Selective inhibition of the 12-lipoxygenase pathway of arachidonic acid metabolism by L-arginine or sodium nitroprusside in intact human platelets.
L-arginine (1-100 microM) or sodium nitroprusside (1-100 microM) caused a concentration dependent decrease in the metabolism of exogenously added arachidonic acid via the 12-lipoxygenase pathway in intact human platelets, as determined by the use of an HPLC assay. NG-monomethyl-L-arginine, but not the D-isomer of this compound, diminished the inhibitory effect of L-arginine. The D isomer of arginine had no effect. The cyclooxygenase pathway was much less susceptible to these effects. This study indicated that nitric oxide formed in intact human platelets selectively inhibited 12-lipoxygenase over that of cyclooxygenase and suggests that such inhibition may be an important regulatory mechanism.
Nakatsuka
M
M
Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
Osawa
Y
Y
D001092:Arachidonate 12-Lipoxygenase / Q000378:metabolism*; D016718:Arachidonic Acid / Q000378:metabolism*; D001120:Arginine / Q000494:pharmacology*; D001792:Blood Platelets / Q000378:metabolism*; D006801:Humans; D066298:In Vitro Techniques; D009599:Nitroprusside / Q000494:pharmacology*
D009599:Nitroprusside; D016718:Arachidonic Acid; D001120:Arginine; D001092:Arachidonate 12-Lipoxygenase