The lack of receptors for atrial natriuretic peptides on human monocytes prevents a rise of cGMP and induction of tumor necrosis factor-alpha synthesis.
Freshly harvested human monocytes were shown to produce tumor necrosis factor-alpha (TNF-alpha) in response to exogenously added or sodium nitroprusside-generated cGMP. In contrast, atrial natriuretic peptide (ANP) that acts by elevating cGMP in a variety of cells, was incapable of inducing TNF-alpha synthesis. This failure was due to a lack of ANP receptors and thus, to the inability of ANP to raise cGMP in human monocytes.
Sprenger
H
H
Institute of Immunology, Philipps University, Marburg, Germany.
Beck
J
J
Nain
M
M
Wesemann
W
W
Gemsa
D
D
D009320:Atrial Natriuretic Factor / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism*; D006367:HeLa Cells / Q000378:metabolism; D006801:Humans; D007378:Interleukins / Q000378:metabolism; D009000:Monocytes / Q000737:chemistry*; D009599:Nitroprusside / Q000378:metabolism; D017461:Receptors, Atrial Natriuretic Factor; D011956:Receptors, Cell Surface / Q000032:analysis*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
D007378:Interleukins; D011956:Receptors, Cell Surface; D014409:Tumor Necrosis Factor-alpha; D009599:Nitroprusside; D009320:Atrial Natriuretic Factor; D000242:Cyclic AMP; D017461:Receptors, Atrial Natriuretic Factor; D006152:Cyclic GMP