Abstract P051: Renal Denervation Normalizes Arterial Pressure but Has No Effect on Renal Inflammation or Glucose Metabolism in Obese Hypertensive C57bl6j Mice

Clinical studies have shown that renal denervation (RDNX) decreases arterial pressure (AP) and improves glucose metabolism in drug resistant obese hypertensive patients. In the present study, we used a murine model of obesity-induced hypertension (HTN) to test the hypothesis that RDNX lowers AP and improves glucose metabolism via an interaction of renal nerves with inflammatory mediators in the kidney. 8-week old C57Bl/6J mice were fed either a low fat diet (LFD; 10 KCal% from fat) or a high fat diet (HFD; 45 KCal% from fat) for 10 weeks. Two parallel protocols were conducted. In a metabolic protocol, body weight, food intake, body-composition and glucose metabolism were measured. In a cardiovascular protocol, radiotelemeters were implanted for measurement of AP. C57Bl6J mice on a HFD exhibited an inflammatory and metabolic syndrome phenotype including increase splenic and renal total T cells, increased fat mass, high blood pressure, hyperglycemia and glucose intolerance as compared to LFD mice. RDNX but not Sham surgery after 12 weeks of HFD normalized AP (116 ± 4 in sham vs. 97± 6 mmHg in RDX HFD mice). RDX had no effect on AP in LFD diet mice. RDX in obese hypertensive mice had no effect on renal T cells or cytokines. Finally, RDX had no effect on glucose metabolism in HFD mice as determined by the glucose tolerance test at 2 weeks after RDX. We conclude that the antihypertensive effect of RDX in obesity-induced hypertension is not associated with improvement in glucose metabolism or renal inflammation in the mouse. ![][1] [1]: /embed/graphic-1.gif