title: Sodium intake regulates renin gene expression differently in the hypothalamus and kidney of rats.
abstract: OBJECTIVE
  To elucidate the different effects of sodium intake on renin messenger RNA (mRNA) in the hypothalamus and the kidney and to investigate the role of hypothalamic renin in sodium-induced hypertension.
  
  
  METHODS
  We investigated the expression of the renin gene in the hypothalamus and the kidney of rats with altered sodium intake and those administered either deoxycorticosterone acetate (DOCA) or sodium. Diets containing a high (8% NaCl), normal (2% NaCl), or low (0.2% NaCl) amount of sodium were administered to 12-week-old male Wistar rats for 10 days or 8 weeks before the rats were killed. Male Wistar rats administered either DOCA or 1% NaCl were killed 2 weeks (during the prehypertensive stage) or 6 weeks (during the hypertensive stage) after the start of treatment. The hypothalamus and kidneys were excised for extraction of total RNA. Competitive polymerase chain reaction of renin mRNA and deletion-mutated renin RNA was performed, and the renin mRNA concentration was calculated.
  
  
  RESULTS
  A high sodium intake for 10 days increased the renin mRNA in the hypothalamus; the hypothalamic renin mRNA had not been suppressed after 8 weeks of a high sodium intake despite the lowering in renal renin mRNA. Renin mRNA levels in the hypothalamus were not suppressed either in the prehypertensive or in the hypertensive stage in rats treated with DOCA or sodium, or both, although the renal renin mRNA was reduced in rats administered DOCA or sodium, or both, compared with that in sham-treated control rats, during both stages.
  
  
  CONCLUSIONS
  The expression of the renin gene is regulated differently in the rat hypothalamus from that in the kidney. The constant expression of the renin gene in the hypothalamus during a chronic high sodium load might be related at least in part to the mechanism of the activated brain renin-angiotensin system in sodium-induced hypertension.
authors.affiliation: Department of Clinical and Laboratory Medicine, Kyoto Prefectural University of Medicine, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Nishimura
authors.forename: A
authors.initials: A
authors.lastname: Nanbu
authors.forename: K
authors.initials: K
authors.lastname: Ohtsuka
authors.forename: H
authors.initials: H
authors.lastname: Takahashi
authors.forename: N
authors.initials: N
authors.lastname: Iwai
authors.forename: M
authors.initials: M
authors.lastname: Kinoshita
authors.forename: M
authors.initials: M
authors.lastname: Yoshimura
mesh_terms: D000818:Animals; D001127:Arginine Vasopressin / Q000652:urine; D001483:Base Sequence; D017931:DNA Primers / Q000235:genetics; D003900:Desoxycorticosterone / Q000633:toxicity; D005786:Gene Expression Regulation; D006439:Hemodynamics; D006973:Hypertension / Q000209:etiology / Q000235:genetics / Q000503:physiopathology; D007031:Hypothalamus / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D008297:Male; D009638:Norepinephrine / Q000652:urine; D009928:Organ Specificity; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012083:Renin / Q000097:blood / Q000235:genetics*; D012982:Sodium, Dietary / Q000008:administration & dosage*
chemical_list: D017931:DNA Primers; D012333:RNA, Messenger; D012982:Sodium, Dietary; D001127:Arginine Vasopressin; D003900:Desoxycorticosterone; D012083:Renin; D009638:Norepinephrine