title: Differential distribution of alpha 2-adrenoceptor subtypes and messenger RNA expression between renal cortex of salt-sensitive and salt-resistant Sabra rats.
abstract: OBJECTIVE
  To assess whether alterations of alpha 2-adrenoceptor subtypes in distribution and gene expression in the renal cortex could explain the predisposition to salt-sensitivity or salt-resistance in Sabra rats.
  
  
  METHODS
  Studies were performed using plasma membranes and RNA preparations from renal cortex of 8- to 10-week-old Sabra salt-sensitive (SBH) and salt-resistant (SBN) rats on a normal-sodium diet.
  
  
  METHODS
  The alpha 2-adrenoceptor subtypes were determined by competition experiments with [3H]-yohimbine or [3H]-RX821002. Their gene expression was studied by RNA-directed complementary DNA synthesis followed by Taq DNA polymerase amplification.
  
  
  RESULTS
  Binding studies showed that alpha 2B- and alpha 2A-adrenoceptor subtypes represented in SBN 72 and 28% of the maximal binding capacities of the two radioligands, respectively. In contrast, only the alpha 2B subtype was detected in the SBH rat. However, the use of guanoxabenz disclosed alpha 2B-adrenoceptors in alpha 2B1 and alpha 2B2 subtypes. The densities of those alpha 2B subtypes appeared to be higher in the SBH rat than in the SBN rat. Messenger RNA corresponding to alpha 2A and alpha 2B subtypes were found both in SBH rats and in SBN rats. The expression of the alpha 2B subtype was permanently higher in the SBH rats than in the SBN rats. The expression of the alpha 2A gene in the SBH rats suggests a specific SBH post-transcriptional regulation resulting in the absence of alpha 2A-adrenoceptor.
  
  
  CONCLUSIONS
  Differences exist in the renal cortex concerning expression and distribution of alpha 2-adrenoceptor subtypes between SBH and SBN rats. From these differences there might result different alpha 2-adrenoceptor-mediated renal functions in SBH and in SBN rats, which could lead to a predisposition to sensitivity or resistance to a high sodium intake.
authors.affiliation: CJF Inserm 94.02, Service de Biochimie de Paris-Ouest, UFR Biomédicale des Saints-Pères, France.
authors.forename: M
authors.initials: M
authors.lastname: Le Jossec
authors.forename: C
authors.initials: C
authors.lastname: Trivalle
authors.forename: J F
authors.initials: JF
authors.lastname: Cloix
authors.forename: R
authors.initials: R
authors.lastname: Pecquery
authors.forename: Y
authors.initials: Y
authors.lastname: Giudicelli
authors.forename: J P
authors.initials: JP
authors.lastname: Dausse
mesh_terms: D000818:Animals; D001483:Base Sequence; D015152:Blotting, Northern; D005784:Gene Amplification; D006973:Hypertension / Q000378:metabolism*; D007672:Kidney Cortex / Q000737:chemistry*; D008297:Male; D008969:Molecular Sequence Data; D012333:RNA, Messenger / Q000032:analysis*; D051381:Rats; D018341:Receptors, Adrenergic, alpha-2 / Q000032:analysis* / Q000235:genetics; D012965:Sodium Chloride / Q000494:pharmacology*; D015016:Yohimbine / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D018341:Receptors, Adrenergic, alpha-2; D015016:Yohimbine; D012965:Sodium Chloride