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Hydronephrosis causes salt-sensitive hypertension in rats

  • Mattias Carlström
  • , Nils Wåhlin
  • , Johan Sällström
  • , Ole Skøtt
  • , Russell Brown
  • , A. Erik G. Persson
  • Uppsala University

Research output: Contribution to journalJournal articleResearchpeer-review

Abstract

BACKGROUND: Hypertension is a common disease in the Western world and approximately 5% of all cases are secondary to kidney malfunction. It is not clear whether unilateral hydronephrosis due to partial obstruction affects blood pressure.

AIM: The aim of this study was to determine whether hypertension develops and to investigate the effects of different salt diets on the blood pressure in hydronephrotic animals.

METHODS: Unilateral partial ureteral obstruction was created in 3-week-old Sprague-Dawley rats. A telemetric device was implanted 4-6 weeks later and blood pressure was measured on normal, low- and high-salt diets. Plasma samples were collected on all diets for renin analysis.

RESULTS: All hydronephrotic animals developed hypertension that correlated to the degree of hydronephrosis. The blood pressure increased slowly with time and was salt sensitive. In severe hydronephrosis, blood pressure increased from 118 +/- 5 mmHg on low salt to 140 +/- 6 mmHg on high salt intake, compared to control levels of 82 +/- 2 and 84 +/- 2 mmHg, respectively. Plasma renin concentration was increased in the hydronephrotic group of animals compared to controls on all diets, but the difference was only significant on a normal salt diet, 165 +/- 15 versus 86 +/- 12 microGU/ml respectively. In animals with severe hydronephrosis the plasma renin levels were lower, and the changes less, than in those with mild and moderate hydronephrosis.

CONCLUSION: This study demonstrates the presence of a salt-sensitive hypertension in hydronephrosis. A systemic effect of the renin-angiotensin system alone cannot be responsible for the hypertension.

Original languageEnglish
JournalJournal of Hypertension
Volume24
Issue number7
Pages (from-to)1437-1443
Number of pages7
ISSN0263-6352
DOIs
Publication statusPublished - 1. Jul 2006

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