title: Association of (pro)renin receptor mRNA expression with angiotensin-converting enzyme mRNA expression in human artery.
abstract: OBJECTIVE
  A significant role of (pro)renin receptor in the pathogenesis of end-organ damage has been suggested only in animal studies. This study was conducted to examine the mRNA expression of (pro)renin receptor in human artery.
  
  
  METHODS
  In 141 kidney failure patients, the mRNA was harvested from arterial fragments obtained during surgery constructing an arteriovenous access for hemodialysis therapy, and expression levels of (pro)renin receptor and other components of the renin-angiotensin system were determined.
  
  
  RESULTS
  Arterial (pro)renin receptor expression was similar in diabetic and non-diabetic patients, although plasma prorenin levels were significantly higher in the diabetic patients than in the non-diabetic patients. The arterial (pro)renin receptor mRNA levels of the hypertensive patients, who had not been treated with either angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers, were significantly lower than those of the patients who had been treated with either drug. Multiple regression analyses showed a significant association with a large coefficient between the arterial mRNA level of the (pro)renin receptor and the arterial mRNA level of ACE; this significant association disappeared in patients who had been treated with either drug.
  
  
  CONCLUSIONS
  (Pro)renin receptor may contribute to the generation of arterial angiotensin II in kidney failure patients.
authors.affiliation: Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
authors.forename: Tomoko
authors.initials: T
authors.lastname: Takemitsu
authors.forename: Atsuhiro
authors.initials: A
authors.lastname: Ichihara
authors.forename: Yuki
authors.initials: Y
authors.lastname: Kaneshiro
authors.forename: Mariyo
authors.initials: M
authors.lastname: Sakoda
authors.forename: Asako
authors.initials: A
authors.lastname: Kurauchi-Mito
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Narita
authors.forename: Kenichiro
authors.initials: K
authors.lastname: Kinouchi
authors.forename: Norimasa
authors.initials: N
authors.lastname: Yamashita
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Itoh
mesh_terms: D000368:Aged; D000450:Aldosterone / Q000097:blood; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001158:Arteries / Q000502:physiology*; D001166:Arteriovenous Shunt, Surgical; D003928:Diabetic Nephropathies / Q000235:genetics / Q000503:physiopathology; D005260:Female; D005786:Gene Expression Regulation / Q000502:physiology; D006801:Humans; D006977:Hypertension, Renal / Q000188:drug therapy / Q000235:genetics / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000235:genetics* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D012333:RNA, Messenger / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000235:genetics*; D012044:Regression Analysis; D012083:Renin / Q000097:blood; D000093342:Prorenin Receptor
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D000450:Aldosterone; D007703:Peptidyl-Dipeptidase A; D012083:Renin; D000093342:Prorenin Receptor