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Nitric oxide synthase inhibitors attenuate human monocyte chemotaxis in vitro
Author(s) -
Belenky Sergei N.,
Robbins Richard A.,
Rubinstein Israel
Publication year - 1993
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.53.5.498
Subject(s) - chemotaxis , monocyte , sodium nitroprusside , nitric oxide , in vitro , omega n methylarginine , nitric oxide synthase , arginine , biology , pharmacology , biochemistry , endocrinology , immunology , receptor , amino acid
Abstract Nitric oxide synthase (NOS) inhibitors have been shown to modulate neutrophil migration. We hypothesized that the NOS inhibitors N G ‐monomethyl‐L‐ arginine (L‐NMMA), N G ‐nitro‐L‐arginine methyl ester (L‐NAME), and L‐canavanine (L‐CAN) also modulate human peripheral blood monocyte chemotaxis. To test this hypothesis, monocyte chemotaxis toward formylmethionyl‐ leucyl‐phenylalanine (fMLP) was assessed using a modified blindwell chemotaxis chamber technique. L‐ NMMA and L‐NAME, but not D‐NMMA or L‐CAN, significantly attenuated fMLP‐induced monocyte chemotaxis (P < .05). L‐Arginine and sodium nitroprusside, but not D‐arginine, reversed NOS inhibitor‐induced responses. Dibutryl cyclic guanyl monophosphate (cGMP) attenuated the inhibitory effects of L‐NMMA on monocyte chemotaxis (P < .05). Finally, fMLP increased cGMP generation by monocytes, which was significantly attenuated by L‐NMMA (P < .05). These data indicate that the L‐arginine/NO biosynthetic pathway regulates human monocyte chemotaxis in vitro.