Increased Arterial Stiffness does not Respond to Renal Denervation in an Animal Model of Secondary Hypertension

Yimin Yao1, Cara Hildreth1, Sheran Li1, Rochelle Boyd1, Zahra Kouchaki, Mark Butlin, Alberto P Avolio2, Paul M Pilowksy3, Jacqueline Kathleen Phillips4

  • 1Dept. of BioMedical Sciences, Faculty of Medicine and Health
  • 2Macquarie University
  • 3Heart Research Institute and University of Sydney
  • 4Faculty of Medicine and Health Sciences, Macquarie University

Details

15:05 - 15:20 | Wed 12 Jul | Greatbatch Room | WeBT11.4

Session: Pulse Transit Time/Arterial Stiffness

Abstract

Renal denervation is a novel device based therapy promoted to reduce high blood pressure. We examined the impact of renal denervation on systolic blood pressure, renal function, and arterial stiffness in the Lewis Polycystic Kidney disease (LPK) rodent model of kidney disease. Animals were subjected to bilateral renal denervation or sham surgeries at age 6 and 12 weeks. Systolic blood pressure was monitored by tail-cuff plethysmography and renal function by urinalysis and creatinine clearance. At age 16 weeks, beat-to-beat aortic pulse wave velocity as a functional indicator of arterial stiffness was determined. Renal denervation produced an overall reduction in blood pressure in the LPK [(denervated 164±4 vs. sham-operated 180±6 mmHg, n = 6 per group, P=0.003)] and delayed, but did not prevent, the decline in renal function. Aortic pulse wave velocity was markedly elevated in the LPK compared with Lewis and was not altered by renal denervation in the LPK however a reduction was seen in the control Lewis animals. These results support the hypothesis that renal nerves contribute to secondary hypertension in conditions such as kidney disease.