title: Upregulation of prolactin receptor in proximal tubular cells was induced in cardiac dysfunction model mice.
abstract: BACKGROUND
  In order to clarify the interaction between cardiac dysfunction and sodium homeostasis in the kidney, we used a murine model of cardiac dysfunction and investigated the effect on sodium transporters in renal tubular cells.
  
  
  METHODS
  Cardiac function was deteriorated by abdominal aortic banding, and the gene expression of sodium transporters in the kidneys was evaluated by real-time RT-PCR and compared with that in the kidneys of control mice.
  
  
  RESULTS
  Gene expression of all three variants of the murine prolactin receptor was enhanced by aortic banding. Upregulated prolactin receptor was distributed in the proximal tubular cells of the pars recta in the deep inner cortex and the outer stripe of the outer medulla. Prolactin has been reported to be a natriuretic hormone that inhibits proximal tubular Na(+)/K(+)-ATPase activity, resulting in reduced sodium reabsorption and the acceleration of natriuresis. Inhibition of endogenous prolactin secretion by bromocriptine administration decreased the urine sodium excretion in both aortic banding and control mice. On the other hand, excess exogenous prolactin administration enhanced urine potassium excretion in aortic banding mice. Furthermore, a high-sodium diet accelerated urinary sodium excretion, which was also significantly decreased by inhibition of endogenous prolactin secretion in aortic banding mice.
  
  
  CONCLUSIONS
  We reported that the prolactin receptor was upregulated by aortic banding treatment. Prolactin-prolactin receptor interaction in the proximal tubular cells of the pars recta should involve a different mechanism of kaliuresis other than inhibition of Na(+)/K(+)-ATPase.
authors.affiliation: Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Niigata, 951-8510, Japan.
authors.forename: Yohei
authors.initials: Y
authors.lastname: Tsuchida
authors.forename: Yoshikatsu
authors.initials: Y
authors.lastname: Kaneko
authors.forename: Tadashi
authors.initials: T
authors.lastname: Otsuka
authors.forename: Kei
authors.initials: K
authors.lastname: Goto
authors.forename: Akihiko
authors.initials: A
authors.lastname: Saito
authors.forename: Keiko
authors.initials: K
authors.lastname: Yamamoto
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Ichiei
authors.initials: I
authors.lastname: Narita
mesh_terms: D058186:Acute Kidney Injury / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001971:Bromocriptine / Q000494:pharmacology; D006332:Cardiomegaly / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D004195:Disease Models, Animal; D006706:Homeostasis; D006727:Hormone Antagonists / Q000494:pharmacology; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008810:Mice, Inbred C57BL; D009318:Natriuresis; D011188:Potassium / Q000652:urine; D011388:Prolactin / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011981:Receptors, Prolactin / Q000235:genetics / Q000378:metabolism*; D015427:Reperfusion Injury / Q000235:genetics / Q000378:metabolism; D012964:Sodium / Q000378:metabolism* / Q000652:urine; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage; D015854:Up-Regulation
chemical_list: D006727:Hormone Antagonists; D011981:Receptors, Prolactin; D017673:Sodium Chloride, Dietary; D001971:Bromocriptine; D011388:Prolactin; D012964:Sodium; D011188:Potassium