title: Disruption of the type 2 dopamine receptor gene causes a sodium-dependent increase in blood pressure in mice.
abstract: BACKGROUND
  Dopamine D(2) receptors (D(2)Rs) are expressed in the kidney. It has not been determined whether D(2)Rs are involved in the mechanism of sodium handling and blood pressure (BP) control.
  
  
  METHODS
  The function of D(2)Rs was investigated in mice disrupted with D(2)R gene (D(2)KO mice). Six-week-old male D(2)KO mice and wild-type (WT) mice were fed high-salt (4% NaCl) or low-salt (0.01% NaCl) diets for 8 weeks.
  
  
  RESULTS
  Before starting the metabolic diet, there were no significant differences in body weight, food consumption, and 24-h urine excretions of creatinine, sodium and potassium. The high-salt diet caused a significant elevation in systolic BP in D(2)KO mice but not in WT mice. Calculation of sodium and potassium balances revealed a significantly high level of sodium retention in D(2)KO mice placed on the high-salt diet. Twenty-four-hour urine norepinephrine excretions and heart rates, indicators of sympathetic activity, were not different in D(2)KO and WT mice on the high-salt diet. Administration of nemonapride, a specific D(2)-like receptor antagonist, to WT mice given 0.9% NaCl in drinking water caused suppression of urinary sodium excretion but had no effect in mice without salt loading.
  
  
  CONCLUSIONS
  These results suggest that D(2) receptors promote sodium excretion during a period of high salt intake. A defect in this mechanism may result in sodium-dependent BP elevation.
authors.affiliation: Department of Medicine and Molecular Science, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Ueda
authors.forename: Ryoji
authors.initials: R
authors.lastname: Ozono
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Oshima
authors.forename: Ai
authors.initials: A
authors.lastname: Yano
authors.forename: Masayuki
authors.initials: M
authors.lastname: Kambe
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Teranishi
authors.forename: Motoya
authors.initials: M
authors.lastname: Katsuki
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Chayama
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000235:genetics*; D001835:Body Weight; D018491:Dopamine Agonists / Q000494:pharmacology; D006973:Hypertension / Q000235:genetics*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009318:Natriuresis / Q000187:drug effects / Q000235:genetics; D009638:Norepinephrine / Q000652:urine; D011188:Potassium / Q000378:metabolism; D019257:Quinpirole / Q000494:pharmacology; D017448:Receptors, Dopamine D2 / Q000235:genetics*; D012982:Sodium, Dietary / Q000494:pharmacology* / Q000652:urine; D014556:Urine
chemical_list: D018491:Dopamine Agonists; D017448:Receptors, Dopamine D2; D012982:Sodium, Dietary; D019257:Quinpirole; D011188:Potassium; D009638:Norepinephrine