title: Alpha 2-adrenoceptors in brain and kidney during development of hypertension in Dahl-Iwai salt-sensitive rats.
abstract: BACKGROUND
  Both renal and extrarenal factors have been considered to contribute to the development of hypertension in Dahl salt-sensitive rats, but contents of both factors have not been established precisely.
  
  
  OBJECTIVE
  To clarify the role of those factors in the sympathetic nervous system, we examined the regulation of alpha2-adrenoceptors in the lower brainstem and the renal tubular basolateral membranes simultaneously during the development of salt-induced hypertension in Dahl-Iwai salt-sensitive rats.
  
  
  METHODS
  Dahl-Iwai salt-sensitive or resistant rats were fed a high (8.0% NaCl)- or low (0.3%)- salt diet from 4 to 6 or 10 weeks of age. At 4, 6 and 10 weeks of age, the plasma membranes of the lower brainstem and the renal tubular basolateral membranes were obtained simultaneously and alpha 2-adrenoceptors were quantified by a radioligand binding assay using 3H-rauwolscine.
  
  
  RESULTS
  In the salt-sensitive rats, systolic blood pressure was significantly higher in those fed a high-salt diet than in those fed a low-salt diet. In the salt-resistant rats, both the high- and the low-salt groups showed similar blood pressure levels. At 6 weeks of age, alpha 2-receptor densities of the salt-sensitive rats fed a high-salt diet were lower in the lower brainstem and higher in the renal basolateral membranes than those fed a low-salt diet. In contrast, in the salt-resistant rats, both the high- and the low-salt groups had similar densities. At 10 weeks of age, the difference between the high- and the low-salt groups in the salt-sensitive rats disappeared in both the brainstem and the renal basolateral membranes.
  
  
  CONCLUSIONS
  Alpha 2-adrenoceptor regulation in the brainstem and the renal basolateral membranes differs between Dahl-Iwai salt-sensitive and salt-resistant rats. The modulation of alpha 2-adrenoceptors by a high salt intake may be essential particularly in the early phase of the development of salt-induced hypertension.
authors.affiliation: Third Department of Internal Medicine, University of The Ryukyus, Okinawa, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Tozawa
authors.forename: S
authors.initials: S
authors.lastname: Takishita
authors.forename: O
authors.initials: O
authors.lastname: Sunagawa
authors.forename: H
authors.initials: H
authors.lastname: Muratani
authors.forename: C
authors.initials: C
authors.lastname: Imai
authors.forename: N
authors.initials: N
authors.lastname: Kawazoe
authors.forename: K
authors.initials: K
authors.lastname: Fukiyama
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001933:Brain Stem / Q000378:metabolism*; D005260:Female; D006973:Hypertension / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D007684:Kidney Tubules / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D011869:Radioligand Assay; D051381:Rats; D018341:Receptors, Adrenergic, alpha-2 / Q000378:metabolism*; D012965:Sodium Chloride / Q000008:administration & dosage
chemical_list: D018341:Receptors, Adrenergic, alpha-2; D012965:Sodium Chloride