Abstract

Renovascular hypertension affects ~1–4% of the hypertensive population and represents the second‐leading cause of secondary hypertension. There is an urgent clinical need to gain insight into the aetiology of renovascular hypertension to form the basis of new treatment targets. We hypothesize that high blood pressure in these conditions aims to sustain perfusion thus optimising organ blood flow and tissue oxygen homeostasis.Male Wistar Rats with (2K1C, n=5) or without (control, n=3) renal artery clip to generate renovascular hypertension were used. Six weeks after renal artery clipping, renal hemodynamics and oxygen metabolism were evaluated under isoflurane anaesthesia. Renal blood flow was measured in the clipped kidney using an ultrasound probe, glomerular filtration rate was measured using FITC‐inulin and the arterio‐venous difference in oxygen content was used to determine the clipped kidney oxygen consumption. Despite mean arterial pressure being higher in the 2K1C group when compared with controls (134±9 vs 97±10 mmHg, p=0.02), blood flow (7±1 vs 7±1 ml/min, p=0.823), glomerular filtration rate (0.42±0.1 vs 0.53±0.1 ml/min, p=0.45) and oxygen consumption (1.0±0.12 vs 0.6±0.1 mlO2/min, p=0.06) were not significantly different between 2K1C and control animalsThis preliminary data suggests that high blood pressure in 2K1C animals is sustaining normal renal perfusion, oxygen homeostasis and renal hemodynamics despite the reduction of arterial diameter.Support or Funding InformationBritish Heart Foundation funded research.

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