Angiotensin II-induced hypertension in rats is only transiently accompanied by lower renal oxygenation

Tonja W. Emans, Daniela Patinha, Jaap A. Joles, Maarten P. Koeners, Ben J. Janssen, C. T. Paul Krediet*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

5 Citations (Web of Science)

Abstract

Activation of the renin-angiotensin system may initiate chronic kidney disease. We hypothesised that renal hypoxia is a consequence of hemodynamic changes induced by angiotensin II and occurs prior to development of severe renal damage. Male Sprague-Dawley rats were infused continuously with angiotensin II (350 ng/kg/min) for 8 days. Mean arterial pressure (n = 5), cortical (n = 6) and medullary (n = 7) oxygenation (pO(2)) were continuously recorded by telemetry and renal tissue injury was scored. Angiotensin II increased arterial pressure gradually to 150 +/- 18 mmHg. This was associated with transient reduction of oxygen levels in renal cortex (by 18 +/- 2%) and medulla (by 17 +/- 6%) at 10 +/- 2 and 6 +/- 1 hours, respectively after starting infusion. Thereafter oxygen levels normalised to pre-infusion levels and were maintained during the remainder of the infusion period. In rats receiving angiotensin II, adding losartan to drinking water (300 mg/L) only induced transient increase in renal oxygenation, despite normalisation of arterial pressure. In rats, renal hypoxia is only a transient phenomenon during initiation of angiotensin II-induced hypertension.
Original languageEnglish
Article number16342
Number of pages9
JournalScientific Reports
Volume8
DOIs
Publication statusPublished - 5 Nov 2018

Keywords

  • KIDNEY TISSUE OXYGENATION
  • END-ORGAN DAMAGE
  • CHRONIC HYPOXIA
  • CONSCIOUS RATS
  • BLOOD-PRESSURE
  • NITRIC-OXIDE
  • TUBULOINTERSTITIAL INJURY
  • DEPENDENT HYPERTENSION
  • TYPE-2 RECEPTORS
  • REMNANT KIDNEY

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