title: Cyclooxygenases 1 and 2 and thromboxane synthase in kidneys of Lyon hypertensive rats.
abstract: Compared with their two normotensive (LN and LL) controls, genetically hypertensive rats of the Lyon strain (LH) exhibit increased renal vascular resistance and a blunted pressure natriuresis function as well as an increased urinary excretion of vasoconstrictor prostanoids. The aim of this study was to assess in the kidneys of these animals the synthesis of vasoconstrictor or sodium-retaining prostanoids. The relative abundance of the mRNAs of cyclooxygenases (COX) 1 and 2 and of thromboxane A2 synthase (TXS), was measured by reverse-transcription polymerase chain reaction (RT-PCR) in renal cortex and medulla dissected in groups of male LH, LN, and LL rats either in baseline conditions or after 1 week of salt loading (1.5% NaCl in the drinking water). In basal conditions, at 3 and 11 weeks of age COX1 was expressed in the kidneys of all rats more markedly in medulla than in cortex. COX2 was poorly expressed in the whole kidney. TXS expression was usually too low to be quantified. No difference could be observed among LH, LN, and LL rats. After salt loading, the expression of COX1 was enhanced in the medulla and that of COX2 reduced in the cortex. LH rats differed from controls by a significantly more marked increase in medullary COX1 expression. The present work excludes any primary generalized increase in the renal expression of the genes that control the synthesis of vasoconstrictor prostanoids in LH rats, but suggests that medullary COX1 is upregulated by salt in these animals.
authors.affiliation: Département de Physiologie et Pharmacologie Clinique, CNRS ESA, Faculté de Pharmacie, Lyon, France. bernard@rockefeller.univ-lyon1.fr
authors.forename: N
authors.initials: N
authors.lastname: Bernard
authors.forename: J
authors.initials: J
authors.lastname: Sacquet
authors.forename: D
authors.initials: D
authors.lastname: Benzoni
authors.forename: J
authors.initials: J
authors.lastname: Sassard
mesh_terms: D000818:Animals; D016375:Antisense Elements (Genetics); D001794:Blood Pressure; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects / Q000502:physiology; D006977:Hypertension, Renal / Q000378:metabolism*; D007527:Isoenzymes / Q000235:genetics* / Q000378:metabolism*; D007672:Kidney Cortex / Q000201:enzymology*; D007679:Kidney Medulla / Q000201:enzymology*; D008297:Male; D008565:Membrane Proteins; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics* / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D011922:Rats, Mutant Strains; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017673:Sodium Chloride, Dietary / Q000494:pharmacology; D013930:Thromboxane-A Synthase / Q000235:genetics / Q000378:metabolism*; D013931:Thromboxanes / Q000096:biosynthesis
chemical_list: D016375:Antisense Elements (Genetics); D007527:Isoenzymes; D008565:Membrane Proteins; D012333:RNA, Messenger; D017673:Sodium Chloride, Dietary; D013931:Thromboxanes; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; C496513:Ptgs1 protein, rat; D013930:Thromboxane-A Synthase