title: Expression of the K+ channel Kir7.1 in the developing rat kidney: role in K+ excretion.
abstract: BACKGROUND
  Coordinated expression of ROMK (luminal K+ channel in the thick ascending limb and the collecting duct) and Na+,K+-ATPase has been demonstrated to be involved in the postnatal development of renal K+ excretion; however, the developmental expression of the basolateral K+ channel Kir7.1 is unknown. The purpose of this study was to elucidate the possible involvement of Kir7.1 in the maturation of renal K+ excretion.
  
  
  METHODS
  Developmental changes in the renal K+ excretion under the condition of K+ overload was investigated by collecting urine from neonatal rats infused with K+ (KCl solution). RNase protection analysis was used to elucidate the expression of Kir7.1 and Na+,K+-ATPase mRNA in pre- and postnatal rats, and the expression of Kir7.1 and ROMK mRNA at 7, 14, and 21 days. Western blotting of Kir7.1, and immunohistochemistry of Kir7.1 and ROMK were used to determine their protein expression.
  
  
  RESULTS
  The ratio of urinary K+ excretion to K+ load increased between 7 and 14 days after birth. In addition, half excretion time of K+ load gradually decreased through the experimental period of 7 and 21 days. Na+,K+-ATPase mRNA levels showed a peak of up-regulation at birth that remained elevated. ROMK1 mRNA levels significantly increased between 7 and 14 days. On the other hand, Kir7.1 mRNA and protein levels significantly increased between 14 and 21 days. Kir7.1 protein in the thick ascending limb was first recognized at 7 days, whereas its expression in the distal convoluted tubule and the cortical collecting duct was found in 21-day-old neonates.
  
  
  CONCLUSIONS
  Our results suggest that Kir7.1 is involved in the development of renal K+ excretion between 14 and 21 days after birth under the condition of K+ overload.
authors.affiliation: Department of Physiology, Kitasato University School of Medicine, Sagamihara, Japan. yosukuki@med.kitasato-u.ac.jp
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Yasuoka
authors.forename: Takao
authors.initials: T
authors.lastname: Shimohama
authors.forename: Mariko
authors.initials: M
authors.lastname: Nishikitani
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Nakamura
authors.forename: Shigehisa
authors.initials: S
authors.lastname: Hirose
authors.forename: Katsumasa
authors.initials: K
authors.lastname: Kawahara
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D018507:Gene Expression Regulation, Developmental; D006947:Hyperkalemia / Q000378:metabolism / Q000503:physiopathology; D007150:Immunohistochemistry; D007668:Kidney / Q000254:growth & development* / Q000502:physiology*; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000235:genetics / Q000378:metabolism; D024661:Potassium Channels, Inwardly Rectifying / Q000235:genetics* / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics / Q000378:metabolism
chemical_list: C510692:Kcnj1 protein, rat; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D012333:RNA, Messenger; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium