Temporal development of baroreceptor dysfunction in a rodent model of chronic kidney disease

Cara M. Hildreth*, Divya Sarma Kandukuri, Ann K. Goodchild, Jacqueline K. Phillips

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)


Altered autonomic control of the cardiovascular system in chronic kidney disease (CKD) contributes to an increased risk of cardiovascular events. The aim of the present study was to determine whether and when autonomic dysfunction occurs in a conscious, telemetered, rodent model of CKD. In Lewis polycystic kidney (LPK; n = 8) and Lewis (n = 8) rats, blood pressure (BP), heart rate (HR), HR variability (HRV), systolic BP variability (SBPV) and baroreflex sensitivity (BRS) were determined from 10 to 16 weeks of age. The LPK rats had higher systolic BP (average across all ages: 230 ± 10 vs 122.6 ± 0.3 mmHg; P < 0.001), increased SBPV (average across all ages: 13.9 ± 1.9 vs 5.2 ± 0.2 mmHg2; P < 0.01) and reduced low-frequency HRV power (average across all ages: 1.5 ± 0.3 vs 2.6 ± 0.2 msec2; P < 0.05). Between 10 and 12 weeks of age, SBPV increased twofold in the LPK rat (8.13 ± 1.05 vs 16.10 ± 1.31 mmHg2 for 10 vs 12 weeks of age, respectively; P < 0.001), coinciding with an approximate 40% reduction in BRS (1.32 ± 0.14 vs 0.79 ± 0.11 ms/mmHg for 10 vs 12 weeks of age, respectively; P < 0.05). There was no difference in BRS between LPK and Lewis rats at 10 weeks of age; however, from 12 weeks onwards, BRS was reduced in LPK rats (0.75 ± 0.01 vs 1.17 ± 0.04 ms/mmHg; P < 0.01). Baroreceptor regulation of HR becomes impaired between 10 and 12 weeks of age in the LPK rat, coinciding with an increase in SBPV. Preventing baroreflex dysfunction in CKD may reduce SBPV and the associated mortality risks.

Original languageEnglish
Pages (from-to)458-465
Number of pages8
JournalClinical and Experimental Pharmacology and Physiology
Issue number7
Publication statusPublished - Jul 2013

Fingerprint Dive into the research topics of 'Temporal development of baroreceptor dysfunction in a rodent model of chronic kidney disease'. Together they form a unique fingerprint.

Cite this