RGD Reference Report - Differential regulation of renal prostaglandin receptor mRNAs by dietary salt intake in the rat. - Rat Genome Database

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Differential regulation of renal prostaglandin receptor mRNAs by dietary salt intake in the rat.

Authors: Jensen, BL  Mann, B  Skott, O  Kurtz, A 
Citation: Jensen BL, etal., Kidney Int. 1999 Aug;56(2):528-37.
RGD ID: 9850282
Pubmed: PMID:10432392   (View Abstract at PubMed)
DOI: DOI:10.1046/j.1523-1755.1999.00564.x   (Journal Full-text)

BACKGROUND: In this study, we tested the hypothesis that prostaglandin (PG) receptor expression in the rat kidney is subject to physiological regulation by dietary salt intake. METHODS: Rats were fed diets with 0.02 or 4% NaCl for two weeks. PG receptor expression was assayed in kidney regions and cells by ribonuclease protection assay and reverse transcription-polymerase chain reaction analysis. Functional correlates were studied by measurement of PGE2-induced cAMP formation and renin secretion in juxtaglomerular (JG) cells isolated from animals on various salt intakes. RESULTS: EP1 and EP3 receptors were predominantly expressed, and the EP2 receptor was exclusively expressed in the rat kidney medulla. The EP4 receptor was strongly expressed in glomeruli and in renin-secreting JG granular cells. IP receptor transcripts were found mainly in cortex. Maintaining rats on a low- or high-NaCl diet did not affect the expression of EP1 or IP receptors, whereas EP4 transcripts in glomeruli were increased twofold by salt deprivation. Consistent with this, we found that PGE2-evoked cAMP production and renin secretion by JG cells from salt-deprived animals were significantly higher compared with cells obtained from salt-loaded animals. In the outer medulla, EP3 transcripts correlated directly with salt intake, and mRNA abundance was increased twofold by a high-NaCl diet. CONCLUSIONS: Our results suggest that subtype-specific, regional changes in PG receptor expression are involved in the renal adaptation to changes in salt intake. The results are in accord with the general concept that renocortical PGE2 stimulates renin secretion and maintains renal blood flow during low-salt states, whereas medullary PGE2 promotes salt excretion in response to a high salt intake.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to salt  IEP 9850282; 9850282 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ptger3  (prostaglandin E receptor 3)
Ptger4  (prostaglandin E receptor 4)


Additional Information