RGD Reference Report - Renal nitric oxide production in rat pregnancy: role of constitutive nitric oxide synthases. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Renal nitric oxide production in rat pregnancy: role of constitutive nitric oxide synthases.

Authors: Smith, CA  Santymire, B  Erdely, A  Venkat, V  Losonczy, G  Baylis, C 
Citation: Smith CA, etal., Am J Physiol Renal Physiol. 2010 Oct;299(4):F830-6. Epub 2010 Jul 14.
RGD ID: 5131941
Pubmed: PMID:20630934   (View Abstract at PubMed)
PMCID: PMC2957259   (View Article at PubMed Central)
DOI: DOI:10.1152/ajprenal.00300.2010   (Journal Full-text)

Functional studies show that increased renal nitric oxide (NO) mediates the renal vasodilation and increased glomerular filtration rate that occur during normal pregnancy. We investigated whether changes in the constitutive NO synthases (NOS), endothelial (eNOS) and neuronal (nNOS), were associated with the increased renal NO production in normal midterm pregnancy in the rat. In kidneys from midterm pregnant (MP: 11-13 days gestation), late-term pregnant (LP: 18-20 days gestation), and similarly aged virgin (V) rats, transcript and protein abundance for eNOS and the nNOSalpha and nNOSbeta splice variants, as well as the rate of L-arginine-to-L-citrulline conversion, were determined as a measure of NOS activity. At MP, renal cortical abundance of the total eNOS protein and phosphorylated (Ser(1177)) eNOS was reduced, and L-arginine-to-L-citrulline conversion in the cortical membrane fraction was decreased; these declines were also seen in LP. There were no changes in the eNOS transcript. In contrast, L-arginine-to-L-citrulline conversion in the soluble fraction of renal cortex increased at MP and then declined at LP. This MP increase was ablated by S-methylthiocitrulline, a nNOS inhibitor. Using Western blotting, we did not detect a change in the protein abundance or transcript of the 160-kDa nNOSalpha, but protein abundance and transcript of the nNOSbeta were increased at MP in cortex. Collectively, these studies suggest that the soluble nNOSbeta is responsible for the increased renal cortical NO production during pregnancy.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
female pregnancy  IEP 5131941; 5131941 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Nos1  (nitric oxide synthase 1)
Nos3  (nitric oxide synthase 3)


Additional Information