title: Hydronephrosis causes salt-sensitive hypertension and impaired renal concentrating ability in mice.
abstract: OBJECTIVE
  Hypertension is a common disease in the industrialized world and approximately 5% of all cases are secondary to kidney malfunction. We have recently shown that hydronephrosis due to partial unilateral ureteral obstruction (PUUO) causes salt-sensitive hypertension in rats. The mechanisms are still unclear, but appear to be intrarenal and primarily located to the diseased kidney. In the present study, we have developed a model for PUUO to study if hydronephrotic mice develop salt-sensitive hypertension.
  
  
  METHODS
  PUUO was created in 3-week-old mice (C57bl/6J). Blood pressure and heart rate were measured telemetrically in adult animals on normal and high salt diets. Metabolism cages were used to study the renal excretion of electrolytes and water. Plasma samples for renin analysis were collected and renal histological changes were evaluated.
  
  
  RESULTS
  All hydronephrotic animals developed salt-sensitive hypertension that correlated to the degree of hydronephrosis. In hydronephrotic animals, blood pressure increased from 114 +/- 1 mmHg on normal salt diet to 120 +/- 2 mmHg on high salt diet, compared with 103 +/- 1 to 104 +/- 1 in controls. Hydronephrotic animals showed increased diuresis and reduced ability to regulate electrolyte concentration. No differences in plasma renin concentration were found between the groups. The parenchymal weight and glomerular area of contralateral kidneys were significantly increased in the hydronephrotic animals. Histopathology of the hydronephrotic kidneys displayed areas with fibrosis, inflammation and glomerular changes.
  
  
  CONCLUSIONS
  This study provides a model for PUUO in mice and demonstrates the presence of salt-sensitive hypertension and an impaired renal concentrating ability in mice which has not been described before.
authors.affiliation: Department of Medical Cell Biology, Division of Integrative Physiology, Uppsala University, Uppsala, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Carlström
authors.forename: J
authors.initials: J
authors.lastname: Sällström
authors.forename: O
authors.initials: O
authors.lastname: Skøtt
authors.forename: E
authors.initials: E
authors.lastname: Larsson
authors.forename: N
authors.initials: N
authors.lastname: Wåhlin
authors.forename: A E G
authors.initials: AE
authors.lastname: Persson
mesh_terms: D000818:Animals; D006339:Heart Rate; D006869:Hydronephrosis / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D006973:Hypertension / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D007668:Kidney / Q000473:pathology; D007671:Kidney Concentrating Ability; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D023421:Models, Animal; D012083:Renin / Q000097:blood; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage; D013686:Telemetry; D014517:Ureteral Obstruction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
chemical_list: D017673:Sodium Chloride, Dietary; D012083:Renin