Abstract 627: Measuring Renal Oxygenation in a Mouse Model of Volume-Dependent Hypertension using BOLD MRI.

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Abstract

Hypertension is closely associated with the progression of kidney damage and dysfunction. Tissue hypoxia in the hypertensive kidney contributes to the progression of kidney damage. Peroxisome proliferator activated receptor-α (PPAR-α) is a nuclear receptor that plays an important role in reducing volume-dependent hypertension. Previous reports demonstrate that a slow pressor dose of Angiotensin II (Ang II) is a model of volume-dependent hypertension. The goal of this study was to determine the role of PPAR-α on renal oxygenation using blood oxygen level-dependent (BOLD) MRI in a model of volume-dependent hypertension. Wild-type (WT) and PPAR-α knockout (KO) mice were imaged using a multiple gradient echo BOLD sequence (12 echoes from 3.2-54ms, TR=900ms) on a 9.4T MRI to measure functional changes in renal oxygenation. Imaging was performed during baseline, day 12 of Ang II (400 ng/kg/min), and 9 days after Ang II-treatment (recovery). T2* relaxation time was measured in the cortex and medulla of the kidney. Cortex T2* values were lower in KO vs WT during baseline (11.0 ± 1.1 ms vs 13.1 ± 1.5 ms), day 12 of Ang II (11.6 ±1.2 ms vs 16.2 ±1.5 ms) and 9 days after Ang II (12.5 ± 0.7 ms vs 15.2 ± 0.3 ms). Medulla T2* values were lower on day 12 of Ang II in KO (16.5 ± 2.5 ms) vs WT (20 ± 1.6 ms) mice. Medulla T2* values were similar between KO and WT mice during baseline and the recovery period. In KO and WT mice, cortex T2* values were lower than that of the medulla, indicative of different metabolic functions between the two tissues. PPAR-α plays an important role in blood pressure regulation and renal oxygenation in the cortex and medulla of the kidney during Ang II-induced hypertension. Hypertension is a risk factor for chronic kidney disease when untreated. BOLD MRI can aid in monitoring renal oxygenation changes during hypertension and determine therapeutic interventions in humans.

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