Differential regulation of renal prostaglandin receptor mRNAs by dietary salt intake in the rat.
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.
Jensen
B L
BL
Institute of Physiology I, University of Regensburg, Germany. bl.jensen@winsloew.sdu.uk
Mann
B
B
Skøtt
O
O
Kurtz
A
A
D000818:Animals; D016375:Antisense Elements (Genetics); D002478:Cells, Cultured; D003001:Cloning, Molecular; D000242:Cyclic AMP / Q000032:analysis; D018076:DNA, Complementary; D015232:Dinoprostone / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D007606:Juxtaglomerular Apparatus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D007678:Kidney Glomerulus / Q000737:chemistry / Q000378:metabolism; D007679:Kidney Medulla / Q000737:chemistry / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D044006:Receptors, Epoprostenol; D011982:Receptors, Prostaglandin / Q000235:genetics; D018078:Receptors, Prostaglandin E / Q000235:genetics*; D058306:Receptors, Prostaglandin E, EP1 Subtype; D058307:Receptors, Prostaglandin E, EP2 Subtype; D058308:Receptors, Prostaglandin E, EP3 Subtype; D058309:Receptors, Prostaglandin E, EP4 Subtype; D012965:Sodium Chloride / Q000494:pharmacology; D012982:Sodium, Dietary / Q000494:pharmacology*
D016375:Antisense Elements (Genetics); D018076:DNA, Complementary; C545636:Ptger1 protein, mouse; C545637:Ptger1 protein, rat; C545645:Ptger2 protein, mouse; C545646:Ptger2 protein, rat; C545648:Ptger3 protein, mouse; C545649:Ptger3 protein, rat; C545651:Ptger4 protein, mouse; C545652:Ptger4 protein, rat; D012333:RNA, Messenger; D044006:Receptors, Epoprostenol; D011982:Receptors, Prostaglandin; D018078:Receptors, Prostaglandin E; D058306:Receptors, Prostaglandin E, EP1 Subtype; D058307:Receptors, Prostaglandin E, EP2 Subtype; D058308:Receptors, Prostaglandin E, EP3 Subtype; D058309:Receptors, Prostaglandin E, EP4 Subtype; D012982:Sodium, Dietary; D012965:Sodium Chloride; D000242:Cyclic AMP; D015232:Dinoprostone