The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Induction of L-arginine transport is inhibited by atrial natriuretic peptide: a peptide hormone as a novel regulator of inducible nitric-oxide synthase substrate availability.

BACKGROUND: The inducible nitric-oxide synthase (iNOS) synthesizes NO from L-arginine. Availability of L-arginine is maintained by a lipopolysaccharide (LPS)-induced induction of the CAT-2B amino acids transporter. Recently, we could show that the cardiovascular hormone atrial natriuretic peptide (ANP) inhibits the induction of iNOS in LPS-stimulated macrophages via its guanylate cyclase-coupled A-receptor. PURPOSE: To investigate whether ANP exerts an effect on LPS-induced L-arginine uptake. METHODS: Murine bone marrow derived macrophages were activated with LPS (1 microg/ml, 20 h) in the presence or absence of ANP or C-type natriuretic peptide (CNP). L-Arginine transport was determined by measuring the uptake of L-[(3)H]arginine. L-[(3)H]Arginine influx was also determined in LPS-activated cells in the presence of N(G)-monomethyl-L-arginine (L-NMMA), competitor amino acids, or ANP. Nitrite accumulation was determined in supernatants of LPS-activated cells cultured in the presence or absence of L-ornithine. RESULTS: ANP dose dependently (10(-8)-10(-6)M) inhibited LPS-induced L-[(3)H]arginine uptake when added simultaneously with LPS, whereas it showed no effect when added simultaneously with L-[(3)H]arginine. The effect was abrogated by the A-receptor antagonist HS-142-1 (10 microg/ml). CNP (10(-6) M) did not influence L-arginine transport. Competitor amino acids (10(-2) M) inhibited L-[(3)H]arginine uptake. An excess of unlabeled L-arginine (10(-2) M) as well as its analog L-NMMA (10(-3) M) also reduced L-[(3)H]arginine influx. L-Arginine uptake was critical for production of NO because L-ornithine significantly decreased LPS-induced nitrite accumulation. CONCLUSION: This work demonstrates that ANP inhibits LPS-induced L-arginine uptake via its guanylate cyclase-coupled A-receptor. Besides its influence on the induction of iNOS, this effect may represent an important and unique mechanism by which ANP regulates NO production in macrophages.[1]

References

 
WikiGenes - Universities