title: Relief of chronic partial ureteral obstruction attenuates salt-sensitive hypertension in rats.
abstract: OBJECTIVE
  The incidence of hydronephrosis due to ureteropelvic junction obstruction is approx. 0.5%. During the last decade, the management of non-symptomatic hydronephrosis has become much more conservative, but the long-term physiological consequences of this policy are not clear. Previously, we have shown that animals with chronic partial unilateral ureteral obstruction develop salt-sensitive hypertension. In this study, the effects of ipsilateral and contralateral nephrectomy and ureterovesicostomy on blood pressure were studied in hydronephrotic animals.
  
  
  METHODS
  Partial unilateral ureteral obstruction was created in 3-week-old male Sprague-Dawley rats and blood pressure was measured telemetrically 4-6 weeks later during a normal and high salt diet before and after uninephrectomy or ureterovesicostomy. Plasma samples for renin assay were collected during both diets before and after ipsilateral nephrectomy.
  
  
  RESULTS
  All hydronephrotic animals developed salt-sensitive hypertension, of different degrees. Before nephrectomy the plasma renin concentration was significantly higher in the hydronephrotic animals than in controls (160 +/- 15 microGU mL(-1) vs. 96 +/- 12 microGU mL(-1), respectively), but after the ipsilateral nephrectomy no differences were found between the groups. In the hydronephrotic animals both ipsilateral nephrectomy and ureterovesicostomy reduced the blood pressure and salt-sensitivity but the former still differed significantly from the controls. In contralaterally, nephrectomized hydronephrotic animals the salt-sensitive hypertension became more pronounced.
  
  
  CONCLUSIONS
  Hydronephrosis in rats causes salt-sensitive hypertension that can be markedly reduced by removing the hydronephrotic kidney or relieving the obstruction by ureterovesicostomy. The mechanisms appear to be intrarenal and primarily located in the diseased kidney, but a secondary mechanism is also present.
authors.affiliation: Department of Medical Cell Biology, Division of Integrative Physiology, University of Uppsala, Uppsala, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Carlström
authors.forename: N
authors.initials: N
authors.lastname: Wåhlin
authors.forename: O
authors.initials: O
authors.lastname: Skøtt
authors.forename: A E G
authors.initials: AE
authors.lastname: Persson
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D006869:Hydronephrosis / Q000097:blood / Q000503:physiopathology*; D006973:Hypertension / Q000097:blood / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology; D008297:Male; D009392:Nephrectomy / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000097:blood; D017673:Sodium Chloride, Dietary / Q000378:metabolism; D014517:Ureteral Obstruction / Q000097:blood / Q000503:physiopathology*; D014519:Ureterostomy / Q000379:methods
chemical_list: D017673:Sodium Chloride, Dietary; D012083:Renin