5) a membrane-permeable non-hydrolyzable analogue of guanosine-3′,5′-cyclic monophosphate (cGMP). Furthermore, the effect of SNP on prostaglandin E2 (PGE2) release was tested. Exogenous and endogenous NO, as well as the guanylyl cyclase activator and cGMP analogue, significantly increased [3H]arachidonic acid release. Both soluble guanylyl cyclase and PLA2 inhibitors counteracted SNP response. Exogenous NO increased PGE2 release, although to a much lesser degree compared with arachidonic acid release.Our results indicate that NO stimulates AA release in WISH cells by activating PLA2 through a cyclic GMP-dependent mechanism.
Published Version
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